greenmedinfo--2020-11-21--Anti-inflammatory effects of persimmon in experimental rodent rheumatoid arthritis.

Persimmon ( L. ) fruits are used in traditional medicine largely due to their claimed beneficial effects on human health .
The aim of this work was to evaluate the anti-inflammatory activity of a persimmon extract in rats with collagen-induced arthritis ( CIA ) .
CIA was induced in Wistar rats through an intradermal injection of an emulsion of bovine type II collagen ( CII ) in complete Freund 's adjuvant ( FCA ) .
Macroscopic evidence of CIA first appeared as periarticular erythema and edema in the hind paws .
The incidence of CIA was 100 % by day @ @ @ @ @ @ @ the severity of CIA progressed for 35 days .
Radiographs revealed focal resorption of bone , with osteophyte formation in the tibiotarsal joint and soft tissue swelling .
The histopathologic features included erosion of the cartilage at the joint margins .
The persimmon extract showed an anti-inflammatory effect given the significant reduction in both the edema volume and radiological alterations attributed to CIA in the bone .
We demonstrate that the administration of persimmon extract attenuates the degree of chronic inflammation and tissue damage characteristic of CIA in rats , most probably by @ @ @ @ @ @ @ .

Persimmon (L.) fruits are used in traditional medicine largely due to their claimed beneficial effects on human health. The aim of this work was to evaluate the anti-inflammatory activity of a persimmon extract in rats with collagen-induced arthritis (CIA). CIA was induced in Wistar rats through an intradermal injection of an emulsion of bovine type II collagen (CII) in complete Freund's adjuvant (FCA). Macroscopic evidence of CIA first appeared as periarticular erythema and edema in the hind paws. The incidence of CIA was 100% by day 27 in the CII-challenged rats, and the severity of CIA progressed for 35 days. Radiographs revealed focal resorption of bone, with osteophyte formation in the tibiotarsal joint and soft tissue swelling. The histopathologic features included erosion of the cartilage at the joint margins. The persimmon extract showed an anti-inflammatory effect given the significant reduction in both the edema volume and radiological alterations attributed to CIA in the bone. We demonstrate that the administration of persimmon extract attenuates the degree of chronic inflammation and tissue damage characteristic of CIA in rats, most probably by the potent antioxidant characteristics of the extract.


greenmedinfo--2020-11-21--The intraocular pressure-lowering effect of persimmon leaves in a model of glaucoma.

The aim of this study was to evaluate the pharmacological efficacy of persimmon leaves in two glaucoma models , microbeads-induced @ @ @ @ @ and DBA/2 mouse .
Thus , we demonstrated that Ethanol Extract of Diospyros kaki ( @ @ @ @ @ pressure ( IOP ) in both mouse models of glaucoma by measurements with a tonometer @ @ @ @ @ revealed that retinal ganglion cell loss and optic nerve damage caused by IOP elevation were @ @ @ @ @ TUNEL assay , H & E staining , and fluorescent staining , while the expression @ @ @ @ @ sGCα-1 ) increased , when EEDK was administered , as revealed by western blot .
@ @ @ @ @ indicating functional scotopic vision was significantly improved in EEDK-administered DBA/2 mice during the 10-week follow-up @ @ @ @ @ electroretinography .
Collectively , our results suggested that EEDK could be an effective therapeutic and @ @ @ @ @ treating retinal degenerative diseases such as glaucoma .

The aim of this study was to evaluate the pharmacological efficacy of persimmon leaves in two glaucoma models, microbeads-induced ocular hypertension (OHT) and DBA/2 mouse. Thus, we demonstrated that Ethanol Extract of Diospyros kaki (EEDK) reduced elevated intraocular pressure (IOP) in both mouse models of glaucoma by measurements with a tonometer. In particular, we revealed that retinal ganglion cell loss and optic nerve damage caused by IOP elevation were markedly diminished as assessed by TUNEL assay, H&E staining, and fluorescent staining, while the expression of soluble guanylate cyclase (sGCα-1) increased, when EEDK was administered, as revealed by western blot. Moreover, the b-wave magnitude indicating functional scotopic vision was significantly improved in EEDK-administered DBA/2 mice during the 10-week follow-up study, as observed with electroretinography. Collectively, our results suggested that EEDK could be an effective therapeutic and IOP-lowering agent for preventing and treating retinal degenerative diseases such as glaucoma.


greenmedinfo--2020-11-21--Anti-inflammatory activities of astringent persimmons stalks of various cultivar types based on the

Anti-inflammatory activities of astringent persimmons stalks of various cultivar types based on the stages of maturity in the Gyeongnam province.

BACKGROUND : Natural products play a significant role in human health in relation to the prevention and treatment of inflammatory conditions .
One of the plants with great medicinal potentials is Diospyros kaki which is mainly cultivated in Asian countries including Korea , Japan , and China .
Astringent D. kaki is a wild species with an astringent taste until they are Ripened .
kaki calyx is a traditional Korean medicine ( TKM ) made from the stalks of astringent D. kaki and is used in treating bed-wetting , vomiting , and hiccupping .
The present study was designed to @ @ @ @ @ @ @ D. kaki stalks based on cultivar types and stages of maturity .
METHODS : The anti-inflammatory effects of the stalk extracts of local astringent D. kaki cultivar species were evaluated on RAW 264.7 cells .
Cell viability was measured using a Cell Counting Kit-8 ( CCK8 ) method .
The anti-inflammatory effects were determined by measuring the nitric oxide ( NO ) concentration of the supernatant .
Cellular signaling pathways were determined by quantitative polymerase chain reactions of inducible nitric oxide synthase ( iNOS ) .
Protein expression of iNOS and phospho-p65 was @ @ @ @ @ @ @ nuclear localization of p65 was determined using confocal imaging in RAW 264.7 cells .
RESULTS : We found that the stage 1 ( 8-9 month ) samples all showed a high percentage of tannic acid content and Gojongsi ( Hamyang ) stalks had the highest content .
The stage 1 samples also showed the highest inhibition of NO production .
Decreases in the expression of iNOS and phosphorylated p65 , and in the nuclear localization of p65 , were dose-dependent .
All the extracts were nontoxic under 100 μg/ml concentration .
CONCLUSION : @ @ @ @ @ @ @ in tannic acid content in astringent D. kaki and their anti-inflammatory effects , in relation to their stage of maturity .
These results are expected to be useful in the verification of the efficacy of oriental medicine and the timing of proper harvest for medical use .

BACKGROUND: Natural products play a significant role in human health in relation to the prevention and treatment of inflammatory conditions. One of the plants with great medicinal potentials is Diospyros kaki which is mainly cultivated in Asian countries including Korea, Japan, and China. Astringent D. kaki is a wild species with an astringent taste until they are Ripened. kaki calyx is a traditional Korean medicine (TKM) made from the stalks of astringent D. kaki and is used in treating bed-wetting, vomiting, and hiccupping. The present study was designed to investigate the potential anti-inflammatory activities of astringent D. kaki stalks based on cultivar types and stages of maturity.
METHODS: The anti-inflammatory effects of the stalk extracts of local astringent D. kaki cultivar species were evaluated on RAW 264.7 cells. Cell viability was measured using a Cell Counting Kit-8 (CCK8) method. The anti-inflammatory effects were determined by measuring the nitric oxide (NO) concentration of the supernatant. Cellular signaling pathways were determined by quantitative polymerase chain reactions of inducible nitric oxide synthase (iNOS). Protein expression of iNOS and phospho-p65 was determined using western blot, and the nuclear localization of p65 was determined using confocal imaging in RAW 264.7 cells.
RESULTS: We found that the stage 1 (8-9 month) samples all showed a high percentage of tannic acid content and Gojongsi (Hamyang) stalks had the highest content. The stage 1 samples also showed the highest inhibition of NO production. Decreases in the expression of iNOS and phosphorylated p65, and in the nuclear localization of p65, were dose-dependent. All the extracts were nontoxic under 100 μg/ml concentration.
CONCLUSION: This study provides insight into the changes in tannic acid content in astringent D. kaki and their anti-inflammatory effects, in relation to their stage of maturity. These results are expected to be useful in the verification of the efficacy of oriental medicine and the timing of proper harvest for medical use.


greenmedinfo--2020-11-21--Anti-obesity effect of fermented persimmon extracts via activation of AMP-activated protein kinase.

There is significant cultivation of persimmon ( Diospyros kaki ) in East Asia , a plant whose fruit has abundant @ @ @ @ @ polyphenols , and dietary fiber .
Persimmon dietary supplements can benefit health by amelioration of @ @ @ @ @ and obesity .
There are also persimmon-based beverages produced via fermentation , such as wines @ @ @ @ @ consumption of these products in East Asia .
Although there is great interest in functional @ @ @ @ @ of fermented persimmon extract ( FPE ) are completely unknown .
We examined the effects @ @ @ @ @ parameters of mice fed a high-fat diet ( HFD ) .
Our results indicated that @ @ @ @ @ approx .
15 % reduction of body weight , reduced abdominal and liver fat , @ @ @ @ @ triglycerides , total cholesterol , and glucose .
FPE also blocked the differentiation of murine @ @ @ @ @ adipocytes .
We suggest that gallic acid is a major bioactive component of FPE , @ @ @ @ @ mediates the beneficial effects of FPE and gallic acid .

There is significant cultivation of persimmon (Diospyros kaki) in East Asia, a plant whose fruit has abundant nutrients, including vitamins, polyphenols, and dietary fiber. Persimmon dietary supplements can benefit health by amelioration of diabetes, cardiovascular disease, and obesity. There are also persimmon-based beverages produced via fermentation, such as wines and vinegars, and increasing consumption of these products in East Asia. Although there is great interest in functional foods, the health effects of fermented persimmon extract (FPE) are completely unknown. We examined the effects of FPE on the metabolic parameters of mice fed a high-fat diet (HFD). Our results indicated that FPE supplementation led to an approx. 15% reduction of body weight, reduced abdominal and liver fat, and reduced serum levels of triglycerides, total cholesterol, and glucose. FPE also blocked the differentiation of murine 3T3-L1 pre-adipocyte cells into mature adipocytes. We suggest that gallic acid is a major bioactive component of FPE, and that AMP-activated protein kinase mediates the beneficial effects of FPE and gallic acid.


greenmedinfo--2020-11-21--Diospyros kaki leaves inhibit HGF/Met signaling-mediated EMT and stemness features in hepatocellular

Diospyros kaki leaves inhibit HGF/Met signaling-mediated EMT and stemness features in hepatocellular carcinoma.

Persimmon ( Diospyros kaki L.f. ) trees are widely cultivated for their edible fruits in Asia .
D. kaki leaves are abundant in phytochemicals that have numerous medicinal properties .
Hepatocyte growth factor ( HGF ) and its receptor Met lead to poor prognosis via the promotion of metastasis and chemoresistance in hepatocellular carcinoma ( HCC ) .
Therefore , inhibitors targeting the HGF/Met pathway are regarded as promising drugs against HCC .
Here , we investigated the effects of D. kaki leaves on HGF-induced epithelial-to-mesenchymal transition ( EMT ) and stemness traits in HCC .
The ethanol extract of @ @ @ @ @ @ @ suppressed HGF-mediated cell migration and invasion through upregulation of CDH1 and downregulation of SNAI1 , VIM , MMP1 , MMP2 , and MMP9 .
Moreover , EEDK increased the cytotoxicity of sorafenib , which was reduced by HGF , and decreased the expression of the stemness markers KRT19 and CD44 .
Additionally , we found a clear correlation between stemness and EMT markers in HCC patients .
Importantly , EEDK reduced Met activity and attenuated HGF-mediated activation of JNK/c-Jun .
Our findings provide new evidence that EEDK can ameliorate HCC with poor prognosis @ @ @ @ @ @ @ .

Persimmon (Diospyros kaki L.f.) trees are widely cultivated for their edible fruits in Asia. D. kaki leaves are abundant in phytochemicals that have numerous medicinal properties. Hepatocyte growth factor (HGF) and its receptor Met lead to poor prognosis via the promotion of metastasis and chemoresistance in hepatocellular carcinoma (HCC). Therefore, inhibitors targeting the HGF/Met pathway are regarded as promising drugs against HCC. Here, we investigated the effects of D. kaki leaves on HGF-induced epithelial-to-mesenchymal transition (EMT) and stemness traits in HCC. The ethanol extract of D. kaki leaves (EEDK) markedly suppressed HGF-mediated cell migration and invasion through upregulation of CDH1 and downregulation of SNAI1, VIM, MMP1, MMP2, and MMP9. Moreover, EEDK increased the cytotoxicity of sorafenib, which was reduced by HGF, and decreased the expression of the stemness markers KRT19 and CD44. Additionally, we found a clear correlation between stemness and EMT markers in HCC patients. Importantly, EEDK reduced Met activity and attenuated HGF-mediated activation of JNK/c-Jun. Our findings provide new evidence that EEDK can ameliorate HCC with poor prognosis and aggressive phenotype by blocking HGF/Met signaling.


greenmedinfo--2020-11-21--Polysaccharide isolated from persimmon leaves suppresses TGF-β1-induced epithelial-to-mesenchymal tr

Polysaccharide isolated from persimmon leaves suppresses TGF-β1-induced epithelial-to-mesenchymal transition in A549 cells.

In the present study , to verify the effect of polysaccharides derived from persimmon leaves ( PLE ) at epithelial-to-mesenchymal @ @ @ @ @ A549 cells were treated with TGF-β1 alone or co-treated with TGF-β1 and PLE ( 50 @ @ @ @ @ PLE-treated cells showed higher expression of E-cadherin and lower expression of N-cadherin and vimentin compared @ @ @ @ @ the levels of transcription factors , including Snail , Slug , and ZEB1 , all @ @ @ @ @ also significantly decreased migration , invasion , and anoikis resistance through TGF-β1 mediated EMT suppression @ @ @ @ @ levels of MMP-2 and MMP-9 while cleaving PARP .
These inhibitory effects of PLE against @ @ @ @ @ , and anoikis resistance weredetermined by activating the canonical SMAD2/3 and non-canonical ERK/p38 signaling pathways @ @ @ @ @ suggest that PLE could be used as a potential chemical therapeutic agent for early metastasis @ @ @ @ @ .

In the present study, to verify the effect of polysaccharides derived from persimmon leaves (PLE) at epithelial-to-mesenchymal transition (EMT), A549 cells were treated with TGF-β1 alone or co-treated with TGF-β1 and PLE (50 and 75 μg/mL). PLE-treated cells showed higher expression of E-cadherin and lower expression of N-cadherin and vimentin compared to TGF-β1-treated cells by inhibiting the levels of transcription factors, including Snail, Slug, and ZEB1, all associated with EMT. PLE also significantly decreased migration, invasion, and anoikis resistance through TGF-β1 mediated EMT suppression, whereby PLE inhibited the levels of MMP-2 and MMP-9 while cleaving PARP. These inhibitory effects of PLE against EMT, migration, invasion, and anoikis resistance weredetermined by activating the canonical SMAD2/3 and non-canonical ERK/p38 signaling pathways. Therefore, these results suggest that PLE could be used as a potential chemical therapeutic agent for early metastasis of lung cancer in vitro.


greenmedinfo--2020-11-21--Total flavonoids isolated from Diospyros kaki leaves induced apoptosis and oxidative stress in human

Total flavonoids isolated from Diospyros kaki leaves induced apoptosis and oxidative stress in human cancer cells.

BACKGROUND/AIM : Persimmon ( Diospyros kaki L. ) leaves are popular as a tea infusion in Asia and their main @ @ @ @ @ The present study aimed to explore the anticancer properties of flavonoids isolated from persimmon leaves @ @ @ @ @ AND METHODS : We investigated the in vitro anti-proliferative activity of PLF against several human @ @ @ @ @ and intracellular reactive oxygen species ( ROS ) induced by PLF were accessed using high-content @ @ @ @ @ The ability of PLF to scavenge free radicals was evaluated by 2,2-diphenyl-1-picrylhydrazyl ( DPPH ) @ @ @ @ @ demonstrated significant inhibition of proliferation of liver , breast , and colorectal cancer cells in @ @ @ @ @ and increased intracellular ROS levels in HCT116 ( colorectal cancer ) and HepG2 ( liver @ @ @ @ @ addition , PLF showed strong free radical scavenging ability .
CONCLUSION : The anti-proliferation activity @ @ @ @ @ was related to the induction of apoptosis and oxidative stress .

BACKGROUND/AIM: Persimmon (Diospyros kaki L.) leaves are popular as a tea infusion in Asia and their main active ingredients are flavonoids. The present study aimed to explore the anticancer properties of flavonoids isolated from persimmon leaves (PLF).
MATERIALS AND METHODS: We investigated the in vitro anti-proliferative activity of PLF against several human cancer cell lines. Apoptosis and intracellular reactive oxygen species (ROS) induced by PLF were accessed using high-content analysis with florescent staining. The ability of PLF to scavenge free radicals was evaluated by 2,2-diphenyl-1-picrylhydrazyl (DPPH) assay.
RESULTS: PLF demonstrated significant inhibition of proliferation of liver, breast, and colorectal cancer cells in vitro. PLF induced apoptosis and increased intracellular ROS levels in HCT116 (colorectal cancer) and HepG2 (liver cancer) cells. In addition, PLF showed strong free radical scavenging ability.
CONCLUSION: The anti-proliferation activity of PLF against cancer cells was related to the induction of apoptosis and oxidative stress.


greenmedinfo--2020-11-21--Anti-cancer potential of persimmon leaves via the PDGFR-Rac-JNK pathway.

Persimmon leaves are known to have some beneficial effects , including ROS elimination , lipid circulation , and neuronal protection @ @ @ @ @ properties and the underlying mechanisms remain unclear .
Herein , we show that treatment with @ @ @ @ @ , Diospyros kaki , leaves ( EEDK ) induces cancer cell death and inhibits cell @ @ @ @ @ energy transfer ( FRET ) technology with genetically-encoded biosensors , we first found that EEDK @ @ @ @ @ in live cells .
Moreover , we found that downstream of the PDGFR-Rac pathway , @ @ @ @ @ .
In contrast , JNK-downstream inhibitors , such as CoCl2 , T-5224 , and pepstatin @ @ @ @ @ death .
Thus , we illustrate that the PDGFR-Rac-JNK signaling axis is triggered by EEDK @ @ @ @ @ death , suggesting the extract of persimmon leaves may be a promising anti-cancer agent .

Persimmon leaves are known to have some beneficial effects, including ROS elimination, lipid circulation, and neuronal protection. However, their anti-cancer properties and the underlying mechanisms remain unclear. Herein, we show that treatment with the ethanol extract of persimmon, Diospyros kaki, leaves (EEDK) induces cancer cell death and inhibits cell proliferation. Using fluorescence resonance energy transfer (FRET) technology with genetically-encoded biosensors, we first found that EEDK stimulates a PDGFR-Rac signaling cascade in live cells. Moreover, we found that downstream of the PDGFR-Rac pathway, JNKs are activated by EEDK. In contrast, JNK-downstream inhibitors, such as CoCl2, T-5224, and pepstatin A, attenuated EEDK-induced cell death. Thus, we illustrate that the PDGFR-Rac-JNK signaling axis is triggered by EEDK, leading to cancer cell death, suggesting the extract of persimmon leaves may be a promising anti-cancer agent.


greenmedinfo--2020-11-21--Persimmon oligomeric proanthocyanidins alleviate ultraviolet B-induced skin damage by regulating oxi

Persimmon oligomeric proanthocyanidins alleviate ultraviolet B-induced skin damage by regulating oxidative stress and inflammatory responses.

Skin damage can be induced by excessive ultraviolet B ( UV-B ) irradiation .
This study aimed to investigate the @ @ @ @ @ oligo-proanthocyanidins ( P-OPC ) against UV-B induced human keratinocyte cells ( HaCaT cells ) and @ @ @ @ @ mechanismsand .
P-OPC was shown to inhibit the production of intracellular reactive oxygen species ( @ @ @ @ @ radiation in both HaCaT cells and mouse skin tissues by increasing the activity of the @ @ @ @ @ dismutase ( SOD ) , glutathione peroxidase ( GSH-Px ) , and glutathione ( GSH @ @ @ @ @ P-OPC was found to suppress cell apoptosis and the production of inflammatory cytokines , TNF-α @ @ @ @ @ , P-OPC could protect skin tissues from UV-B-induced damage by suppressing oxidant stress , acute @ @ @ @ @ MAPK and NF-κB signalling pathways .
These results indicate the potential of P-OPC as a @ @ @ @ @ skin damage .

Skin damage can be induced by excessive ultraviolet B (UV-B) irradiation. This study aimed to investigate the potential protective activity of persimmon oligo-proanthocyanidins (P-OPC) against UV-B induced human keratinocyte cells (HaCaT cells) and skin damage and its underlying mechanismsand. P-OPC was shown to inhibit the production of intracellular reactive oxygen species (ROS) induced by UVB radiation in both HaCaT cells and mouse skin tissues by increasing the activity of the antioxidant enzyme system [superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and glutathione (GSH)]. Furthermore, P-OPC was found to suppress cell apoptosis and the production of inflammatory cytokines, TNF-α, and IL-6. Overall, P-OPC could protect skin tissues from UV-B-induced damage by suppressing oxidant stress, acute inflammation, and cell apoptosisregulating MAPK and NF-κB signalling pathways. These results indicate the potential of P-OPC as a photochemo-protective agent against UV-B induced skin damage.


greenmedinfo--2020-11-21--Antioxidant and α-glucosidase inhibitory capacity of nonextractable polyphenols in Mopan persimmon.

This study was to evaluate and compare the polyphenols contents , antioxidant capacities , andα-glucosidase inhibitory abilities of extractable and @ @ @ @ @ NEP ) in Mopan persimmon .
The results showed that total phenols content of NEP @ @ @ @ @ that of EP , and the hydrolyzed NEP compounds displayed higher antioxidant capacity than EP @ @ @ @ @ ORAC assays .
Meanwhile , NEP also exhibited inhibition capacity of α-glucosidase and were higher @ @ @ @ @ In addition , an in vitro model of gastrointestinal digestion was used for the release @ @ @ @ @ content and ORAC values were obviously increased in gastric digestionstage .
The result indicated that @ @ @ @ @ which has often been overlooked and discarded in the past , possessed higher polyphenols content @ @ @ @ @ .

This study was to evaluate and compare the polyphenols contents, antioxidant capacities, andα-glucosidase inhibitory abilities of extractable and nonextractable polyphenols (EP and NEP) in Mopan persimmon. The results showed that total phenols content of NEP was 5 times higher than that of EP, and the hydrolyzed NEP compounds displayed higher antioxidant capacity than EP in vitro by DPPH,ORAC assays. Meanwhile, NEP also exhibited inhibition capacity of α-glucosidase and were higher than that of acarbose. In addition, an in vitro model of gastrointestinal digestion was used for the release of NEP, the polyphenols content and ORAC values were obviously increased in gastric digestionstage. The result indicated that NEP in Mopan persimmon, which has often been overlooked and discarded in the past, possessed higher polyphenols content and antioxidant capacity than EP.


greenmedinfo--2020-11-21--Diospyros mespiliformis and M. whitei show antimalarial effects against resistant Plasmodium berghei

Diospyros mespiliformis and M. whitei show antimalarial effects against resistant Plasmodium berghei infection.

ETHNOPHARMACOLOGICAL RELEVANCE : Diospyros mespiliformis Hochst .
ex A. DC .
and Mondia whitei ( Hook.f . )
Skeels are traditionally used in Africa for the treatment of malaria .
However , scientific evidence to substantiate this folkloric claim and their effects on liver mitochondria during malaria treatment have not been reported .
AIM OF THE STUDY : This study investigated the efficacy of D. mespiliformis and M. whitei against chloroquine-sensitive and resistant strains of malarial parasites in mice .
It also investigated the toxicity and protection against cellular organelles like mitochondria .
MATERIALS AND METHODS : Male Swiss mice @ @ @ @ @ @ @ ANKA ) strain of Plasmodium berghei and were treated via oral gavage with methanol extracts of D. mespiliformis and M. whitei reconstituted in dimethylsulfoxide as vehicle ( DMSO , 5 % v/v ) for five consecutive days .
Percentage parasite load and clearance were assessed by microscopy .
The infected control was treated with the vehicle .
Hematological indices were assessed using standard procedures .
Alanine aminotransferase ( ALT ) , aspartate aminotransferase ( AST ) and alkaline phosphatase ( ALP ) were determined using assay kits .
Hepatic mitochondria were isolated via @ @ @ @ @ @ @ mPT ) , ATPase ( mATPase ) activity and lipid peroxidation ( mLPO ) were determined spectroscopically .
Liver tissue histology was carried out by standard laboratory procedures .
Phytochemical analysis of both extracts were performed using LC-MS to identify the most prominent compounds from each of the extracts .
RESULTS : After treatment on day 5 , D. mespiliformis and M. whitei at 400 mg/kg decreased mean values for : percentage parasitemia ( 5.0±1.0 , 2.0±0.2 ) , increased Packed Cell Volume ( PCV ) ( 36.0±1.4 , 36.0±0.0 % ) and @ @ @ @ @ @ @ ) relative to the untreated control ( 20.0±5.2 ; 30.0±0.0 % ; 1.4±1.4X10mm , respectively ) .
At the same dose , D. mespiliformis and M. whitei decreased ALT ( 8.0±3.8 , 24.2±4.0U/L ) , AST ( 6.2±0.8 , 8.0±0.9U/L ) and ALP ( 56.0±0.7 , 51.0± 1.0U/L ) activities compared to the infected control ( 77.0±10.9U/L , 14.0±0.7U/L and 76.0±6.0U/L , respectively ) .
Both D. mespiliformis and M. whitei reversed mPT opening , decreased mATPase enhancement and mLPO , relative tothe control .
Histopathology of the liver showed extensive hemorrhagic lesions @ @ @ @ @ @ @ control while both D. mespiliformis and M. whitei were well tolerated at the highest dose .
The LC-MS analysis of D. mespiliformis showed the presence of betulinic acid , tocopherol and kaempferol with antimalarial and antioxidant properties while the M. whitei sample contained coumarin and chlorogenic acid that have antimalarial and hepato-protective properties .
CONCLUSIONS : Diospyros mespiliformis and M. whitei show antimalarial effects against resistant Plasmodium berghei infection , enhanced cell viability , mito-protection and are not toxic in mice .

ETHNOPHARMACOLOGICAL RELEVANCE: Diospyros mespiliformis Hochst. ex A. DC. and Mondia whitei (Hook.f.) Skeels are traditionally used in Africa for the treatment of malaria. However, scientific evidence to substantiate this folkloric claim and their effects on liver mitochondria during malaria treatment have not been reported.
AIM OF THE STUDY: This study investigated the efficacy of D. mespiliformis and M. whitei against chloroquine-sensitive and resistant strains of malarial parasites in mice. It also investigated the toxicity and protection against cellular organelles like mitochondria.
MATERIALS AND METHODS: Male Swiss mice were infected with a chloroquine resistant (ANKA) strain of Plasmodium berghei and were treated via oral gavage with methanol extracts of D. mespiliformis and M. whitei reconstituted in dimethylsulfoxide as vehicle (DMSO, 5% v/v) for five consecutive days. Percentage parasite load and clearance were assessed by microscopy. The infected control was treated with the vehicle. Hematological indices were assessed using standard procedures. Alanine aminotransferase (ALT), aspartate aminotransferase (AST) and alkaline phosphatase (ALP) were determined using assay kits. Hepatic mitochondria were isolated via centrifugation, and their permeability transition (mPT), ATPase (mATPase) activity and lipid peroxidation (mLPO) were determined spectroscopically. Liver tissue histology was carried out by standard laboratory procedures. Phytochemical analysis of both extracts were performed using LC-MS to identify the most prominent compounds from each of the extracts.
RESULTS: After treatment on day 5, D. mespiliformis and M. whitei at 400 mg/kg decreased mean values for: percentage parasitemia (5.0±1.0, 2.0±0.2), increased Packed Cell Volume (PCV) (36.0±1.4, 36.0±0.0%) and platelets (2.0±1.4, 2.0±2.8 X 10mm) relative to the untreated control (20.0±5.2; 30.0±0.0%; 1.4±1.4X10mm, respectively). At the same dose, D. mespiliformis and M. whitei decreased ALT (8.0±3.8, 24.2±4.0U/L), AST (6.2±0.8, 8.0±0.9U/L) and ALP (56.0±0.7, 51.0± 1.0U/L) activities compared to the infected control (77.0±10.9U/L, 14.0±0.7U/L and 76.0±6.0U/L, respectively). Both D. mespiliformis and M. whitei reversed mPT opening, decreased mATPase enhancement and mLPO, relative tothe control. Histopathology of the liver showed extensive hemorrhagic lesions and severe disseminated congestion in the infected control while both D. mespiliformis and M. whitei were well tolerated at the highest dose. The LC-MS analysis of D. mespiliformis showed the presence of betulinic acid, tocopherol and kaempferol with antimalarial and antioxidant properties while the M. whitei sample contained coumarin and chlorogenic acid that have antimalarial and hepato-protective properties.
CONCLUSIONS: Diospyros mespiliformis and M. whitei show antimalarial effects against resistant Plasmodium berghei infection, enhanced cell viability, mito-protection and are not toxic in mice.


greenmedinfo--2020-11-21--Apple polyphenols extract alleviated dextran sulfate sodium-induced ulcerative colitis.

To investigate and compare the preventive effects of apple polyphenols extract ( APE ) with phloretin on dextran sulfate sodium ( DSS ) -induced ulcerative colitis ( UC ) , 60 male mice were treated with 125 or 500 mg/ ( kg bw d ) APE or 100 mg/ ( kg bw d ) phloretin , the single-ingredient of APE , for continuous 3 weeks by intragastric administration , meanwhile , mice were provided with 3 % DSS dissolved in drinking water to induce UC during the third week .
Both APE and phloretin significantly ameliorated DSS-induced UC by inhibiting @ @ @ @ @ @ @ and mucosa damage .
Except the same mechanisms of the inhibited activation of NF-κB signaling , decreased hyodeoxycholic acid level and increased abundance of Verrucomicrobia at phylum and Bacteroides and Akkermansia at genus , APE increased β-muricholic acid level and decreased Bacterodetes abundance , while phloretin decreased Firmicutes abundance .
Furthermore , APE treatment showed much lower disease activity index score , less body weight loss and lighter spleen than phloretin .
Thus , our study supported the potentiality of APE as a promising dietary intervention for the prevention of experimental UC .

To investigate and compare the preventive effects of apple polyphenols extract (APE) with phloretin on dextran sulfate sodium (DSS)-induced ulcerative colitis (UC), 60 male mice were treated with 125 or 500 mg/(kg bw d) APE or 100 mg/(kg bw d) phloretin, the single-ingredient of APE, for continuous 3 weeks by intragastric administration, meanwhile, mice were provided with 3% DSS dissolved in drinking water to induce UC during the third week. Both APE and phloretin significantly ameliorated DSS-induced UC by inhibiting body weight loss, preventing colon shortening and mucosa damage. Except the same mechanisms of the inhibited activation of NF-κB signaling, decreased hyodeoxycholic acid level and increased abundance of Verrucomicrobia at phylum and Bacteroides and Akkermansia at genus, APE increased β-muricholic acid level and decreased Bacterodetes abundance, while phloretin decreased Firmicutes abundance. Furthermore, APE treatment showed much lower disease activity index score, less body weight loss and lighter spleen than phloretin. Thus, our study supported the potentiality of APE as a promising dietary intervention for the prevention of experimental UC.


greenmedinfo--2020-11-23--Galangin ameliorated pulmonary fibrosis in vivo and in vitro by regulating epithelial-mesenchymal tr

Galangin ameliorated pulmonary fibrosis in vivo and in vitro by regulating epithelial-mesenchymal transition.

Pulmonary fibrosis ( PF ) is a disease that is characterized by abnormal epithelial-mesenchymal transition ( EMT ) and persistent inflammatory injury , with high mortality and poor prognosis , but the current therapies are accompanied by certain adverse side effects .
In this study , we investigated the role of galangin ( GA ) , an anti-inflammatory and anti-tumoral phytochemical extracted from galangal , in preventing and curing bleomycin ( BLM ) -induced pulmonary fibrosis and the underlying mechanism .
Histopathological staining confirmed that GA dramatically moderated bleomycin-induced pulmonary fibrosis in mice .
Compared with the vehicle treatment , @ @ @ @ @ @ @ and increased the expression of E-cadherin .
The expression ofα-Smooth muscle actin ( α-SMA ) , which is a myofibroblast marker , was also suppressed .
In addition , GA diminished the increase in the numbers of CD4CD69and CD8CD69T cells and dendritic cells induced by bleomycin , and reduced the residence of inflammatory cells in the lung tissues .
Notably , GA inhibited the TGF-β1-induced EMT and fibroblast differentiation in vitro , which further confirmed the potential protective effect of GA on pulmonary fibrosis .
Taken together , our results suggest that GA @ @ @ @ @ @ @ fibrosis by attenuating EMT and inflammatory damage andmay have prevent potential of pulmonary fibrosis .

Pulmonary fibrosis (PF) is a disease that is characterized by abnormal epithelial-mesenchymal transition (EMT) and persistent inflammatory injury, with high mortality and poor prognosis, but the current therapies are accompanied by certain adverse side effects. In this study, we investigated the role of galangin (GA), an anti-inflammatory and anti-tumoral phytochemical extracted from galangal, in preventing and curing bleomycin (BLM)-induced pulmonary fibrosis and the underlying mechanism. Histopathological staining confirmed that GA dramatically moderated bleomycin-induced pulmonary fibrosis in mice. Compared with the vehicle treatment, GA treatment inhibited the expression of vimentin and increased the expression of E-cadherin. The expression ofα-Smooth muscle actin (α-SMA), which is a myofibroblast marker, was also suppressed. In addition, GA diminished the increase in the numbers of CD4CD69and CD8CD69T cells and dendritic cells induced by bleomycin, and reduced the residence of inflammatory cells in the lung tissues. Notably, GA inhibited the TGF-β1-induced EMT and fibroblast differentiation in vitro, which further confirmed the potential protective effect of GA on pulmonary fibrosis. Taken together, our results suggest that GA exerts a beneficial effect on bleomycin-induced pulmonary fibrosis by attenuating EMT and inflammatory damage andmay have prevent potential of pulmonary fibrosis.


greenmedinfo--2020-11-22--Galangin suppresses proliferation, migration, and invasion of human glioblastoma cells.

Background : Galangin ( GLN ) , a pure natural flavonoid compound found in plants , has been shown to exert anti-cancer effects against multiple cancer types , including glioma .
However , its underlying molecular mechanism remains unclear .
Epithelial-to-mesenchymal transition ( EMT ) performs an important function in the genesis and development of cancer .
Skp2 , a pivotal component of SCFE3 ubiquitin ligase , has been shown to function as an oncogene in GBM invasion that contributes to the EMT process .
Thus , we explored whether GLN inhibited Skp2-mediated EMT and the mechanism underlying the Skp2 @ @ @ @ @ @ @ , wound healing assay and transwell assay were used to examine cell proliferation , migration , and invasion after treatment with or without GLN .
RT-PCR and Western blotting analysis were performed to evaluate mRNA and protein expression , respectively .
Co-immunoprecipitation was conducted to detect ubiquitinated Skp2 levels in vitro and in vivo after GLN treatment .
Bioluminescence imaging was performed to examine the intracranial tumor size of U87 xenograft mice .
Microscale thermophoresis ( MST ) experiment was used to detect interactions between Skp2 and GLN .
Results : GLN suppressed @ @ @ @ @ @ @ invasion , and also downregulated the expression of Skp2 and mesenchymal markers ( Zeb1 , N-cadherin , snail , vimentin ) in vitro .
Moreover , the overexpression of Skp2 in GBM cells decreased the effect of GLN on EMT .
Furthermore , we demonstrated that GLN degraded skp2 protein through the ubiquitination proteasome pathway and directly interacted with skp2 protein , as shown through the MST assay .
Conclusion : This study is the first to identify Skp2 as a novel target of GLN for the treatment of GBM and report of @ @ @ @ @ @ @ pathway .
Results from our study indicated the potential of GLN for the treatment of GBM through ubiquitin-mediated degradation of Skp2 .

Background: Galangin (GLN), a pure natural flavonoid compound found in plants, has been shown to exert anti-cancer effects against multiple cancer types, including glioma. However, its underlying molecular mechanism remains unclear. Epithelial-to-mesenchymal transition (EMT) performs an important function in the genesis and development of cancer. Skp2, a pivotal component of SCFE3 ubiquitin ligase, has been shown to function as an oncogene in GBM invasion that contributes to the EMT process. Thus, we explored whether GLN inhibited Skp2-mediated EMT and the mechanism underlying the Skp2 degradation pathway.
Methods: CCK-8 assay, wound healing assay and transwell assay were used to examine cell proliferation, migration, and invasion after treatment with or without GLN. RT-PCR and Western blotting analysis were performed to evaluate mRNA and protein expression, respectively. Co-immunoprecipitation was conducted to detect ubiquitinated Skp2 levels in vitro and in vivo after GLN treatment. Bioluminescence imaging was performed to examine the intracranial tumor size of U87 xenograft mice. Microscale thermophoresis (MST) experiment was used to detect interactions between Skp2 and GLN.
Results: GLN suppressed GBM cell growth, migration, and invasion, and also downregulated the expression of Skp2 and mesenchymal markers (Zeb1, N-cadherin, snail, vimentin) in vitro. Moreover, the overexpression of Skp2 in GBM cells decreased the effect of GLN on EMT. Furthermore, we demonstrated that GLN degraded skp2 protein through the ubiquitination proteasome pathway and directly interacted with skp2 protein, as shown through the MST assay.
Conclusion: This study is the first to identify Skp2 as a novel target of GLN for the treatment of GBM and report of Skp2 protein degradation in a ubiquitination proteasome pathway. Results from our study indicated the potential of GLN for the treatment of GBM through ubiquitin-mediated degradation of Skp2.


greenmedinfo--2020-11-22--Genipin enhances the antitumor effect of elesclomol in A549 lung cancer cells.

The uncoupling protein-2 ( UCP2 ) serves a role in tumor aggressiveness and anticancer resistance , which is considered to be associated with its ability to attenuate reactive oxygen species ( ROS ) production .
We hypothesized that UCP2 may protect cancer cells from elesclomol-induced cytotoxicity , and that this may be overcome by blocking UCP2 function with genipin .
In A549 lung cancer cells that exhibited high UCP2 expression , treatment with elesclomol alone induced limited changes in glucose uptake , ROS production and cell survival .
By contrast , both UCP2 knockdown and genipin treatment mildly reduced glucose @ @ @ @ @ @ @ cell survival .
Combining genipin and elesclomol further reduced glucose uptake and increased cellular and mitochondrial ROS production .
Moreover , co-treatment with genipin and elesclomol reduced the colony forming capacity to 50.6±7.4 % and the cell survival to 42.0±3.4 % of that in the control cells ( both P < 0.001 ) .
Suppression of cell survival by treatment with elesclomol and genipin was enhanced in the presence of an exogenous ROS inducer and attenuated by a ROS scavenger .
The cytotoxic effects of combining genipin and elesclomol were accompanied by reduced @ @ @ @ @ @ @ as demonstrated by Annexin V assay and increased protein cleavage of PARP and caspase-3 .
Finally , in an A549×enograft mouse model , tumor growth was only modestly retarded by treatment with elesclomol or genipin alone , but was markedly suppressed by combining the two drugs compared with that in the control group ( P=0.008 ) .
Therefore , high UCP2 expression may limit the antitumor effect of elesclomol by attenuating ROS responses , and this may be overcome by co-treatment with genipin ; combining elesclomol and genipin may be an effective strategy @ @ @ @ @ @ @

The uncoupling protein-2 (UCP2) serves a role in tumor aggressiveness and anticancer resistance, which is considered to be associated with its ability to attenuate reactive oxygen species (ROS) production. We hypothesized that UCP2 may protect cancer cells from elesclomol-induced cytotoxicity, and that this may be overcome by blocking UCP2 function with genipin. In A549 lung cancer cells that exhibited high UCP2 expression, treatment with elesclomol alone induced limited changes in glucose uptake, ROS production and cell survival. By contrast, both UCP2 knockdown and genipin treatment mildly reduced glucose uptake, increased ROS production and decreased cell survival. Combining genipin and elesclomol further reduced glucose uptake and increased cellular and mitochondrial ROS production. Moreover, co-treatment with genipin and elesclomol reduced the colony forming capacity to 50.6±7.4% and the cell survival to 42.0±3.4% of that in the control cells (both P<0.001). Suppression of cell survival by treatment with elesclomol and genipin was enhanced in the presence of an exogenous ROS inducer and attenuated by a ROS scavenger. The cytotoxic effects of combining genipin and elesclomol were accompanied by reduced mitochondrial membrane potential and occurred through apoptosis as demonstrated by Annexin V assay and increased protein cleavage of PARP and caspase-3. Finally, in an A549×enograft mouse model, tumor growth was only modestly retarded by treatment with elesclomol or genipin alone, but was markedly suppressed by combining the two drugs compared with that in the control group (P=0.008). Therefore, high UCP2 expression may limit the antitumor effect of elesclomol by attenuating ROS responses, and this may be overcome by co-treatment with genipin; combining elesclomol and genipin may be an effective strategy for treating cancers with high UCP2.


greenmedinfo--2020-11-22--Galangin attenuated cerebral ischemia-reperfusion injury.

AIMS : To evaluate the impact of galangin treatment on cerebral ischemia-reperfusion ( I/R ) injury in gerbils and to identify potential mechanisms of the protective effect of galangin on hippocampal neurons after I/R injury .
PRINCIPAL METHODS : A cerebral ischemia model using bilateral common carotid artery ligation in gerbils was established .
The Morris water maze ( MWM ) test was used to evaluate the learning and memory ability of gerbils .
The cell viability was evaluated with an MTT assay .
The levels of lipid peroxide biomarkers were measured to estimate the injury due to lipid peroxide @ @ @ @ @ @ @ micrography , immunofluorescence and Nissl staining .
Western blot and quantitative real-time polymerase chain reaction ( qRT-PCR ) were used to measure the molecular characteristics .
KEY FINDINGS : In the MWM , gerbils treated with galangin after I/R injury showed significant improvements in learning and memory .
In addition , galangin treatment reduced the levels of lipid peroxide in the brains of gerbils that underwent I/R as well as reduced the amount of cell death and increased the expression of SLC7A11 and glutathione peroxidase 4 ( GPX4 ) .
Furthermore , the @ @ @ @ @ @ @ decreased in galangin-treated gerbils , and the effect of galangin was weakened when SLC7A11 was knocked down .
These results show that galangin can inhibit ferroptosis by enhancing the expressions of SLC7A11 and GPX4 as well as reduce neuronal cell death .
SIGNIFICANCE : Galangin inhibits ferroptosis through activation of the SLC7A11/GPX4 axis and has a protective effect on hippocampal neurons in gerbils after I/R .

AIMS: To evaluate the impact of galangin treatment on cerebral ischemia-reperfusion (I/R) injury in gerbils and to identify potential mechanisms of the protective effect of galangin on hippocampal neurons after I/R injury.
PRINCIPAL METHODS: A cerebral ischemia model using bilateral common carotid artery ligation in gerbils was established. The Morris water maze (MWM) test was used to evaluate the learning and memory ability of gerbils. The cell viability was evaluated with an MTT assay. The levels of lipid peroxide biomarkers were measured to estimate the injury due to lipid peroxide. The morphology was detected by electron micrography, immunofluorescence and Nissl staining. Western blot and quantitative real-time polymerase chain reaction (qRT-PCR) were used to measure the molecular characteristics.
KEY FINDINGS: In the MWM, gerbils treated with galangin after I/R injury showed significant improvements in learning and memory. In addition, galangin treatment reduced the levels of lipid peroxide in the brains of gerbils that underwent I/R as well as reduced the amount of cell death and increased the expression of SLC7A11 and glutathione peroxidase 4 (GPX4). Furthermore, the expression of the marker of ferroptosis was decreased in galangin-treated gerbils, and the effect of galangin was weakened when SLC7A11 was knocked down. These results show that galangin can inhibit ferroptosis by enhancing the expressions of SLC7A11 and GPX4 as well as reduce neuronal cell death.
SIGNIFICANCE: Galangin inhibits ferroptosis through activation of the SLC7A11/GPX4 axis and has a protective effect on hippocampal neurons in gerbils after I/R.


greenmedinfo--2020-11-22--Sayer Ji's Livestream: "The Xenogen Hypothesis: Why Viruses Are Vectors of Resilience"

Sayer Ji discusses an alternative explanation for the role of viruses in informational transfer within biological systems , and how conventional views on both bodily symptoms and viruses overlook the elegance and intelligence of nature .
He covers the topic in relation to COVID , the conventional medical system , natural health , and related topics .
XENOGEN CONCEPT SUMMARY : The newly coined word combines the terms xeno- ( `` foreign '' / '' other '' ) -- as in xenohormetic -- with `` -gen '' ( `` to produce/give birth to ) -- as in pathogen -- to @ @ @ @ @ @ @ based information-carrying biomolecules found naturally within the human holobiont , such as virion particles or exosomes , have in generating the symptoms commonly referred to as diseases such as `` cold '' or `` flu , '' but which , in actuality , represent a xenohormetic response that creates a set of self-regulatory/detoxifying programs ( i.e .
`` symptoms '' ) that result in greater resiliency in both the individual and the group , i.e .
contribute to `` herd immunity . ''
While the vector of information -- the `` virus , @ @ @ @ @ @ @ the `` exosome '' - can be viewed as `` the cause '' of the set of biological programs that are induced by it , it functions as a carrier of information ( like a text message ) , which can used by the body , if needed , instead of being penetrated and dominated by it ; the agency is retained within the organisms and is not transferred to the `` particle . ''
So-called pathogenic responses , therefore , induced by informational vectors , such as fever , diarrhea , malaise @ @ @ @ @ @ @ function as biologically indispensable mechanisms for mediating genotype-to-immunophenotype expression , and therefore can be re-envisioned within the `` xenogen hypothesis '' framework to be biologically useful , if not at times life-saving .
For example , lethal conditions such as cancer , or deadly opportunistic infections with certain bacteria , can be averted through the induction of episodic , seasonal `` healing crises . ''
While not directly addressed in this livestream , Sayer also believes that the groundbreaking work of Luc Montagnier , Nobel Prize winning virologist , may help explain the @ @ @ @ @ @ @ . ''
Sayer believes that Montagnier 's work* proving DNA teleportation reveals how it is possible that an electromagnetic signal from a body undergoing xenohormetic detoxification/self-regulation could cause the assembly of exosomes or virion particles identical to the `` sick '' individual within that of a susceptible body .
This will be explored in future livestreams .
*https : //www.popsci.com/science/articl ...
The mammalian virome in genetic analysis of health and disease pathogenesis https : //youtu.be/TRVxTBuvChU Plant-Derived Exosomes as Cross-Species Messengers and Beacons of Epigenetics https : //www.greenmedinfo.com/blog/plant-derived-exosomes-cross-species-messengers-and-beacons-epigenetics Why Everything You Learned About Viruses @ @ @ @ @ @ @ 2014 influenza virion study ) https : //www.greenmedinfo.com/blog/why-only-thing-influenza-may-kill-germ-theory How the Microbiome Undermines the Ego , Vaccine Policy , and Patriarchy https : //www.greenmedinfo.com/blog/how-microbiome-destroyed-ego-vaccine-policy-and-patriarchy Join and use Stand for Health Freedom : https : //www.standforhealthfreedom.com My first mention of the Xenogen hypothesis ( for more study ) COVID-19 -- is it really about a virus ?
https : //youtu.be/rp4wXSku8Ik Get live updates via our Telegram Channel : https : //t.me/sayeregengmi Learn more about information referenced in this video at www.questioningcovid.com Support Greenmedinfo.com and Sayer 's work by becoming a member here : https : @ @ @ @ @ @ @ : //www.greenmedinfo.com/donation/how-you-can-support-our-mission

Visit our Re-post guidelines This article is copyrighted by GreenMedInfo LLC, 2023
Sayer Ji discusses an alternative explanation for the role of viruses in informational transfer within biological systems, and how conventional views on both bodily symptoms and viruses overlook the elegance and intelligence of nature. He covers the topic in relation to COVID, the conventional medical system, natural health, and related topics.
XENOGEN CONCEPT SUMMARY: The newly coined word xenogen combines the terms xeno- ("foreign"/"other") -- as in xenohormetic -- with "-gen" ("to produce/give birth to) -- as in pathogen -- to describe the role that certain nucleic acid based information-carrying biomolecules found naturally within the human holobiont, such as virion particles or exosomes, have in generating the symptoms commonly referred to as diseases such as "cold" or "flu," but which, in actuality, represent a xenohormetic response that creates a set of self-regulatory/detoxifying programs (i.e. "symptoms") that result in greater resiliency in both the individual and the group, i.e. contribute to "herd immunity."
While the vector of information -- the "virus," the "particle," or the "exosome" - can be viewed as "the cause" of the set of biological programs that are induced by it, it functions as a carrier of information (like a text message), which can used by the body, if needed, instead of being penetrated and dominated by it; the agency is retained within the organisms and is not transferred to the "particle."
So-called pathogenic responses, therefore, induced by informational vectors, such as fever, diarrhea, malaise, mucus formation, etc., may function as biologically indispensable mechanisms for mediating genotype-to-immunophenotype expression, and therefore can be re-envisioned within the "xenogen hypothesis" framework to be biologically useful, if not at times life-saving. For example, lethal conditions such as cancer, or deadly opportunistic infections with certain bacteria, can be averted through the induction of episodic, seasonal "healing crises."
While not directly addressed in this livestream, Sayer also believes that the groundbreaking work of Luc Montagnier, Nobel Prize winning virologist, may help explain the role of psychogenicity in "viral contagion." Sayer believes that Montagnier's work* proving DNA teleportation reveals how it is possible that an electromagnetic signal from a body undergoing xenohormetic detoxification/self-regulation could cause the assembly of exosomes or virion particles identical to the "sick" individual within that of a susceptible body. This will be explored in future livestreams. *https://www.popsci.com/science/articl...
Related content and references:
Related content: ZERO Evidence that COVID Fulfills Koch's 4 Germ Theory Postulates - Dr. Andrew Kaufman & Sayer Ji https://youtu.be/sSBQUIEUbQ8
The mammalian virome in genetic analysis of health and disease pathogenesis https://youtu.be/TRVxTBuvChU
Plant-Derived Exosomes as Cross-Species Messengers and Beacons of Epigenetics https://www.greenmedinfo.com/blog/plant-derived-exosomes-cross-species-messengers-and-beacons-epigenetics
Why Everything You Learned About Viruses is WRONG View (discussion of the 2014 influenza virion study) https://www.greenmedinfo.com/blog/why-only-thing-influenza-may-kill-germ-theory
How the Microbiome Undermines the Ego, Vaccine Policy, and Patriarchy https://www.greenmedinfo.com/blog/how-microbiome-destroyed-ego-vaccine-policy-and-patriarchy
COVID-19 Death Recording Manipulation Explained https://www.greenmedinfo.com/blog/covid-19-death-recording-manipulation-explained
Join and use Stand for Health Freedom: https://www.standforhealthfreedom.com
My first mention of the Xenogen hypothesis (for more study) COVID-19 -- is it really about a virus? https://youtu.be/rp4wXSku8Ik
Get live updates via our Telegram Channel: https://t.me/sayeregengmi
Join our newsletter for direct updates: https://www.greenmedinfo.com
Learn more about information referenced in this video at www.questioningcovid.com
Sayer Ji and Kelly Brogan's membership community, Vital Life Project: https://kellybroganmd.mykajabi.com/vital-life-project-offer
Support Greenmedinfo.com and Sayer's work by becoming a member here: https://www.greenmedinfo.com/membership Or make a donation: https://www.greenmedinfo.com/donation/how-you-can-support-our-mission


greenmedinfo--2020-11-22--Astragaloside IV can effectively protect the blood-brain barrier and reduce the area of cerebral inf

Astragaloside IV can effectively protect the blood-brain barrier and reduce the area of cerebral infarction.

Background : Previous studies proved that AS-IV could prevent blood-brain barrier ( BBB ) against an increase in permeability .
However , its underlying molecular mechanism has not been enlightened yet .
The aim of the study is to reveal the potential protective mechanism of astragaloside IV ( AS-IV ) on the blood-brain barrier after ischemia-reperfusion .
Methods : In vivo , AS-IV neurological protection was measured by Long 's five-point scale and 2,3,5-triphenyltetrazolium chloride staining .
AS-IV protection for BBB was observed by Evans blue extravasation technique .
Endoplasmic reticulum stress and apoptosis-related protein levels were measured by western @ @ @ @ @ @ @ , cell apoptosis was analyzed by western blot and flow cytometry.Endoplasmic reticulum stress-related protein levels were quantified through western blot .
Results : AS-IV treatment could decrease the infarct size in rats ' brain and protect the BBB against Evans blue permeating through brain , after ischemia/reperfusion , significantly .
Further , ischemia/reperfusion or oxygen-glucose deprivation/reperfusion was found to have an increase in endothelial cell apoptosis proteins , such as Bax , Bcl-2 , and caspase-3 , and endoplasmic reticulum stress-associated proteins , such as phosphorylated PERK and eIF2 , Bip , and @ @ @ @ @ @ @ treatment .
Conclusions : AS-IV can effectively protect the blood-brain barrier and reduce the area of cerebral infarction via inhibiting endoplasmic reticulum stress-mediated apoptosis in endothelial cells .

Background: Previous studies proved that AS-IV could prevent blood-brain barrier (BBB) against an increase in permeability. However, its underlying molecular mechanism has not been enlightened yet. The aim of the study is to reveal the potential protective mechanism of astragaloside IV (AS-IV) on the blood-brain barrier after ischemia-reperfusion.
Methods: In vivo, AS-IV neurological protection was measured by Long's five-point scale and 2,3,5-triphenyltetrazolium chloride staining. AS-IV protection for BBB was observed by Evans blue extravasation technique. Endoplasmic reticulum stress and apoptosis-related protein levels were measured by western blot with AS-IV intervention. In vitro, cell apoptosis was analyzed by western blot and flow cytometry.Endoplasmic reticulum stress-related protein levels were quantified through western blot.
Results: AS-IV treatment could decrease the infarct size in rats' brain and protect the BBB against Evans blue permeating through brain, after ischemia/reperfusion, significantly. Further, ischemia/reperfusion or oxygen-glucose deprivation/reperfusion was found to have an increase in endothelial cell apoptosis proteins, such as Bax, Bcl-2, and caspase-3, and endoplasmic reticulum stress-associated proteins, such as phosphorylated PERK and eIF2, Bip, and CHOP, which were attenuated by AS-IV treatment.
Conclusions: AS-IV can effectively protect the blood-brain barrier and reduce the area of cerebral infarction via inhibiting endoplasmic reticulum stress-mediated apoptosis in endothelial cells.


greenmedinfo--2020-11-22--Astragaloside IV inhibits cell proliferation and metastasis of breast cancer.

Astragaloside IV ( ASV ) , which has several pharmacological abilities , shows potential therapeutic effects on certain cancers by @ @ @ @ @ noncoding RNA ( lncRNA ) .
However , the anticancer role that ASV plays by @ @ @ @ @ remains unknown .
In this study , we first demonstrated that the lncRNA of TRHDE @ @ @ @ @ ) was downregulated in breast cancer tissues and cells .
Low TRHDE-AS1 expression is associated @ @ @ @ @ with breast cancer and potentially contributes to the aggressive tumor biology of breast cancer .
@ @ @ @ @ TRHDE-AS1 expression in a dose- and time-dependent manner in breast cancer cells .
By upregulating @ @ @ @ @ cancer cell growth and metastasis both in vitro and in vivo .
Taken together , @ @ @ @ @ participates in the anticancer role of ASV in breast cancer , which provides evidence for @ @ @ @ @ breast cancer therapy .

Astragaloside IV (ASV), which has several pharmacological abilities, shows potential therapeutic effects on certain cancers by regulating the expression of long noncoding RNA (lncRNA). However, the anticancer role that ASV plays by regulating lncRNAs in breast cancer remains unknown. In this study, we first demonstrated that the lncRNA of TRHDE antisense RNA 1 (TRHDE-AS1) was downregulated in breast cancer tissues and cells. Low TRHDE-AS1 expression is associated with poor outcomes in patients with breast cancer and potentially contributes to the aggressive tumor biology of breast cancer. Furthermore, ASV significantly increased TRHDE-AS1 expression in a dose- and time-dependent manner in breast cancer cells. By upregulating TRHDE-AS1, ASV repressed breast cancer cell growth and metastasis both in vitro and in vivo. Taken together, our data indicated that TRHDE-AS1 participates in the anticancer role of ASV in breast cancer, which provides evidence for the application of ASV for breast cancer therapy.


greenmedinfo--2020-11-22--Astragaloside IV and echinacoside benefit neuronal properties via direct effects and through upregul

Astragaloside IV and echinacoside benefit neuronal properties via direct effects and through upregulation of SOD1 astrocyte function in vitro.

Amyotrophic lateral sclerosis ( ALS ) , also known as a major type of motor neuron disease , is a disease characterized by the degeneration of both upper and lower motor neurons .
Astragaloside IV ( AST ) is one of the most effective compounds isolated from Astragalus membranaceus .
Echinacoside ( ECH ) is also an active constituent in Cistanche tubulosa .
These two herbs had been used in treating disease described like ALS in ancient China under the guidance of traditional Chinese medicine theory and now they are still being used extensively for ALS in current Chinese medicine @ @ @ @ @ @ @ has effect on ALS disease condition is still unclear .
Survivals of primary cultured neuron and astrocyte were determined by the MTS assay .
Proteins including GLT1 and GFAP , from SOD1 G93A Tg ( transgenic ) astrocyte lysate were determined by Western blot .
Synaptic markers , PSD95 and VGLUT1 , were stained by immunofluorescence and observed by a confocal microscope .
Proper dilution of AST and ECH was confirmed to be not harmful to both astrocytes and neurons .
AST and ECH enhanced neuronal synaptic markers density or intensity/area in different @ @ @ @ @ @ @ significantly rescue SOD1 astrocyte conditional medium-treated neuronal survival and synapse loss .
Ten micromolars ECH could significantly rescue the suppressed GLT1 level expressed by SOD1 Tg astrocyte .
This present research proved that AST and ECH could benefit neuronal properties and rescue certain dysfunction , such as GLT1 low expression , loss of neuron-supporting function , of astrocytes under SOD1 condition .

Amyotrophic lateral sclerosis (ALS), also known as a major type of motor neuron disease, is a disease characterized by the degeneration of both upper and lower motor neurons. Astragaloside IV (AST) is one of the most effective compounds isolated from Astragalus membranaceus. Echinacoside (ECH) is also an active constituent in Cistanche tubulosa. These two herbs had been used in treating disease described like ALS in ancient China under the guidance of traditional Chinese medicine theory and now they are still being used extensively for ALS in current Chinese medicine practice, but whether AST or ECH has effect on ALS disease condition is still unclear. Survivals of primary cultured neuron and astrocyte were determined by the MTS assay. Proteins including GLT1 and GFAP, from SOD1 G93A Tg (transgenic) astrocyte lysate were determined by Western blot. Synaptic markers, PSD95 and VGLUT1, were stained by immunofluorescence and observed by a confocal microscope. Proper dilution of AST and ECH was confirmed to be not harmful to both astrocytes and neurons. AST and ECH enhanced neuronal synaptic markers density or intensity/area in different aspects. Both AST and ECH could significantly rescue SOD1 astrocyte conditional medium-treated neuronal survival and synapse loss. Ten micromolars ECH could significantly rescue the suppressed GLT1 level expressed by SOD1 Tg astrocyte. This present research proved that AST and ECH could benefit neuronal properties and rescue certain dysfunction, such as GLT1 low expression, loss of neuron-supporting function, of astrocytes under SOD1 condition.


greenmedinfo--2020-11-22--Potential of natural astaxanthin in alleviating the risk of cytokine storm in COVID-19.

Host excessive inflammatory immune response to SARS-CoV-2 infection is thought to underpin the pathogenesis of COVID-19 associated severe pneumonitis and acute lung injury ( ALI ) or acute respiratory distress syndrome ( ARDS ) .
Once an immunological complication like cytokine storm occurs , anti-viral based monotherapy alone is not enough .
Additional anti-inflammatory treatment is recommended .
It must be noted that anti-inflammatory drugs such as JAK inhibitors , IL-6 inhibitors , TNF-α inhibitors , colchicine , etc.
, have been either suggested or are under trials for managing cytokine storm in COVID-19 infections .
Natural astaxanthin ( ASX @ @ @ @ @ @ @ and has antioxidant , anti-inflammatory , and immunomodulatory properties .
There is evidence from preclinical studies that supports its preventive actions against ALI/ARDS .
Moreover , ASX has a potent PPARs activity .
Therefore , it is plausible to speculate that ASX could be considered as a potential adjunctive supplement .
Here , we summarize the mounting evidence where ASX is shown to exert protective effect by regulating the expression of pro-inflammatory factors IL-1β , IL-6 , IL-8 and TNF-α .
We present reports where ASX is shown to prevent against oxidative damage @ @ @ @ @ @ @ by regulating signaling pathways like NF-ĸB , NLRP3 and JAK/STAT .
These evidences provide a rationale for considering natural astaxanthin as a therapeutic agent against inflammatory cytokine storm and associated risks in COVID-19 infection and this suggestion requires further validation with clinical studies .

Host excessive inflammatory immune response to SARS-CoV-2 infection is thought to underpin the pathogenesis of COVID-19 associated severe pneumonitis and acute lung injury (ALI) or acute respiratory distress syndrome (ARDS). Once an immunological complication like cytokine storm occurs, anti-viral based monotherapy alone is not enough. Additional anti-inflammatory treatment is recommended. It must be noted that anti-inflammatory drugs such as JAK inhibitors, IL-6 inhibitors, TNF-α inhibitors, colchicine, etc., have been either suggested or are under trials for managing cytokine storm in COVID-19 infections. Natural astaxanthin (ASX) has a clinically proven safety profile and has antioxidant, anti-inflammatory, and immunomodulatory properties. There is evidence from preclinical studies that supports its preventive actions against ALI/ARDS. Moreover, ASX has a potent PPARs activity. Therefore, it is plausible to speculate that ASX could be considered as a potential adjunctive supplement. Here, we summarize the mounting evidence where ASX is shown to exert protective effect by regulating the expression of pro-inflammatory factors IL-1β, IL-6, IL-8 and TNF-α. We present reports where ASX is shown to prevent against oxidative damage and attenuate exacerbation of the inflammatory responses by regulating signaling pathways like NF-ĸB, NLRP3 and JAK/STAT. These evidences provide a rationale for considering natural astaxanthin as a therapeutic agent against inflammatory cytokine storm and associated risks in COVID-19 infection and this suggestion requires further validation with clinical studies.


greenmedinfo--2020-11-22--Astaxanthin protects retinal ganglion cells from acute glaucoma via the Nrf2/HO-1 pathway.

The death of retinal ganglion cells ( RGCs ) during acute glaucoma causes progressive degeneration of the retinal nerve and irreversible blindness .
Astaxanthin ( AST ) is a type of xanthophyll carotenoids and naturally synthesized by multiple halobios .
It has been reported to protect the retina from acute glaucoma due to its anti-oxidative and anti-neuroinflammatory properties .
However , the mechanism underlying this process remains unclear .
We designed a mouse model with acute glaucoma and AST was administered by oral gavage .
Hematoxylin and eosin staining was utilized to evaluate the condition of retina and the number @ @ @ @ @ @ @ was performed to evaluate the mRNA levels of Bax and Bcl2 while Western blot assay was used to determine the protein levels of Bax , Bcl2 , Nrf2 and HO-1 .
AST protected the retinal integrity of mice with acute glaucoma .
The apoptosis of RGCs induced by ischemia and reperfusion was repressed by AST .
The protective functions of AST on the retinal and ganglion cells decreased with the knock-down of Nrf2 .
AST promoted the activation of Nrf2 and Ho-1 in the RGCs of the model mice .
AST protected the @ @ @ @ @ @ @ alleviated the severe retinopathy symptoms through the Nrf2/Ho-1 pathway .

The death of retinal ganglion cells (RGCs) during acute glaucoma causes progressive degeneration of the retinal nerve and irreversible blindness. Astaxanthin (AST) is a type of xanthophyll carotenoids and naturally synthesized by multiple halobios. It has been reported to protect the retina from acute glaucoma due to its anti-oxidative and anti-neuroinflammatory properties. However, the mechanism underlying this process remains unclear. We designed a mouse model with acute glaucoma and AST was administered by oral gavage. Hematoxylin and eosin staining was utilized to evaluate the condition of retina and the number of ganglion cells was counted. QRT-PCR was performed to evaluate the mRNA levels of Bax and Bcl2 while Western blot assay was used to determine the protein levels of Bax, Bcl2, Nrf2 and HO-1. AST protected the retinal integrity of mice with acute glaucoma. The apoptosis of RGCs induced by ischemia and reperfusion was repressed by AST. The protective functions of AST on the retinal and ganglion cells decreased with the knock-down of Nrf2. AST promoted the activation of Nrf2 and Ho-1 in the RGCs of the model mice. AST protected the RGCs from apoptosis during acute glaucoma and alleviated the severe retinopathy symptoms through the Nrf2/Ho-1 pathway.


greenmedinfo--2020-11-22--Astaxanthin improves serum cytokine expression and semen quality of diabetes mellitus KKAy mice.

The present study aims to explore the effects of astaxanthin on the semen quality of diabetes mellitus ( DM ) @ @ @ @ @ of 60 DM KKAy mice with similar body weights and initial blood glucose and serum @ @ @ @ @ four groups , namely , one control and three astaxanthin treatments ( 10 , 50 @ @ @ @ @ ) .
Results show that oral astaxanthin administration reduced fasting blood glucose and serum total @ @ @ @ @ , insulin and nitrate oxide levels in the testis of DM KKAy mice .
Astaxanthin @ @ @ @ @ cholesterol , protein and superoxide dismutase levels in the testis ; serum interleukin-11 , tumour @ @ @ @ @ ; and sperm density , sperm movement and normal morphology rate of DM KKAy mice @ @ @ @ @ , astaxanthin can effectively affect serum cytokines and ameliorate semenquality of DM KKAy mice ; @ @ @ @ @ developed as an adjuvant drug to treat diabetes mellitus-induced infertility .

The present study aims to explore the effects of astaxanthin on the semen quality of diabetes mellitus (DM) KKAy mice. A total of 60 DM KKAy mice with similar body weights and initial blood glucose and serum lipid levels were assigned to four groups, namely, one control and three astaxanthin treatments (10, 50, or 100 mg/kg astaxanthin). Results show that oral astaxanthin administration reduced fasting blood glucose and serum total cholesterol, low-density lipoprotein cholesterol, insulin and nitrate oxide levels in the testis of DM KKAy mice. Astaxanthin also improved the high-density lipoprotein cholesterol,protein and superoxide dismutase levels in the testis; serum interleukin-11, tumour necrosis factor-α and interferon-γ levels; and sperm density, sperm movement and normal morphology rate of DM KKAy mice. Based on the results, astaxanthin can effectively affect serum cytokines and ameliorate semenquality of DM KKAy mice; thus, it may be developed as an adjuvant drug to treat diabetes mellitus-induced infertility.


greenmedinfo--2020-11-22--Antioxidant and anti‑inflammatory mechanisms of action of astaxanthin in cardiovascular diseases.

Cardiovascular diseases are the most common cause of mortality worldwide .
Oxidative stress and inflammation are pathophysiological processes involved in @ @ @ @ @ ; thus , anti‑inflammatory and antioxidant agents that modulate redox balance have become research targets @ @ @ @ @ molecular mechanisms of action and therapeutic properties .
Astaxanthin , a carotenoid of the xanthophyll @ @ @ @ @ properties due to its molecular structure andits arrangement in the plasma membrane , factors that @ @ @ @ @ oxygen and nitrogen species .
This carotenoid also has prominent anti‑inflammatory activity , possibly interrelated @ @ @ @ @ and is also involved in the modulation of lipid and glucose metabolism .
Considering the @ @ @ @ @ on cardiovascular health evidenced by preclinical and clinical studies , the aim of the present @ @ @ @ @ molecular and cellular mechanisms associated with the antioxidant and anti‑inflammatory properties of this carotenoid in @ @ @ @ @ .
The beneficial properties and safety profile of astaxanthin indicate that this compound may be @ @ @ @ @ as an adjuvant in the treatment of cardiovascular diseases .

Cardiovascular diseases are the most common cause of mortality worldwide. Oxidative stress and inflammation are pathophysiological processes involved in the development of cardiovascular diseases; thus, anti‑inflammatory and antioxidant agents that modulate redox balance have become research targets so as to evaluate their molecular mechanisms of action and therapeutic properties. Astaxanthin, a carotenoid of the xanthophyll group, has potent antioxidant properties due to its molecular structure andits arrangement in the plasma membrane, factors that favor the neutralization of reactive oxygen and nitrogen species. This carotenoid also has prominent anti‑inflammatory activity, possibly interrelated with its antioxidant effect, and is also involved in the modulation of lipid and glucose metabolism. Considering the potential beneficial effects of astaxanthin on cardiovascular health evidenced by preclinical and clinical studies, the aim of the present review was to describe the molecular and cellular mechanisms associated with the antioxidant and anti‑inflammatory properties of this carotenoid in cardiovascular diseases, particularly atherosclerosis. The beneficial properties and safety profile of astaxanthin indicate that this compound may be used for preventing progression or as an adjuvant in the treatment of cardiovascular diseases.


greenmedinfo--2020-11-22--Astaxanthin alleviates oxidative damage in acute pancreatitis via direct antioxidant mechanisms.

BACKGROUND/AIMS : Astaxanthin ( ATX ) is a naturally occurring carotenoid and a potent antioxidant .
Various anti-inflammatory effects of ATX have been examined .
We aimed to investigate the protective effect of ATX and its mechanism in a cerulein-induced acute pancreatitis rat model .
MATERIALS AND METHODS : The rats were randomized into 2 main groups as control ( C ) and acute pancreatitis group ( AP ) .
AP group was subsequently divided into subgroups as AP+vehicle ( AP ) , AP+ATX , and ATX+peroxisome proliferator-activated receptor-alpha antagonist GW6471 ( ATX+GW ) groups .
To induce AP , @ @ @ @ @ @ @ , intraperitonally [ ip ] ) at 1 hour intervals , whereas the C group received saline .
The AP group was treated with vehicle olive oil , ATX 40 mg/kg/orally , or GW6471 and ATX ( GW1 mg/kg/ip ; ATX ; 40 mg/kg/peroral ) .
Treatments were administered after the 1st cerulein injection .
At the 7th hour afterthe final injection , the rats were killed and the pancreatic tissue was used for the determination of malondialdehyde ( MDA ) , glutathione ( GSH ) , and myeloperoxidase ( MPO ) activities @ @ @ @ @ @ @ , lipase , and histopathological analyses were performed .
RESULTS : Elevated serum lipase and amylase levels in the vehicle-treated AP group ( p < 0.01 ) decreased in the ATX and ATX+GW groups ( p < 0.05 ) .
In the AP groups , GSH was reduced and MDA , MPO , luminol , and lucigenin levels were increased ( p < 0.05-0.001 ) .
ATX reversed these changes ( p < 0.05-0.001 ) .
The vehicle-treated group revealed significant severe cytoplasmic degeneration and vacuolization , whereas ATX ameliorated these destructions .
@ @ @ @ @ @ @ of ATX biochemically or histologically .
CONCLUSION : ATX has a potent protective effect on AP via its radical scavenging and antioxidant properties .
Therefore , we believe that ATX may have therapeutic potential .

BACKGROUND/AIMS: Astaxanthin (ATX) is a naturally occurring carotenoid and a potent antioxidant. Various anti-inflammatory effects of ATX have been examined. We aimed to investigate the protective effect of ATX and its mechanism in a cerulein-induced acute pancreatitis rat model.
MATERIALS AND METHODS: The rats were randomized into 2 main groups as control (C) and acute pancreatitis group (AP). AP group was subsequently divided into subgroups as AP+vehicle (AP), AP+ATX, and ATX+peroxisome proliferator-activated receptor-alpha antagonist GW6471 (ATX+GW) groups. To induce AP, the rats were administered cerulein (50µg/kg, intraperitonally [ip]) at 1 hour intervals, whereas the C group received saline. The AP group was treated with vehicle olive oil, ATX 40 mg/kg/orally, or GW6471 and ATX (GW1 mg/kg/ip; ATX; 40 mg/kg/peroral). Treatments were administered after the 1st cerulein injection. At the 7th hour afterthe final injection, the rats were killed and the pancreatic tissue was used for the determination of malondialdehyde (MDA), glutathione (GSH), and myeloperoxidase (MPO) activities and luminol-lucigenin chemiluminescence levels. Serum amylase, lipase, and histopathological analyses were performed.
RESULTS: Elevated serum lipase and amylase levels in the vehicle-treated AP group (p<0.01) decreased in the ATX and ATX+GW groups (p<0.05). In the AP groups, GSH was reduced and MDA, MPO, luminol, and lucigenin levels were increased (p<0.05-0.001). ATX reversed these changes (p<0.05-0.001). The vehicle-treated group revealed significant severe cytoplasmic degeneration and vacuolization, whereas ATX ameliorated these destructions. GW6471 did not abolish the positive effects of ATX biochemically or histologically.
CONCLUSION: ATX has a potent protective effect on AP via its radical scavenging and antioxidant properties. Therefore, we believe that ATX may have therapeutic potential.


greenmedinfo--2020-11-22--Attenuation of the Na/K‑ATPase/Src/ROS amplification signaling pathway by astaxanthin ameliorates my

Attenuation of the Na/K‑ATPase/Src/ROS amplification signaling pathway by astaxanthin ameliorates myocardial cell oxidative stress injury.

The 3S , 3'S‑ASTaxanthin ( 3S , 3'S‑AST ) isomer has strong antioxidant activity ; however , its protective roles and potential mechanisms against oxidative stress damage in cardiomyocytes have not been investigated .
Na+/K+‑ATPase ( NKA ) /Src signal activation has an important role in increasing reactive oxygen species ( ROS ) production .
The aim of the present study was to investigate the protective effects and mechanism of 3S , 3'S‑AST on hydrogen peroxide ( H2O2 ) ‑induced oxidative stress injury in H9c2 myocardial cells .
The protective effects of 3S , 3'S‑AST on H2O2‑induced H9c2 cell injurywas @ @ @ @ @ @ @ kinase myocardial band content , cell viability and nuclear morphology .
The antioxidant effect was investigated by analyzing ROS accumulation and malondialdehyde , glutathione ( GSH ) peroxidase , GSH and glutathione reductase activity levels .
The protein expression levels of Bax , Bcl‑2 , caspase‑3 and cleaved caspase‑3 were analyzed using western blotting to determine cardiomyocyte apoptosis .
Western blot analysis of the phosphorylation levels of Src and Erk1/2 were also performed to elucidate the molecular mechanism involved .
Theresults showed that 3S , 3'S‑AST reduced the release of LDH and promoted @ @ @ @ @ @ @ and cell apoptosis induced by H2O2 .
Furthermore , 3S , 3'S‑AST also restored apoptosis‑related Bax and Bcl‑2 protein expression levels in H2O2‑treated H9c2 cells .
The phosphorylation levels of Src and Erk1/2 were significantly higher in the H2O2 treatment group , whereas 3S , 3'S‑AST pretreatment significantly decreased the levels of phosphorylated ( p ) ‑Src and p‑ERK1/2 .
The results provided evidence that 3S , 3'S‑AST exhibited a cardioprotective effect against oxidative stress injury by attenuating NKA/Src/Erk1/2‑modulated ROS amplification .

The 3S, 3'S‑ASTaxanthin (3S, 3'S‑AST) isomer has strong antioxidant activity; however, its protective roles and potential mechanisms against oxidative stress damage in cardiomyocytes have not been investigated. Na+/K+‑ATPase (NKA)/Src signal activation has an important role in increasing reactive oxygen species (ROS) production. The aim of the present study was to investigate the protective effects and mechanism of 3S, 3'S‑AST on hydrogen peroxide (H2O2)‑induced oxidative stress injury in H9c2 myocardial cells. The protective effects of 3S, 3'S‑AST on H2O2‑induced H9c2 cell injurywas observed by measuring lactate dehydrogenase and creatine kinase myocardial band content, cell viability and nuclear morphology. The antioxidant effect was investigated by analyzing ROS accumulation and malondialdehyde, glutathione (GSH) peroxidase, GSH and glutathione reductase activity levels. The protein expression levels of Bax, Bcl‑2, caspase‑3 and cleaved caspase‑3 were analyzed using western blotting to determine cardiomyocyte apoptosis. Western blot analysis of the phosphorylation levels of Src and Erk1/2 were also performed to elucidate the molecular mechanism involved. Theresults showed that 3S, 3'S‑AST reduced the release of LDH and promoted cell viability, and attenuated ROS accumulation and cell apoptosis induced by H2O2. Furthermore, 3S, 3'S‑AST also restored apoptosis‑related Bax and Bcl‑2 protein expression levels in H2O2‑treated H9c2 cells. The phosphorylation levels of Src and Erk1/2 were significantly higher in the H2O2 treatment group, whereas 3S, 3'S‑AST pretreatment significantly decreased the levels of phosphorylated (p)‑Src and p‑ERK1/2. The results provided evidence that 3S, 3'S‑AST exhibited a cardioprotective effect against oxidative stress injury by attenuating NKA/Src/Erk1/2‑modulated ROS amplification.


greenmedinfo--2020-11-22--Cognitive effects of astaxanthin pretreatment on recovery from traumatic brain injury.

Traumatic brain injury ( TBI ) , caused by mechanical impact to the brain , is a leading cause of death and disability among young adults , with slow and often incomplete recovery .
Preemptive treatment strategies may increase the injury resilience of high-risk populations such as soldiers and athletes .
In this work , the xanthophyll carotenoid Astaxanthin was examined as a potential nutritional preconditioning method in mice ( sabra strain ) to increase their resilience prior to TBI in a closed head injury ( CHI ) model .
The effect of Astaxanthin pretreatment on heat shock protein ( @ @ @ @ @ @ @ CHI was explored by gavage or free eating ( in pellet form ) for 2 weeks before CHI .
Assessment of neuromotor function by the neurological severity score ( NSS ) revealed significant improvement in the Astaxanthin gavage-treated group ( 100 mg/kg , ATX ) during recovery compared to the gavage-treated olive oil group ( OIL ) , beginning at 24 h post-CHI and lasting throughout 28 days ( < 0.007 ) .
Astaxanthin pretreatment in pellet form produced a smaller improvement in NSS vs. posttreatment at 7 days post-CHI ( < 0.05 @ @ @ @ @ @ @ the novel object recognition test ( ORT ) and the Y Maze test revealed an advantage for Astaxanthin administration via free eating vs. standard chow during recovery post-CHI ( ORT at 3 days , < 0.035 ; improvement in Y Maze score from 2 to 29 days , < 0.02 ) .
HSP profile and anxiety ( open field test ) were not significantly affected by Astaxanthin .
In conclusion , astaxanthin pretreatment may contribute to improved recovery post-TBI in mice and is influenced by the form of administration .

Traumatic brain injury (TBI), caused by mechanical impact to the brain, is a leading cause of death and disability among young adults, with slow and often incomplete recovery. Preemptive treatment strategies may increase the injury resilience of high-risk populations such as soldiers and athletes. In this work, the xanthophyll carotenoid Astaxanthin was examined as a potential nutritional preconditioning method in mice (sabra strain) to increase their resilience prior to TBI in a closed head injury (CHI) model. The effect of Astaxanthin pretreatment on heat shock protein (HSP) dynamics and functional outcome after CHI was explored by gavage or free eating (in pellet form) for 2 weeks before CHI. Assessment of neuromotor function by the neurological severity score (NSS) revealed significant improvement in the Astaxanthin gavage-treated group (100 mg/kg, ATX) during recovery compared to the gavage-treated olive oil group (OIL), beginning at 24 h post-CHI and lasting throughout 28 days (<0.007). Astaxanthin pretreatment in pellet form produced a smaller improvement in NSS vs. posttreatment at 7 days post-CHI (<0.05). Cognitive and behavioral evaluation using the novel object recognition test (ORT) and the Y Maze test revealed an advantage for Astaxanthin administration via free eating vs. standard chow during recovery post-CHI (ORT at 3 days,<0.035; improvement in Y Maze score from 2 to 29 days,<0.02). HSP profile and anxiety (open field test) were not significantly affected by Astaxanthin. In conclusion, astaxanthin pretreatment may contribute to improved recovery post-TBI in mice and is influenced by the form of administration.


greenmedinfo--2020-11-22--The promising effects of astaxanthin on lung diseases.

Astaxanthin ( ASX ) is a naturally occurring xanthophyll carotenoid .
Both in vitro and in vivo studies have shown that it is a potent antioxidant with anti-inflammatory properties .
Lung cancer is the leading cause of cancer death worldwide , whereas other lung diseases such as chronic obstructive pulmonary disease , emphysema , and asthma are of high prevalence .
In the past decade , mounting evidence has suggested a protective role for ASX against lung diseases .
This article reviews the potential role of ASX in protecting against lung diseases , including lung cancer .
It also summarizes @ @ @ @ @ @ @ protects against pulmonary diseases , including regulating the nuclear factor erythroid 2-related factor/heme oxygenase-1 pathway , NF-κB signaling , mitogen-activated protein kinase signaling , Janus kinase-signal transducers and activators of transcription-3 signaling , the phosphoinositide 3-kinase/Akt pathway , and modulating immune response .
Several future directions are proposed in this review .
However , most in vitro and in vivostudies have used ASX at concentrations that are not achievable by humans .
Also , no clinical trials have been conducted and/or reported .
Thus , preclinical studies with ASX treatment within physiological concentrations @ @ @ @ @ @ @ to examine the health benefits of ASX withrespect to lung diseases .

Astaxanthin (ASX) is a naturally occurring xanthophyll carotenoid. Both in vitro and in vivo studies have shown that it is a potent antioxidant with anti-inflammatory properties. Lung cancer is the leading cause of cancer death worldwide, whereas other lung diseases such as chronic obstructive pulmonary disease, emphysema, and asthma are of high prevalence. In the past decade, mounting evidence has suggested a protective role for ASX against lung diseases. This article reviews the potential role of ASX in protecting against lung diseases, including lung cancer. It also summarizes the underlying molecular mechanisms by which ASX protects against pulmonary diseases, including regulating the nuclear factor erythroid 2-related factor/heme oxygenase-1 pathway, NF-κB signaling, mitogen-activated protein kinase signaling, Janus kinase-signal transducers and activators of transcription-3 signaling, the phosphoinositide 3-kinase/Akt pathway, and modulating immune response. Several future directions are proposed in this review. However, most in vitro and in vivostudies have used ASX at concentrations that are not achievable by humans. Also, no clinical trials have been conducted and/or reported. Thus, preclinical studies with ASX treatment within physiological concentrations as well as human studies are required to examine the health benefits of ASX withrespect to lung diseases.


greenmedinfo--2020-11-22--Astaxanthin counteracts vascular calcification in vitro.

Vascular calcification ( VC ) is a critical contributor to the rising cardiovascular risk among at-risk populations such as those with diabetes or renal failure .
The pathogenesis of VC involves an uprising of oxidative stress , for which antioxidants can be theoretically effective .
However , astaxanthin , a potent antioxidant , has not been tested before for the purpose of managing VC .
To answer this question , we tested the efficacy of astaxanthin against VC using the high phosphate ( HP ) -induced vascular smooth muscle cell ( VSMC ) calcification model .
RNAs from treated groups @ @ @ @ @ @ @ consistency and inter-group differential expressions identified .
Candidate hub genes were selected , followed by validation in experimental models and functional characterization .
We showed that HP induced progressive calcification among treated VSMCs , while astaxanthin dose-responsively and time-dependently ameliorated calcification severities .
Transcriptomic profiling revealed that 3491 genes exhibited significant early changes during VC progression , among which 26 potential hub genes were selected based on closeness ranking and biologic plausibility .
SOD2 was validated in the VSMC model , shown to drive the deactivation of cellular senescence and enhance antioxidative defenses @ @ @ @ @ @ @ oxygen species ( ROS ) levels without HP , but significantly lowered ROS production in HP-treated VSMCs .
SOD2 knockdown prominently abolished the anti-calcification effect of astaxanthin on HP-treated VSMCs , lending support to our findings .
In conclusion , we demonstrated for the first time that astaxanthin could be a potential candidate treatment for VC , through inducing the up-regulation of SOD2 early during calcification progression and potentially suppressing vascular senescence .

Vascular calcification (VC) is a critical contributor to the rising cardiovascular risk among at-risk populations such as those with diabetes or renal failure. The pathogenesis of VC involves an uprising of oxidative stress, for which antioxidants can be theoretically effective. However, astaxanthin, a potent antioxidant, has not been tested before for the purpose of managing VC. To answer this question, we tested the efficacy of astaxanthin against VC using the high phosphate (HP)-induced vascular smooth muscle cell (VSMC) calcification model. RNAs from treated groups underwent Affymetrix microarray screening, with intra-group consistency and inter-group differential expressions identified. Candidate hub genes were selected, followed by validation in experimental models and functional characterization. We showed that HP induced progressive calcification among treated VSMCs, while astaxanthin dose-responsively and time-dependently ameliorated calcification severities. Transcriptomic profiling revealed that 3491 genes exhibited significant early changes during VC progression, among which 26 potential hub genes were selected based on closeness ranking and biologic plausibility. SOD2 was validated in the VSMC model, shown to drive the deactivation of cellular senescence and enhance antioxidative defenses. Astaxanthin did not alter intracellular reactive oxygen species (ROS) levels without HP, but significantly lowered ROS production in HP-treated VSMCs. SOD2 knockdown prominently abolished the anti-calcification effect of astaxanthin on HP-treated VSMCs, lending support to our findings. In conclusion, we demonstrated for the first time that astaxanthin could be a potential candidate treatment for VC, through inducing the up-regulation of SOD2 early during calcification progression and potentially suppressing vascular senescence.


greenmedinfo--2020-11-22--Astaxanthin and its effects in inflammatory responses and inflammation-associated diseases: recent a

Astaxanthin and its effects in inflammatory responses and inflammation-associated diseases: recent advances and future directions.

Astaxanthin is a natural lipid-soluble and red-orange carotenoid .
Due to its strong antioxidant property , anti-inflammatory , anti-apoptotic , @ @ @ @ @ has gained growing interest as a multi-target pharmacological agent against various diseases .
In the @ @ @ @ @ mechanisms of astaxanthin involved in targeting for inflammatory biomarkers and multiple signaling pathways , including @ @ @ @ @ , ERK1/2 , JNK , p38 MAPK , and JAK-2/STAT-3 , have been described .
@ @ @ @ @ anti-inflammatory effects of astaxanthin in neurological diseases , diabetes , gastrointestinal diseases , hepatic and @ @ @ @ @ skin disorders , are highlighted .
In addition to the protective effects of astaxanthin in @ @ @ @ @ , we also summarize recent advances for the inconsistent roles of astaxanthin in infectious diseases @ @ @ @ @ that the exact function of astaxanthin in response to different pathogen infection and the potential @ @ @ @ @ viral infectious diseases should be important research directions in the future .

Astaxanthin is a natural lipid-soluble and red-orange carotenoid. Due to its strong antioxidant property, anti-inflammatory, anti-apoptotic, and immune modulation, astaxanthin has gained growing interest as a multi-target pharmacological agent against various diseases. In the current review, the anti-inflammation mechanisms of astaxanthin involved in targeting for inflammatory biomarkers and multiple signaling pathways, including PI3K/AKT, Nrf2, NF-κB, ERK1/2, JNK, p38 MAPK, and JAK-2/STAT-3, have been described. Furthermore, the applications of anti-inflammatory effects of astaxanthin in neurological diseases, diabetes, gastrointestinal diseases, hepatic and renal diseases, eye and skin disorders, are highlighted. In addition to the protective effects of astaxanthin in various chronic and acute diseases, we also summarize recent advances for the inconsistent roles of astaxanthin in infectious diseases, and give our view that the exact function of astaxanthin in response to different pathogen infection and the potential protective effects of astaxanthin in viral infectious diseases should be important research directions in the future.


greenmedinfo--2020-11-23--The combination of ginger powder and zinc supplement improves the fructose-induced metabolic syndrom

The combination of ginger powder and zinc supplement improves the fructose-induced metabolic syndrome.

Although studies have shown that ginger , as an herbal remedy and zinc are able to improve inflammation , oxidative stress , autophagy , and metabolism of lipid and glucose , their molecular mechanisms are unknown .
Therefore , this study was aimed to examine the therapeutic effects of ginger with zinc supplement for eight weeks on fructose-induced metabolic syndrome ( MS ) .
Ninety-six adult male Sprague Dawley rats ( 220 g ± 20 ) were randomly assigned to twelve controlled and treated groups .
After the last treatment session , the level of lipid profiles , glucose , @ @ @ @ @ @ @ and liver enzymes as biomarkers to evaluate liver function in serum were measured .
The level of antioxidant enzymes and lipid peroxidation to evaluate the oxidative status and the TNF-α level as a biomarker to assess the state of inflammation in liver were also measured .
The level of zinc along with the expression of NF-κB , mTORC1 , PPAR-α , SREBP-1c , and Nrf2 in liver was also evaluated .
The level of metabolic factors and liver enzymes in serum along with lipid peroxidation and TNF-α in liver increased ; zinc and @ @ @ @ @ @ @ MS compared to control rats ( p

Although studies have shown that ginger, as an herbal remedy and zinc are able to improve inflammation, oxidative stress, autophagy, and metabolism of lipid and glucose, their molecular mechanisms are unknown. Therefore, this study was aimed to examine the therapeutic effects of ginger with zinc supplement for eight weeks on fructose-induced metabolic syndrome (MS). Ninety-six adult male Sprague Dawley rats (220 g ± 20) were randomly assigned to twelve controlled and treated groups. After the last treatment session, the level of lipid profiles, glucose, insulin, and leptin as metabolic factors and liver enzymes as biomarkers to evaluate liver function in serum were measured. The level of antioxidant enzymes and lipid peroxidation to evaluate the oxidative status and the TNF-α level as a biomarker to assess the state of inflammation in liver were also measured. The level of zinc along with the expression of NF-κB, mTORC1, PPAR-α, SREBP-1c, and Nrf2 in liver was also evaluated. The level of metabolic factors and liver enzymes in serum along with lipid peroxidation and TNF-α in liver increased; zinc and antioxidant enzymes levels decreased in rats with MS compared to control rats (p < .05). The hepatic expression of SREBP-1c, NF-κB and mTORC1 were upregulated and the expression of PPAR-α and Nrf2 were downregulated in rats with MS compared to control rats (p < .05). Treatment with different doses of ginger, zinc, and the combination of them could improve metabolic, inflammatory oxidative stress factors, and expression of the above genes in rats with MS compared to the MS group (p < .05). It can be concluded that ginger, zinc, and the combination of them could improve oxidative damage, inflammation, and autophagy induced by fructose and could adjust the glucose and lipid metabolism and the homeostasis of zinc in rats with MS. PRACTICAL APPLICATIONS: Due to the increasing prevalence of metabolic diseases, the use of plant compounds such as ginger has attracted widespread attention. Ginger as an herbal remedy with predominant pharmacological properties due to its availability, cheapness, and lack of side effects is also very popular for the treatment of metabolic disorders in folk medicine. Moreover, enhancing its medicinal properties with supplements such as zinc can be widely welcomed. This study was actually performed with the aim of investigating the effects of ginger + zinc supplement on MS. The results showed that the ginger + zinc supplement could improveoxidative damage, inflammation, and autophagy caused by fructose and adjust the glucose and lipid metabolism and the homeostasis of zinc in rats with MS. The results of this study support the hypothesis that ginger can be used as a very suitable option for the production of medicinal supplements tomaintain human health.