greenmedinfo--2020-07-30--Magnolol may effectively enhance anti-hepatocellular carcinoma ability of radiation.

BACKGROUND/AIM : Radiation ( RT ) induced ERK/NF-κB in hepatocellular carcinoma ( HCC ) has been reported in our previous @ @ @ @ @ toxicity of RT or triggers a radioresistance effect .
Thus , combining RT with a @ @ @ @ @ HCC to RT .
Magnolol , a bioactive compound , was known to have anti-inflammatory @ @ @ @ @ , we aimed to investigate whether magnolol may enhance anti-HCC efficacy of RT in vivo @ @ @ @ @ We established a Hep3B bearing mouse to evaluate the efficacy of the combination treatment of @ @ @ @ @ : Most significantly , tumor volume and tumor weight inhibition was found in the combination @ @ @ @ @ also illustrated the suppression of RT-induced ERK/NF-κB-related proteins expression by magnolol .
In addition , @ @ @ @ @ as caspase-3 and -9 , were markedly increased in the combination group .
CONCLUSION : @ @ @ @ @ ability of RT by downregulating the expression of ERK/NF-κB-related proteins and increasing the expression of @ @ @

BACKGROUND/AIM: Radiation (RT) induced ERK/NF-κB in hepatocellular carcinoma (HCC) has been reported in our previous works; it weakens the toxicity of RT or triggers a radioresistance effect. Thus, combining RT with a suitable NF-κB inhibitor may sensitize HCC to RT. Magnolol, a bioactive compound, was known to have anti-inflammatory and anti-tumor functions. Here, we aimed to investigate whether magnolol may enhance anti-HCC efficacy of RT in vivo.
MATERIALS AND METHODS: We established a Hep3B bearing mouse to evaluate the efficacy of the combination treatment of magnolol and RT.
RESULTS: Most significantly, tumor volume and tumor weight inhibition was found in the combination group. Tumor immunohistochemistry staining also illustrated the suppression of RT-induced ERK/NF-κB-related proteins expression by magnolol. In addition, intrinsic apoptosis-related proteins, such as caspase-3 and -9, were markedly increased in the combination group.
CONCLUSION: Magnolol may effectively enhance anti-HCC ability of RT by downregulating the expression of ERK/NF-κB-related proteins and increasing the expression of apoptosis-related proteins.


greenmedinfo--2020-07-30--Magnolol ameliorates behavioural impairments and neuropathology in a transgenic model of Alzheimer's

Magnolol ameliorates behavioural impairments and neuropathology in a transgenic model of Alzheimer's disease.

Alzheimer 's disease ( AD ) is a common neurodegenerative disease characterized by progressive memory loss .
Magnolol ( MN ) , the main active ingredient of , possesses anti-AD effects in several experimental models of AD .
In this study , we aimed to explore whether MN could ameliorate the cognitive deficits in TgCRND8 transgenic mice and to elucidate its molecular mechanisms .
Male TgCRND8 mice were orally administered with MN ( 20 and 40 mg/kg ) daily for 4 consecutive months , followed by assessing the spatial learning and memory functions using the open-field , radial arm maze @ @ @ @ @ @ @ The results demonstrated that MN ( 20 and 40 mg/kg ) could markedly ameliorate the cognitive deficits in TgCRND8 mice.In addition , MN significantly increased the expression of postsynaptic density protein 93 ( PSD93 ) , PSD-95 , synapsin-1 , synaptotagmin-1 , synaptophysin ( SYN ) , and interleukin-10 ( IL-10 ) , while markedly reduced the protein levels of tumor necrosis factor alpha ( TNF- ) , IL-6 , IL-1 , A , and A , and modulated the amyloid precursor protein ( APP ) processing and phosphorylation .
Immunofluorescence showed that @ @ @ @ @ @ @ ( Iba-1 ) and astrocytes ( GFAP ) in the hippocampus and cerebral cortex of TgCRND8 mice .
Mechanistic studies revealed that MN could significantly increase the ratios of p-GSK-3 ( Ser9 ) /GSK-3 , p-Akt ( Ser473 ) /Akt , and p-NF-B p65/NF-B p65 .
These findings indicate that MN exerted cognitive deficits improving effects via suppressing neuroinflammation , amyloid pathology , and synaptic dysfunction through regulating the PI3K/Akt/GSK-3and NF-B pathways , suggesting that MN is a promising naturally occurring polyphenol worthy of further developing into a therapeutic agent for AD treatment @

Alzheimer's disease (AD) is a common neurodegenerative disease characterized by progressive memory loss. Magnolol (MN), the main active ingredient of, possesses anti-AD effects in several experimental models of AD. In this study, we aimed to explore whether MN could ameliorate the cognitive deficits in TgCRND8 transgenic mice and to elucidate its molecular mechanisms. Male TgCRND8 mice were orally administered with MN (20 and 40 mg/kg) daily for 4 consecutive months, followed by assessing the spatial learning and memory functions using the open-field, radial arm maze, and novel object recognition tests. The results demonstrated that MN (20 and 40 mg/kg) could markedly ameliorate the cognitive deficits in TgCRND8 mice.In addition, MN significantly increased the expression of postsynaptic density protein 93 (PSD93), PSD-95, synapsin-1, synaptotagmin-1, synaptophysin (SYN), and interleukin-10 (IL-10), while markedly reduced the protein levels of tumor necrosis factor alpha (TNF-), IL-6, IL-1, A, and A, and modulated the amyloid precursor protein (APP) processing and phosphorylation. Immunofluorescence showed that MN significantly suppressed the activation of microglia (Iba-1) and astrocytes (GFAP) in the hippocampus and cerebral cortex of TgCRND8 mice. Mechanistic studies revealed that MN could significantly increase the ratios of p-GSK-3(Ser9)/GSK-3, p-Akt (Ser473)/Akt, and p-NF-B p65/NF-B p65. These findings indicate that MN exerted cognitive deficits improving effects via suppressing neuroinflammation, amyloid pathology, and synaptic dysfunction through regulating the PI3K/Akt/GSK-3and NF-B pathways, suggesting that MN is a promising naturally occurring polyphenol worthy of further developing into a therapeutic agent for AD treatment.


greenmedinfo--2020-07-30--The protective effect of hesperetin in osteoarthritis: an in vitro and in vivo study

Osteoarthritis ( OA ) , a progressive joint disorder , is principally characterized by the degeneration and destruction of articular cartilage .
Previous research studies demonstrated that inflammation and ECM degradation play a major role in OA development .
Hesperetin , the aglycone of neohesperidin found in the peel of Citrus aurantium L. ( Rutaceae ) , demonstrated in several studies potential anti-inflammatory activity in a variety of diseases .
However , the mechanisms by which hesperetin plays a protective role in osteoarthritis ( OA ) are not completely understood .
In this study , we found the anti-inflammatory effects @ @ @ @ @ @ @ in both in vitro and in vivo experiments .
In vitro , IL-1β-induced expression of inducible nitric oxide synthase ( iNOS ) , cyclooxygenase-2 ( COX-2 ) , nitric oxide ( NO ) , tumor necrosis factor alpha ( TNF-α ) , prostaglandin E2 ( PGE2 ) , and interleukin-6 ( IL-6 ) were inhibited by hesperetin .
Moreover , hesperetin down-regulated the IL-1β-stimulated matrix metalloproteinase-13 ( MMP-13 ) and thrombospondin motifs 5 ( ADAMTS-5 ) while up-regulating collagen type II and aggrecan .
Mechanistically , we revealed that hesperetin suppressed nuclear factor @ @ @ @ @ @ @ activating the nuclear factor ( erythroid-derived 2 ) -like 2 ( Nrf2 ) in IL-1β-induced chondrocytes .
Hesperetin-induced repression of OA development is shown using a DMM model .
Taken together , our findings suggest that hesperetin may be a novel potential therapeutic agent for repressing the development of OA .

Osteoarthritis (OA), a progressive joint disorder, is principally characterized by the degeneration and destruction of articular cartilage. Previous research studies demonstrated that inflammation and ECM degradation play a major role in OA development. Hesperetin, the aglycone of neohesperidin found in the peel of Citrus aurantium L. (Rutaceae), demonstrated in several studies potential anti-inflammatory activity in a variety of diseases. However, the mechanisms by which hesperetin plays a protective role in osteoarthritis (OA) are not completely understood. In this study, we found the anti-inflammatory effects of hesperetin in the progression of OA in both in vitro and in vivo experiments. In vitro, IL-1β-induced expression of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), nitric oxide (NO), tumor necrosis factor alpha (TNF-α), prostaglandin E2 (PGE2), and interleukin-6 (IL-6) were inhibited by hesperetin. Moreover, hesperetin down-regulated the IL-1β-stimulated matrix metalloproteinase-13 (MMP-13) and thrombospondin motifs 5 (ADAMTS-5) while up-regulating collagen type II and aggrecan. Mechanistically, we revealed that hesperetin suppressed nuclear factor kappa B (NF-κB) signaling by activating the nuclear factor (erythroid-derived 2)-like 2 (Nrf2) in IL-1β-induced chondrocytes. Hesperetin-induced repression of OA development is shown using a DMM model. Taken together, our findings suggest that hesperetin may be a novel potential therapeutic agent for repressing the development of OA.


greenmedinfo--2020-07-30--M. officinalis extract can be used as an antiviral food material to control norovirus foodborne dise

M. officinalis extract can be used as an antiviral food material to control norovirus foodborne diseases.

Norovirus is a major cause of foodborne disease and nonbacterial gastroenteritis globally .
This study evaluated the antiviral effects ofextract @ @ @ @ @ constituents against human norovirus surrogates , murine norovirus ( MNV ) and feline calicivirus ( @ @ @ @ @ model food systems .
Pretreatment or cotreatment of.extract at 1 mg/mL reduced MNV and FCV @ @ @ @ @ Honokiol and magnolol , which are the major polyphenols in the extract , showed significant @ @ @ @ @ FCV .
The virus-infected cells that were treated with.extract exhibited significantly increased glutathione levels ( @ @ @ @ @ levels in apple , orange , and plum juices and by 0.9 and 1.6 log @ @ @ @ @ when they were treated with the extract at 5 mg/mL .
Therefore , the present @ @ @ @ @ used as an antiviral food material to control norovirus foodborne diseases .

Norovirus is a major cause of foodborne disease and nonbacterial gastroenteritis globally. This study evaluated the antiviral effects ofextract and its honokiol and magnolol constituents against human norovirus surrogates, murine norovirus (MNV) and feline calicivirus (FCV), and in model food systems. Pretreatment or cotreatment of.extract at 1 mg/mL reduced MNV and FCV titers by 0.6-1.8 log. Honokiol and magnolol, which are the major polyphenols in the extract, showed significant antiviral effects against MNV and FCV. The virus-infected cells that were treated with.extract exhibited significantly increased glutathione levels ( < 0.05). The extract, honokiol, and magnolol revealed ferric ion-reducing and 2,2-diphenyl-1-picrylhydrazyl radical scavenging activities in a dose-dependent manner. Furthermore, MNV and FCV titers were reduced by>1.6 log or to undetectable levels in apple, orange, and plum juices and by 0.9 and 1.6 log in milk, respectively, when they were treated with the extract at 5 mg/mL. Therefore, the present study suggests that.extract can be used as an antiviral food material to control norovirus foodborne diseases.


greenmedinfo--2020-07-31--L-theanine reduced the development of knee osteoarthritis.

The etiology of osteoarthritis ( OA ) is multifactorial , with no effective disease-modifying-drugs .
L-theanine has been reported to inhibit inflammatory responses in some diseases and this study aimed to investigate the effect of L-theanine on Interleukin-1 ( IL-1 ) β-stimulated chondrocytes , and in an injury-induced OA rat model .
Primary chondrocytes were stimulated by IL-1β ( 10 ng/mL ) for 24 h and then co-cultured with L-theanine for 24 h. The effects of L-theanine on IL-1β-stimulated expression of pro-inflammatory cytokines and hydrolytic enzyme were analyzed using Western blotting , quantitative polymerase chain reaction ( q-PCR ) and @ @ @ @ @ @ @ .
An immunofluorescence assay was used to detect nuclear factor kappa B ( NF-κB ) phosphorylation .
OA was induced by anterior cruciate ligament transection ( ACLT ) surgery in rats and celecoxib was used as a positive control .
OA severity was measured using the Osteoarthritis Research Society International ( OARSI ) grading system to describe histological changes .
The results showed that L-theanine decreased the expression of pro-inflammatory mediators , including cyclooxygenase-2 ( COX-2 ) , prostaglandin E2 ( PGE-2 ) , inducible nitric oxide synthase ( iNOS ) , and @ @ @ @ @ @ @ in vivo and in vitro .
L-theanine treatment inhibited IL-1β-induced upregulation of matrix metalloproteinases ( MMP ) -3 and MMP-13 , as well as inhibited NF-κB p65 activation .
In vivo animal model showed that L-theanine administration ( 200 mg/kg ) significantly alleviated OA lesions and decreased OARSI score .
Our data indicated that L-theanine decreased inflammatory cytokines and protected extracellular matrix degradation through inhibition of the NF-κB pathway , and L-theanine may be considered a promising therapeutic strategy in OA prevention .

The etiology of osteoarthritis (OA) is multifactorial, with no effective disease-modifying-drugs. L-theanine has been reported to inhibit inflammatory responses in some diseases and this study aimed to investigate the effect of L-theanine on Interleukin-1(IL-1)β-stimulated chondrocytes, and in an injury-induced OA rat model. Primary chondrocytes were stimulated by IL-1β (10 ng/mL) for 24 h and then co-cultured with L-theanine for 24 h. The effects of L-theanine on IL-1β-stimulated expression of pro-inflammatory cytokines and hydrolytic enzyme were analyzed using Western blotting, quantitative polymerase chain reaction (q-PCR) and enzyme-linked immunosorbent assay (ELISA) kits. An immunofluorescence assay was used to detect nuclear factor kappa B (NF-κB) phosphorylation. OA was induced by anterior cruciate ligament transection (ACLT) surgery in rats and celecoxib was used as a positive control. OA severity was measured using the Osteoarthritis Research Society International (OARSI) grading system to describe histological changes. The results showed that L-theanine decreased the expression of pro-inflammatory mediators, including cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE-2), inducible nitric oxide synthase (iNOS), and nitric oxide (NO), both in vivo and in vitro. L-theanine treatment inhibited IL-1β-induced upregulation of matrix metalloproteinases (MMP)-3 and MMP-13, as well as inhibited NF-κB p65 activation. In vivo animal model showed that L-theanine administration (200 mg/kg) significantly alleviated OA lesions and decreased OARSI score. Our data indicated that L-theanine decreased inflammatory cytokines and protected extracellular matrix degradation through inhibition of the NF-κB pathway, and L-theanine may be considered a promising therapeutic strategy in OA prevention.


greenmedinfo--2020-07-31--Protective effects of L-theanine on rats with dextran sulfate sodium-induced inflammatory bowel dise

Protective effects of L-theanine on rats with dextran sulfate sodium-induced inflammatory bowel disease.

The aim of this study is to evaluate the anti-inflammatory and protective effects of L-theanine in inflammatory bowel disease ( IBD ) and to identify the underlying molecular mechanisms .
Rats were pre-treated with L-theanine at 0 , 50 , 200 , or 800 mg/kg/day .
IBD was induced in rats using dextran sulfate sodium ( DSS ) .
Histopathological analysis suggests that L-theanine can suppress DSS-induced IBD with significant inhibition of inflammation in large and small intestinal tissues .
Moreover , the 200 mg/kg/day L-theanine-treated DSS group had higher body and small intestine weights , a lower disease activity @ @ @ @ @ @ @ the DSS group without pre-treatment .
In RNA sequencing and tandem mass tag labeling analyses , large number of mRNAs and proteins expression level differed when compared with the DSS-induced rats with and without 200 mg/kg/day L-theanine pre-treatment .
Moreover , Kyoto Encyclopedia of Genes and Genomes pathway analysis indicates the anti-inflammatory activities of L-theanine in DSS-induced IBD , with a high representation of genes in '' Cholesterol metabolism '' and '' Retinol metabolism '' pathways .
Analysis of protein-protein interaction networks further indicates the involvement of these two pathways .
These studies @ @ @ @ @ @ @ DSS-induced IBD through molecular mechanisms involving cholesterol and retinol metabolism .

The aim of this study is to evaluate the anti-inflammatory and protective effects of L-theanine in inflammatory bowel disease (IBD) and to identify the underlying molecular mechanisms. Rats were pre-treated with L-theanine at 0, 50, 200, or 800 mg/kg/day. IBD was induced in rats using dextran sulfate sodium (DSS). Histopathological analysis suggests that L-theanine can suppress DSS-induced IBD with significant inhibition of inflammation in large and small intestinal tissues. Moreover, the 200 mg/kg/day L-theanine-treated DSS group had higher body and small intestine weights, a lower disease activity index and expression of inflammatory factors than the DSS group without pre-treatment. In RNA sequencing and tandem mass tag labeling analyses, large number of mRNAs and proteins expression level differed when compared with the DSS-induced rats with and without 200 mg/kg/day L-theanine pre-treatment. Moreover, Kyoto Encyclopedia of Genes and Genomes pathway analysis indicates the anti-inflammatory activities of L-theanine in DSS-induced IBD, with a high representation of genes in"Cholesterol metabolism"and"Retinol metabolism"pathways. Analysis of protein-protein interaction networks further indicates the involvement of these two pathways. These studies suggest that medium-dose L-theanine pre-treatment could ameliorate DSS-induced IBD through molecular mechanisms involving cholesterol and retinol metabolism.


greenmedinfo--2020-07-31--Cystine and Theanine may be beneficial for preventing oxaliplatin-induced peripheral neuropathy.

Oxaliplatin frequently causes severe peripheral neuropathy as a dose-limiting toxicity .
However , this toxicity lacks a strategy for prevention @ @ @ @ @ , which includes precursors for the biosynthesis of glutathione .
In this study , we @ @ @ @ @ on oxaliplatin-induced peripheral neuropathy using an in vivo model .
Repeated injection of oxaliplatin ( @ @ @ @ @ week for 2 weeks ) caused mechanical allodynia , cold hyperalgesia and axonal degeneration of @ @ @ @ @ .
Mechanical allodynia and axonal degeneration , but not cold hyperalgesia , were ameliorated by @ @ @ @ @ 200 mg/kg orally ( p.o . )
] and Theanine ( 80 mg/kg p.o. )
@ @ @ @ @ Cystine and Theanine to rats significantly increased the glutathione level in the sciatic nerve compared @ @ @ @ @ Furthermore , Cystine and Theanine did not attenuate the tumour cytotoxicity of oxaliplatin in C-26 @ @ @ @ @ findings suggest that Cystine and Theanine may be beneficial for preventing oxaliplatin-induced peripheral neuropathy .

Oxaliplatin frequently causes severe peripheral neuropathy as a dose-limiting toxicity. However, this toxicity lacks a strategy for prevention. Cystine/Theanine is a supplement, which includes precursors for the biosynthesis of glutathione. In this study, we investigated the effects of Cystine/Theanine on oxaliplatin-induced peripheral neuropathy using an in vivo model. Repeated injection of oxaliplatin (4 mg/kg intraperitoneally twice a week for 2 weeks) caused mechanical allodynia, cold hyperalgesia and axonal degeneration of the sciatic nerve in rats. Mechanical allodynia and axonal degeneration, but not cold hyperalgesia, were ameliorated by daily co-administration of Cystine [200 mg/kg orally(p.o.)] and Theanine (80 mg/kg p.o.). Moreover, co-administration of Cystine and Theanine to rats significantly increased the glutathione level in the sciatic nerve compared with the oxaliplatin group. Furthermore, Cystine and Theanine did not attenuate the tumour cytotoxicity of oxaliplatin in C-26 tumour cell-bearing mice. These findings suggest that Cystine and Theanine may be beneficial for preventing oxaliplatin-induced peripheral neuropathy.


greenmedinfo--2020-07-31--Astaxanthin may inhibit gastric diseases associated with H. pylori infection.

( ) infection leads to the massive apoptosis of the gastric epithelial cells , causing gastric ulcers , gastritis , and gastric adenocarcinoma .
Autophagy is a cellular recycling process that plays important roles in cell death decisions and can protect cells by preventing apoptosis .
Upon the induction of autophagy , the level of the autophagy substrate p62 is reduced and the autophagy-related ratio of microtubule-associated proteins 1A/1B light chain 3B ( LC3B ) -II/LC3B-I is heightened .
AMP-activated protein kinase ( AMPK ) and mammalian target of rapamycin ( mTOR ) are involved in the regulation of autophagy @ @ @ @ @ @ @ potent anti-oxidant that plays anti-inflammatory and anti-cancer roles in various cells .
In the present study , we examined whether AST inhibits-induced apoptosis through AMPK-mediated autophagy in the human gastric epithelial cell line AGS ( adenocarcinoma gastric ) in vitro .
In this study , induced apoptosis .
Compound C , an AMPK inhibitor , enhanced the-induced apoptosis of AGS cells .
In contrast , metformin , an AMPK activator , suppressed-induced apoptosis , showing that AMPK activation inhibits-induced apoptosis .
AST inhibited-induced apoptosis by increasing the phosphorylation of AMPK and decreasing the @ @ @ @ @ @ @ ) and mTOR in-stimulated cells .
The number of LC3B puncta in-stimulated cells increased with AST .
These results suggest that AST suppresses the-induced apoptosis of AGS cells by inducing autophagy through the activation of AMPK and the downregulation of its downstream target , mTOR .
In conclusion , AST may inhibit gastric diseases associated withinfection by increasing autophagy through the activation of the AMPK pathway .

() infection leads to the massive apoptosis of the gastric epithelial cells, causing gastric ulcers, gastritis, and gastric adenocarcinoma. Autophagy is a cellular recycling process that plays important roles in cell death decisions and can protect cells by preventing apoptosis. Upon the induction of autophagy, the level of the autophagy substrate p62 is reduced and the autophagy-related ratio of microtubule-associated proteins 1A/1B light chain 3B (LC3B)-II/LC3B-I is heightened. AMP-activated protein kinase (AMPK) and mammalian target of rapamycin (mTOR) are involved in the regulation of autophagy. Astaxanthin (AST) is a potent anti-oxidant that plays anti-inflammatory and anti-cancer roles in various cells. In the present study, we examined whether AST inhibits-induced apoptosis through AMPK-mediated autophagy in the human gastric epithelial cell line AGS (adenocarcinoma gastric) in vitro. In this study,induced apoptosis. Compound C, an AMPK inhibitor, enhanced the-induced apoptosis of AGS cells. In contrast, metformin, an AMPK activator, suppressed-induced apoptosis, showing that AMPK activation inhibits-induced apoptosis. AST inhibited-induced apoptosis by increasing the phosphorylation of AMPK and decreasing the phosphorylation of RAC-alpha serine/threonine-protein kinase (Akt) and mTOR in-stimulated cells. The number of LC3B puncta in-stimulated cells increased with AST. These results suggest that AST suppresses the-induced apoptosis of AGS cells by inducing autophagy through the activation of AMPK and the downregulation of its downstream target, mTOR. In conclusion, AST may inhibit gastric diseases associated withinfection by increasing autophagy through the activation of the AMPK pathway.


greenmedinfo--2020-07-31--Astaxanthin supplementation may be effective for some types of normal tension glaucoma in which glut

Astaxanthin supplementation may be effective for some types of normal tension glaucoma in which glutamate neurotoxicity and oxidative stress are involved.

Astaxanthin ( AST ) , a natural marine carotenoid , possess a wide variety of biological functions .
In particular , as a strong antioxidant , AST effectively scavenges oxygen free radicals and reduces oxidative stress .
In addition , recentstudies have suggested that AST attenuates glutamate-induced apoptosis and cytotoxicity .
The glutamate/aspartate transporter ( GLAST ) deficient ( GLAST ) mouse is a mouse model of normal tension glaucoma ( NTG ) caused by both the glutamate neurotoxicity and oxidative stress in the retina .
In the present study , we investigated the effects of AST on the ganglion @ @ @ @ @ @ @ damage , using spectral domain-optical coherence tomography .
As a result , AST significantly attenuated the thinning of ganglion cell complex in GLASTmice in comparison to an AST-free control group .
Our results suggest the possibility that AST has protective effects against glutamate neurotoxicity and oxidative stress in the retina .
At present , the only treatment for NTG that is available in the clinical setting is to reduce the IOP as much as possible .
Thus , our results suggest that AST supplementation may be effective for some types of NTG in @ @ @ @ @ @ @ involved .

Astaxanthin (AST), a natural marine carotenoid, possess a wide variety of biological functions. In particular, as a strong antioxidant, AST effectively scavenges oxygen free radicals and reduces oxidative stress. In addition, recentstudies have suggested that AST attenuates glutamate-induced apoptosis and cytotoxicity. The glutamate/aspartate transporter (GLAST) deficient (GLAST) mouse is a mouse model of normal tension glaucoma (NTG) caused by both the glutamate neurotoxicity and oxidative stress in the retina. In the present study, we investigated the effects of AST on the ganglion cell complex, indicator of glaucomatous structural damage, using spectral domain-optical coherence tomography. As a result, AST significantly attenuated the thinning of ganglion cell complex in GLASTmice in comparison to an AST-free control group. Our results suggest the possibility that AST has protective effects against glutamate neurotoxicity and oxidative stress in the retina. At present, the only treatment for NTG that is available in the clinical setting is to reduce the IOP as much as possible. Thus, our results suggest that AST supplementation may be effective for some types of NTG in which glutamate neurotoxicity and oxidative stress are involved.


greenmedinfo--2020-07-31--Astaxanthin has anti-migration and invasion effects against human glioblastoma cells.

OBJECTIVES : The study was to investigate anti-migration and invasion effects of astaxanthin ( ATX ) , a natural carotenoid @ @ @ @ @ , against A172 human glioblastoma cells .
MATERIALS AND METHODS : Cell viability after ATX @ @ @ @ @ assays .
Tumor cell migration and invasion were observed by scratch and Boyden chamber assays @ @ @ @ @ MMP-2 and activity of MMP-9 were observed by immunoblotting and gelatin zymography , respectively .
@ @ @ @ @ 150µM was not toxic to A172 cells at 48 h post-treatment .
In contrast , @ @ @ @ @ µM significantly decreased migration and invasion of A172 cells at 24 and 48 h post-treatment @ @ @ @ @ is associated with the reduction of MMP-2 and MMP-9 expressions in a dose-dependentmanner .
CONCLUSION @ @ @ @ @ ATX has anti-migration and invasion effects against human glioblastoma cells and might be applicable for @ @ @ @ @ glioblastoma .

OBJECTIVES: The study was to investigate anti-migration and invasion effects of astaxanthin (ATX), a natural carotenoid derivative distributed in marine environments, against A172 human glioblastoma cells.
MATERIALS AND METHODS: Cell viability after ATX treatment was measured by MTT assays. Tumor cell migration and invasion were observed by scratch and Boyden chamber assays, respectively. Expression of MMP-2 and activity of MMP-9 were observed by immunoblotting and gelatin zymography, respectively.
RESULTS: ATX up to 150µM was not toxic to A172 cells at 48 h post-treatment. In contrast, ATX at 50 and 100 µM significantly decreased migration and invasion of A172 cells at 24 and 48 h post-treatment. Metastatic-reducing effect of ATX is associated with the reduction of MMP-2 and MMP-9 expressions in a dose-dependentmanner.
CONCLUSION: This finding indicated that ATX has anti-migration and invasion effects against human glioblastoma cells and might be applicable for the protection against metastasis of glioblastoma.


greenmedinfo--2020-07-31--Astaxanthin exerted a dose-dependent protective effect on photoreceptor cells against damage mediate

Astaxanthin exerted a dose-dependent protective effect on photoreceptor cells against damage mediated by blue light LED exposure.

Light-emitting diodes ( LEDs ) are widely used and energy-efficient light sources in modern life that emit higher levels of short-wavelength blue light .
Excessive blue light exposure may damage the photoreceptor cells in our eyes .
Astaxanthin , a xanthophyll that is abundantly available in seafood , is a potent free radical scavenger and anti-inflammatory agent .
We used a 661W photoreceptor cell line to investigate the protective effect of astaxanthin on blue light LED-induced retinal injury .
The cells were treated with various concentrations of astaxanthin and then exposed to blue light LED .
Our results showed that @ @ @ @ @ @ @ cell apoptosis and prevented cell death .
Moreover , the protective effect was concentration dependent .
Astaxanthin suppressed the production of reactive oxygen species and oxidative stress biomarkers and diminished mitochondrial damage induced by blue light exposure .
Western blot analysis confirmed that astaxanthin activated the PI3K/Akt pathway , induced the nuclear translocation of Nrf2 , and increased the expression of phase II antioxidant enzymes .
The expression of antioxidant enzymes and the suppression of apoptosis-related proteins eventually protected the 661W cells against blue light LED-induced cell damage .
Thus , our results @ @ @ @ @ @ @ effect on photoreceptor cells against damage mediated by blue light LED exposure .

Light-emitting diodes (LEDs) are widely used and energy-efficient light sources in modern life that emit higher levels of short-wavelength blue light. Excessive blue light exposure may damage the photoreceptor cells in our eyes. Astaxanthin, a xanthophyll that is abundantly available in seafood, is a potent free radical scavenger and anti-inflammatory agent. We used a 661W photoreceptor cell line to investigate the protective effect of astaxanthin on blue light LED-induced retinal injury. The cells were treated with various concentrations of astaxanthin and then exposed to blue light LED. Our results showed that pretreatment with astaxanthin inhibited blue light LED-induced cell apoptosis and prevented cell death. Moreover, the protective effect was concentration dependent. Astaxanthin suppressed the production of reactive oxygen species and oxidative stress biomarkers and diminished mitochondrial damage induced by blue light exposure. Western blot analysis confirmed that astaxanthin activated the PI3K/Akt pathway, induced the nuclear translocation of Nrf2, and increased the expression of phase II antioxidant enzymes. The expression of antioxidant enzymes and the suppression of apoptosis-related proteins eventually protected the 661W cells against blue light LED-induced cell damage. Thus, our results demonstrated that astaxanthin exerted a dose-dependent protective effect on photoreceptor cells against damage mediated by blue light LED exposure.


greenmedinfo--2020-07-31--Astragaloside IV alleviates the brain damage induced by subarachnoid hemorrhage.

Subarachnoid hemorrhage ( SAH ) caused brain damage accounts for more than 20 % death of patients with cerebrovascular diseases .
We aimed to investigate the effects of Astragaloside IV ( AS-IV ) on SAH-induced brain damage and its underlying mechanism .
SAH rat model was established and treated with or without AS-IV .
Brain injury and function were evaluated by neurological score , brain water content , Nissl staining , and behavioral experiments using Morris water maze .
The protein expression related to SAH caused inflammation and neuron apoptosis were assessed .
As expected , after 24 h of @ @ @ @ @ @ @ score and the number of intact neurons were significantly reduced in SAH rats compared to sham rats , but AS-IV treatment dramatically elevated the two scores and the number of intact neuron number .
Brain water content that increased after SAH was also declinedin AS-IV treated rats compared to untreated rats .
In addition , SAH rats treated with AS-IV also showed better neurological outcomes than untreated SAH rats including shorter escape time and swimming distance , longer quadrant stay in the Morris water maze and increased fall latency from the rod rotating @ @ @ @ @ @ @ rats , the anti-apoptosis pathway phosphoinositide 3-kinase ( PI3K ) / protein kinase B ( Akt ) was activated while nuclear factor-κB ( NF-κB ) signaling was markedly repressed by AS-IV .
Several apoptosis associated genes including FoxO1 , Bim , Bax and a typical apoptosis marker cleaved-caspase-3 were all downregulated by AS-IV .
In conclusion , this study found a protective role of AS-IV in SAH-induced brain injury through regulating PI3K and NF-κB signaling pathways .

Subarachnoid hemorrhage (SAH) caused brain damage accounts for more than 20 % death of patients with cerebrovascular diseases. We aimed to investigate the effects of Astragaloside IV (AS-IV) on SAH-induced brain damage and its underlying mechanism. SAH rat model was established and treated with or without AS-IV. Brain injury and function were evaluated by neurological score, brain water content, Nissl staining, and behavioral experiments using Morris water maze. The protein expression related to SAH caused inflammation and neuron apoptosis were assessed. As expected, after 24 h of SAH, Garcia score, beam balance score and the number of intact neurons were significantly reduced in SAH rats compared to sham rats, but AS-IV treatment dramatically elevated the two scores and the number of intact neuron number. Brain water content that increased after SAH was also declinedin AS-IV treated rats compared to untreated rats. In addition, SAH rats treated with AS-IV also showed better neurological outcomes than untreated SAH rats including shorter escape time and swimming distance, longer quadrant stay in the Morris water maze and increased fall latency from the rod rotating. In addition, in the SAH rats, the anti-apoptosis pathway phosphoinositide 3-kinase (PI3K)/ protein kinase B (Akt) was activated while nuclear factor-κB (NF-κB) signaling was markedly repressed by AS-IV. Several apoptosis associated genes including FoxO1, Bim, Bax and a typical apoptosis marker cleaved-caspase-3 were all downregulated by AS-IV. In conclusion, this study found a protective role of AS-IV in SAH-induced brain injury through regulating PI3K and NF-κB signaling pathways.


greenmedinfo--2020-07-31--Astragaloside IV as a potential antioxidant against diabetic ketoacidosis.

OBJECT : Astragaloside IV ( AS IV ) has antioxidative and anti-apoptotic properties , however , its effects on juvenile mice with diabetic ketoacidosis ( DKA ) have not been determined .
This study aims to explore the effect and mechanism of Astragaloside IV ( AS-IV ) on juvenile mice with DKA .
METHODS : DKA model was established through intraperitoneal injection of streptozotocin ( STZ ) and alloxan ( ALX ) .
DKA mice were divided into Control group , DKA group , DKA+AS-IV group , DKA+AS-IV+SP600125 group , DKA+AS-IV+Anisomycin group , DKA+AS-IV+GV248 group and DKA+AS-IV+GV248-Nrf2 group .
To @ @ @ @ @ @ @ , JNK inhibitor SP600125 and activator Anisomycin were injected .
The effects of AS-IV on antioxidant capacity and pathologies of pancreatic tissues in DKA juvenile mice were assessed .
The expression of JNK/Nrf2 signal pathway was measured by Western blot .
RESULTS : DKA juvenile mouse models were successfully established , evidenced by elevated blood glucose and blood ketone , suppressed insulin and pH value , and notable injuries in pancreatic tissues .
Gavage of AS-IV can enhance antioxidant capacity of pancreatic tissue and ameliorate injuries in pancreatic tissues .
AS-IV increased insulin @ @ @ @ @ @ @ glucose in DKA juvenile mice .
In pancreatic tissues of DKA juvenile mice , protein level of p-JNK/JNK in pancreatic tissue and Nrf2 in the nuclei were increased after administration of AS-IV .
Inhibition on JNK/Nrf2 signal pathway would impair the favorable effect of AS-IV on DKA juvenile mice , while antioxidant capacity , insulin level and blood glucose were improved in DKA juvenile mice injected an activator of JNK/Nrf2 pathway .
CONCLUSION : Collectively , AS-IV can enhance the antioxidant capacity of DKA juvenile mice to decrease blood glucose and to increase @ @ @ @ @ @ @ action may be realized through the JNK/Nrf2 pathway .

OBJECT: Astragaloside IV (AS IV) has antioxidative and anti-apoptotic properties, however, its effects on juvenile mice with diabetic ketoacidosis (DKA) have not been determined. This study aims to explore the effect and mechanism of Astragaloside IV (AS-IV) on juvenile mice with DKA.
METHODS: DKA model was established through intraperitoneal injection of streptozotocin (STZ) and alloxan (ALX). DKA mice were divided into Control group, DKA group, DKA+AS-IV group, DKA+AS-IV+SP600125 group, DKA+AS-IV+Anisomycin group, DKA+AS-IV+GV248 group and DKA+AS-IV+GV248-Nrf2 group. To verify the implication of JNK signal pathway, JNK inhibitor SP600125 and activator Anisomycin were injected. The effects of AS-IV on antioxidant capacity and pathologies of pancreatic tissues in DKA juvenile mice were assessed. The expression of JNK/Nrf2 signal pathway was measured by Western blot.
RESULTS: DKA juvenile mouse models were successfully established, evidenced by elevated blood glucose and blood ketone, suppressed insulin and pH value, and notable injuries in pancreatic tissues. Gavage of AS-IV can enhance antioxidant capacity of pancreatic tissue and ameliorate injuries in pancreatic tissues. AS-IV increased insulin level, in addition to suppressing blood glucose in DKA juvenile mice. In pancreatic tissues of DKA juvenile mice, protein level of p-JNK/JNK in pancreatic tissue and Nrf2 in the nuclei were increased after administration of AS-IV. Inhibition on JNK/Nrf2 signal pathway would impair the favorable effect of AS-IV on DKA juvenile mice, while antioxidant capacity, insulin level and blood glucose were improved in DKA juvenile mice injected an activator of JNK/Nrf2 pathway.
CONCLUSION: Collectively, AS-IV can enhance the antioxidant capacity of DKA juvenile mice to decrease blood glucose and to increase serum insulin secretion. The mechanism of action may be realized through the JNK/Nrf2 pathway.


greenmedinfo--2020-07-31--Astragaloside IV protects retinal pigment epithelial cells from apoptosis by upregulating miR-128 ex

Astragaloside IV protects retinal pigment epithelial cells from apoptosis by upregulating miR-128 expression.

The present study aimed to investigate the protective effects exerted by astragaloside‑IV ( AIV ) on retinal pigment epithelial ( RPE ) cells of rats with diabetes mellitus ( DM ) , and to explore the underlying molecular mechanisms .
For this purpose , a rat model of DM was established by injecting rats with an intraperitoneal injection of streptozotocin .
AIV was then intragastrically administered .
An electroretinogram ( ERG ) was used to assess retinopathy and TUNEL staining was used to detect the level of apoptosis of RPE cells .
Western blot analysis was used to determine protein @ @ @ @ @ @ @ in vivo .
AIV was found to be able to significantly increase body weight and decrease blood glucose levels in rats with DM in a dose‑dependent manner .
Compared with the rats with DM , the rat rod cell response a wave , b wave , maximum response b wave , photopic ( photo ) ‑ERG b wave and oscillatory potential ( OP ) p4 wave latency significantly decreased and the amplitude of OP Os1 wave increased significantly in the rats with DM treated with AIV for 11 weeks .
In addition , @ @ @ @ @ @ @ RPE cells from rats with DM and significantly decreased the protein expression levels of Bax/Bcl‑2 , Fas/FasL , active caspase‑3 , active caspase‑8 , active caspase‑9 , homeobox B3 ( HOXB3 ) , p‑phosphoinositide 3‑kinase ( PI3K ) /PI3K , p‑AKT/AKT and p‑p70S6K1/p70S6K1 , whereas it significantly increased miR‑128 expression in the RPE cells from rats with DM .
In vitro , AIV significantly inhibited the high glucose ( HG ) ‑induced apoptosis of RPE cells by increasing miR‑128 expression and Bcl‑2 and FasL protein expression in vivo .
On the whole , @ @ @ @ @ @ @ that AIV treatment protects RPE cells of diabetic rats from apoptosis , and that these effects may be associated with the upregulationof miR‑128 expression .

The present study aimed to investigate the protective effects exerted by astragaloside‑IV (AIV) on retinal pigment epithelial (RPE) cells of rats with diabetes mellitus (DM), and to explore the underlying molecular mechanisms. For this purpose, a rat model of DM was established by injecting rats with an intraperitoneal injection of streptozotocin. AIV was then intragastrically administered. An electroretinogram (ERG) was used to assess retinopathy and TUNEL staining was used to detect the level of apoptosis of RPE cells. Western blot analysis was used to determine protein expression in RPE cells in vitro and in vivo. AIV was found to be able to significantly increase body weight and decrease blood glucose levels in rats with DM in a dose‑dependent manner. Compared with the rats with DM, the rat rod cell response a wave, b wave, maximum response b wave, photopic (photo)‑ERG b wave and oscillatory potential (OP) p4 wave latency significantly decreased and the amplitude of OP Os1 wave increased significantly in the rats with DM treated with AIV for 11 weeks. In addition, AIV significantly decreased the apoptotic levels of RPE cells from rats with DM and significantly decreased the protein expression levels of Bax/Bcl‑2, Fas/FasL, active caspase‑3, active caspase‑8, active caspase‑9, homeobox B3 (HOXB3), p‑phosphoinositide 3‑kinase (PI3K)/PI3K, p‑AKT/AKT and p‑p70S6K1/p70S6K1, whereas it significantly increased miR‑128 expression in the RPE cells from rats with DM. In vitro, AIV significantly inhibited the high glucose (HG)‑induced apoptosis of RPE cells by increasing miR‑128 expression and Bcl‑2 and FasL protein expression in vivo. On the whole, the findings of the present study demonstrate that AIV treatment protects RPE cells of diabetic rats from apoptosis, and that these effects may be associated with the upregulationof miR‑128 expression.


greenmedinfo--2020-07-31--Astragaloside IV alleviates mouse slow transit constipation.

Gut microbiota and short-chain fatty acids ( SCFAs ) are associated with the development of various human diseases .
In this study , we examined the role of astragaloside IV in modulating mouse gut microbiota structure and the generation of SCFAs , as well as in slow transit constipation ( STC ) .
An STC model was established by treating mice with loperamide , in which the therapeutic effects of astragaloside IV were evaluated .
The microbiota community structure and SCFA content were analysed by 16S rRNA gene sequencing and gas chromatography-mass spectrometry , respectively .
The influence of butyrate @ @ @ @ @ @ @ model and Cajal cells ( ICC ) .
Astragaloside IV promoted defecation , improved intestinal mobility , suppressed ICC loss and alleviated colonic lesions in STC mice .
Alterations in gut microbiota community structure in STC mice , such as decreased Lactobacillus reuteri diversity , were improved following astragaloside IV treatment .
Moreover , astragaloside IV up-regulated butyric acid and valeric acid , but decreased isovaleric acid , in STC mouse stools .
Butyrate promoted defecation , improved intestinal mobility , and enhanced ICC proliferation by regulating the AKT-NF-κB signalling pathway .
Astragaloside @ @ @ @ @ @ @ and inhibited ICC loss by regulating the gut microbiota community structure and generating butyric acid .

Gut microbiota and short-chain fatty acids (SCFAs) are associated with the development of various human diseases. In this study, we examined the role of astragaloside IV in modulating mouse gut microbiota structure and the generation of SCFAs, as well as in slow transit constipation (STC). An STC model was established by treating mice with loperamide, in which the therapeutic effects of astragaloside IV were evaluated. The microbiota community structure and SCFA content were analysed by 16S rRNA gene sequencing and gas chromatography-mass spectrometry, respectively. The influence of butyrate on STC was assessed using a mouse model and Cajal cells (ICC). Astragaloside IV promoted defecation, improved intestinal mobility, suppressed ICC loss and alleviated colonic lesions in STC mice. Alterations in gut microbiota community structure in STC mice, such as decreased Lactobacillus reuteri diversity, were improved following astragaloside IV treatment. Moreover, astragaloside IV up-regulated butyric acid and valeric acid, but decreased isovaleric acid, in STC mouse stools. Butyrate promoted defecation, improved intestinal mobility, and enhanced ICC proliferation by regulating the AKT-NF-κB signalling pathway. Astragaloside IV promoted intestinal transit in STC mice and inhibited ICC loss by regulating the gut microbiota community structure and generating butyric acid.


greenmedinfo--2020-07-31--Astragaloside protects rat brain from microwave-induced functional injuries via restoring acetylchol

Astragaloside protects rat brain from microwave-induced functional injuries via restoring acetylcholine and normalizing electroencephalogram.

Studies from our group and others have reported that 30 mW/cmmicrowave could damage the structures of rat hippocampus , as well as impair the neuronal functions .
The neuroprotective effects of astragaloside , purified from Astragalus membranaceus , have been demonstrated in animal models of neurodegenerative diseases .
In this study , we found that 30 mW/cmmicrowave impaired spatial learning and memory ability in rats , while astragaloside could significantly alleviate the injuries .
The pathological analysis also showed that astragaloside protected neurons from microwave-induced damages , such as mitochondrial swelling and cavitation , rough endoplasmic reticulum swelling and dilation @ @ @ @ @ @ @ aggregation .
Moreover , microwave-induced structural damage of synapse resulted in downregulation of acetylcholine , an important neurotransmitter for information transmission , while astragaloside could protect the structure of synapse , as well as restore the acetylcholine level in rat hippocampus .
Furthermore , astragaloside also accelerated the recovery of brain electroencephalogram ( EEG ) after microwave exposure , indicating that astragaloside could promote the normalization of neuronal functions .
In conclusion , astragaloside protected the morphological structures and restored acetylcholine level in rat hippocampus , which could improve brain functions via normalizing @ @ @ @ @ @ @ be a promising candidate to treat microwave-induced injuries of central nervous system ( CNS ) .

Studies from our group and others have reported that 30 mW/cmmicrowave could damage the structures of rat hippocampus, as well as impair the neuronal functions. The neuroprotective effects of astragaloside, purified from Astragalus membranaceus, have been demonstrated in animal models of neurodegenerative diseases. In this study, we found that 30 mW/cmmicrowave impaired spatial learning and memory ability in rats, while astragaloside could significantly alleviate the injuries. The pathological analysis also showed that astragaloside protected neurons from microwave-induced damages, such as mitochondrial swelling and cavitation, rough endoplasmic reticulum swelling and dilation, synaptic gap disappearing, and vesicle aggregation. Moreover, microwave-induced structural damage of synapse resulted in downregulation of acetylcholine, an important neurotransmitter for information transmission, while astragaloside could protect the structure of synapse, as well as restore the acetylcholine level in rat hippocampus. Furthermore, astragaloside also accelerated the recovery of brain electroencephalogram (EEG) after microwave exposure, indicating that astragaloside could promote the normalization of neuronal functions. In conclusion, astragaloside protected the morphological structures and restored acetylcholine level in rat hippocampus, which could improve brain functions via normalizing brain EEG. Therefore, astragaloside might be a promising candidate to treat microwave-induced injuries of central nervous system (CNS).


greenmedinfo--2020-07-31--Astragaloside IV improves neurobehavior and promotes hippocampal neurogenesis.

Astragaloside IV ( AST ) as the main active ingredient of Astragalus membranaceus .
Clinical and laboratory-based studies have demonstrated the effects of AST on cerebral protection and angiogenesis after ischemia stroke .
In addition , several reports investigated the effect of AST on proliferation of neural stem cells .
The current study was aimed to evaluate the influence of AST on neurogenesis in hippocampal dentate gyrus ( DG ) of MCAO rats and to explore the possible mechanisms .
In this study , the neurobehavioral tests ( Ludmila Belayev 12-point scoring , Screen test , fore limb placing test @ @ @ @ @ @ @ effect of AST treatment against functional deficit of MCAO rats .
The immunofluorescence staining , western-blot and qRT-PCR was performed to evaluate the effects of AST on proliferation , differentiation and maturity of neural stemr cells in hippocampus .
Moreover , we investigated the possible mechanism of the AST treatment in promoting neurogenesis after ischemic stroke .
The findings indicated that AST treatment ameliorated the neurobehavior of MCAO rats .
The results indicated that AST treatment possessed the potential to improve proprioceptive sense and motor function of MCAO rats .
AST treatment sustained @ @ @ @ @ @ @ recovery in MCAO rats .
The results suggested that AST improved neurobehavior deficit after ischemic stroke .
Furthermore , AST promoted neurogenesis through upregulating the expressing of BNDF/TrkB signaling pathway .
Therefore AST might be a promising therapeutic agent for ischemic stroke .

Astragaloside IV (AST) as the main active ingredient of Astragalus membranaceus. Clinical and laboratory-based studies have demonstrated the effects of AST on cerebral protection and angiogenesis after ischemia stroke. In addition, several reports investigated the effect of AST on proliferation of neural stem cells. The current study was aimed to evaluate the influence of AST on neurogenesis in hippocampal dentate gyrus (DG) of MCAO rats and to explore the possible mechanisms. In this study, the neurobehavioral tests (Ludmila Belayev 12-point scoring, Screen test, fore limb placing test) had been employed to investigate the effect of AST treatment against functional deficit of MCAO rats. The immunofluorescence staining, western-blot and qRT-PCR was performed to evaluate the effects of AST on proliferation, differentiation and maturity of neural stemr cells in hippocampus. Moreover, we investigated the possible mechanism of the AST treatment in promoting neurogenesis after ischemic stroke. The findings indicated that AST treatment ameliorated the neurobehavior of MCAO rats. The results indicated that AST treatment possessed the potential to improve proprioceptive sense and motor function of MCAO rats. AST treatment sustained neuronal viability and stimulates sensorimotor integration functional recovery in MCAO rats. The results suggested that AST improved neurobehavior deficit after ischemic stroke. Furthermore, AST promoted neurogenesis through upregulating the expressing of BNDF/TrkB signaling pathway. Therefore AST might be a promising therapeutic agent for ischemic stroke.


greenmedinfo--2020-07-31--Astragaloside IV promotes anti-photoaging by enhancing the proliferation and paracrine activity of a

Astragaloside IV promotes anti-photoaging by enhancing the proliferation and paracrine activity of adipose-derived stem cells.

Photoaging is a degenerative biological process .
As a kind of pluripotent stem cells , adipose-derived stem cells ( ADSCs ) are widely used in the treatment of photoaging .
Therefore , we aimed to find an effective way to improve the anti-aging ability of ADSCs .
In this study , we isolated ADSCs and assessed multi-lineage differentiation ability and markers .
Cultured ADSCs were preconditioned with astragaloside IV ( ASI ) at 10-7M , 10-6M , and 10-5M .
Cell proliferation was assessed by CCK-8 assay and cytokine secretion by ELISA .
A fibroblast photoaging model was established and @ @ @ @ @ @ @ .
Matrix metalloproteinase-1 ( MMP1 ) and type I procollagen ( PC-I ) secreted by human dermal fibroblasts ( HDFs ) were measured by ELISA .
The effects of ASI-treated ADSCs on skin texture , including dermal thickness , collagen content , and microvessel density , in a photoaging animal model were analyzed using H & E staining , Masson staining , and CD31 immunohistochemistry , respectively .
We found that 10-6M ASI could significantly promote cell proliferation and stimulate robust secretion of growth factors in ADSCs .
Furthermore , our data showed @ @ @ @ @ @ @ ultraviolet B ( UVB ) -induced decrease of PC-I secretion and increase of MMP-1 release in fibroblasts .
Moreover , in photoaged skin of nude mice , ASI-treated ADSCs significantly increased dermal thickness , collagen content , and microvessel density .
Our results indicated that preconditioning with ASI stimulated ADSCs to secrete more useful growth factors and activate dermal fibroblasts and thus could be a potentially safe strategy to improve ADSC-based therapy .

Photoaging is a degenerative biological process. As a kind of pluripotent stem cells, adipose-derived stem cells (ADSCs) are widely used in the treatment of photoaging. Therefore, we aimed to find an effective way to improve the anti-aging ability of ADSCs. In this study, we isolated ADSCs and assessed multi-lineage differentiation ability and markers. Cultured ADSCs were preconditioned with astragaloside IV (ASI) at 10-7M, 10-6M, and 10-5M. Cell proliferation was assessed by CCK-8 assay and cytokine secretion by ELISA. A fibroblast photoaging model was established and co-cultured with normal ADSCs or ASI-treated ADSCs. Matrix metalloproteinase-1 (MMP1) and type I procollagen (PC-I) secreted by human dermal fibroblasts (HDFs) were measured by ELISA. The effects of ASI-treated ADSCs on skin texture, including dermal thickness, collagen content, and microvessel density, in a photoaging animal model were analyzed using H&E staining, Masson staining, and CD31 immunohistochemistry, respectively. We found that 10-6M ASI could significantly promote cell proliferation and stimulate robust secretion of growth factors in ADSCs. Furthermore, our data showed that ASI-treated ADSCs could markedly reverse the ultraviolet B (UVB)-induced decrease of PC-I secretion and increase of MMP-1 release in fibroblasts. Moreover, in photoaged skin of nude mice, ASI-treated ADSCs significantly increased dermal thickness, collagen content, and microvessel density. Our results indicated that preconditioning with ASI stimulated ADSCs to secrete more useful growth factors and activate dermal fibroblasts and thus could be a potentially safe strategy to improve ADSC-based therapy.


greenmedinfo--2020-07-31--S. platensis could be an adjunctive therapy for the management of type 2 diabetes.

Spirulina platensis has been found to be useful in the treatment of type 2 diabetes .
The present study aims to elucidate the effects of ethanol extract and butanol fraction of S. platensis on insulin release and glucose homoeostasis in type 2 diabetic rats , together with their mechanism of actions .
In vitro and in vivo methods were used including cellular studies to determine potential role of ion channels and cAMP in the insulinotropic actions of the extracts .
The ethanol extract and butanol fraction stimulated insulin release from mouse islets and pancreaticβ-cells in a concentration-dependent manner .
The @ @ @ @ @ @ @ from perfused rat pancreas .
The insulin-releasing action was augmented by glucose , isobutylmethylxanthine , tolbutamide and a depolarising concentration of KCl .
The insulin secretory effect was attenuated with diazoxide and verapamil and by omission of extracellular Ca2+ .
Butanol fraction was found to significantly inhibit dipeptidyl peptidase IV enzyme activity .
Moreover , butanol fraction improved glucose tolerance following oral glucose administration ( 2·5 g/kg body weight ( b.w. )
) .
The butanol fraction was tested on 24 h starved rats given an oral sucrose load ( 2·5 g/kg b.w @ @ @ @ @ @ @ carbohydrate digestion and absorption .
S. platensis substantially decreased postprandial hyperglycaemia after oral sucrose load and increased unabsorbed sucrose content throughout the gut .
During in situ intestinal perfusion with glucose , the butanol fraction reduced glucose absorption and promoted gut motility .
Finally , chronic oral administration of butanol fraction for 28 d significantly decreased blood glucose , increased plasma insulin , pancreatic insulin stores , liver glycogen and improved lipid profile .
The characterisation of active compounds from butanol fraction revealed the presence of p-coumaric acid , β-carotene , catechin and @ @ @ @ @ @ @ S. platensis could be an adjunctive therapy for the management of type 2 diabetes .

Spirulina platensis has been found to be useful in the treatment of type 2 diabetes. The present study aims to elucidate the effects of ethanol extract and butanol fraction of S. platensis on insulin release and glucose homoeostasis in type 2 diabetic rats, together with their mechanism of actions. In vitro and in vivo methods were used including cellular studies to determine potential role of ion channels and cAMP in the insulinotropic actions of the extracts. The ethanol extract and butanol fraction stimulated insulin release from mouse islets and pancreaticβ-cells in a concentration-dependent manner. The butanol fraction also similarly stimulated insulin release from perfused rat pancreas. The insulin-releasing action was augmented by glucose, isobutylmethylxanthine, tolbutamide and a depolarising concentration of KCl. The insulin secretory effect was attenuated with diazoxide and verapamil and by omission of extracellular Ca2+. Butanol fraction was found to significantly inhibit dipeptidyl peptidase IV enzyme activity. Moreover, butanol fraction improved glucose tolerance following oral glucose administration (2·5 g/kg body weight (b.w.)). The butanol fraction was tested on 24 h starved rats given an oral sucrose load (2·5 g/kg b.w.) to examine possible effects on carbohydrate digestion and absorption. S. platensis substantially decreased postprandial hyperglycaemia after oral sucrose load and increased unabsorbed sucrose content throughout the gut. During in situ intestinal perfusion with glucose, the butanol fraction reduced glucose absorption and promoted gut motility. Finally, chronic oral administration of butanol fraction for 28 d significantly decreased blood glucose, increased plasma insulin, pancreatic insulin stores, liver glycogen and improved lipid profile. The characterisation of active compounds from butanol fraction revealed the presence of p-coumaric acid, β-carotene, catechin and other antioxidant polyphenols. In conclusion, S. platensis could be an adjunctive therapy for the management of type 2 diabetes.


greenmedinfo--2020-07-31--Ferulic acid protects cardiomyocytes from TNF-α/cycloheximide-induced apoptosis.

Acute myocardial infarction ( AMI ) results in irreversible cardiac cell damage or death because of decreased blood flow to the heart .
Apoptosis plays an important role in the process of tissue damage after myocardial infarction ( MI ) , which has pathological and therapeutic implications .
Ferulic acid ( FA ) is a phenolic acid endowed with strong antioxidative and cytoprotective activities .
The present study aimed to investigate whether FA protects cardiomyocytes from apoptosis by regulating autophagy , which is a cellular self-digestion process , and one of the first lines of defense against oxidative stress .
@ @ @ @ @ @ @ ng/mL ) and cycloheximide ( CHX , 5 μg/mL ) in rat H9c2 cardiomyocytes .
FA-inhibited TNF-α/CHX-induced apoptosis was determined by the quantification of TUNEL-positive cells , and the effect was associated with decreased ROS production and inhibited caspase3 activation .
FA treatment enhanced autophagy and increased autophagy-associated protein expression , leading to an inhibition of mTOR signaling .
When co-treated with 3-methyladenine ( 3-MA ) , an autophagy inhibitor , the anti-apoptotic effect of FA was attenuated .
In an in vivo mouse MI model , FA treatment decreased the apoptotic cell @ @ @ @ @ @ @ improved cardiac performance , as determined by histological and echocardiographic assessments .
Taken collectively , these results suggest that FA could protect cardiomyocytes from apoptosis by enhancing autophagy .

Acute myocardial infarction (AMI) results in irreversible cardiac cell damage or death because of decreased blood flow to the heart. Apoptosis plays an important role in the process of tissue damage after myocardial infarction (MI), which has pathological and therapeutic implications. Ferulic acid (FA) is a phenolic acid endowed with strong antioxidative and cytoprotective activities. The present study aimed to investigate whether FA protects cardiomyocytes from apoptosis by regulating autophagy, which is a cellular self-digestion process, and one of the first lines of defense against oxidative stress. Apoptosis was induced by TNF-α (10 ng/mL) and cycloheximide (CHX, 5 μg/mL) in rat H9c2 cardiomyocytes. FA-inhibited TNF-α/CHX-induced apoptosis was determined by the quantification of TUNEL-positive cells, and the effect was associated with decreased ROS production and inhibited caspase3 activation. FA treatment enhanced autophagy and increased autophagy-associated protein expression, leading to an inhibition of mTOR signaling. When co-treated with 3-methyladenine (3-MA), an autophagy inhibitor, the anti-apoptotic effect of FA was attenuated. In an in vivo mouse MI model, FA treatment decreased the apoptotic cell number, reduced infarct size, and improved cardiac performance, as determined by histological and echocardiographic assessments. Taken collectively, these results suggest that FA could protect cardiomyocytes from apoptosis by enhancing autophagy.


greenmedinfo--2020-07-31--Transcriptomic analysis of multi-drug resistant Escherichia coli K-12 strain in response to Lavandul

Transcriptomic analysis of multi-drug resistant Escherichia coli K-12 strain in response to Lavandula angustifolia essential oil.

To better understand the synergistic antibacterial activity between piperacillin andessential oil ( LEO ) against multidrug-resistant , we performed microarray @ @ @ @ @ used alone and in combination with piperacillin against the non-treated control .
In total , @ @ @ @ @ after the combination of LEO and piperacillin treatment .
Among the up-regulated genes , ,are @ @ @ @ @ and nitrotoluene degradation , which were observed only in the LEO-piperacillin combinatory treatment .
Four @ @ @ @ @ result , andwere validated by qRT-PCR as these genes showed differential expression consistently in the @ @ @ @ @ analysis showed that there was upregulation of genes involved in several biological processes including fructose @ @ @ @ @ system ( PTS ) , lipopolysaccharide biosynthesis and nitrotoluene degradation .
Genes involved in microbial @ @ @ @ @ found both up- and down-regulated in LEO-piperacillin combinatory treatment .
Our study provides new information @ @ @ @ @ occur during the LEO and piperacillin interaction against the multidrug-resistant bacteria and contributes to unravel @ @ @ @ @ .

To better understand the synergistic antibacterial activity between piperacillin andessential oil (LEO) against multidrug-resistant, we performed microarray transcriptomic analysis of LEO when used alone and in combination with piperacillin against the non-treated control. In total, 90 genes were differentially expressed after the combination of LEO and piperacillin treatment. Among the up-regulated genes,,are known to control microbial metabolism and nitrotoluene degradation, which were observed only in the LEO-piperacillin combinatory treatment. Four candidate genes from the microarray result,andwere validated by qRT-PCR as these genes showed differential expression consistently in the two methods. Biochemical pathway analysis showed that there was upregulation of genes involved in several biological processes including fructose and mannose metabolism, phosphotransferase system (PTS), lipopolysaccharide biosynthesis and nitrotoluene degradation. Genes involved in microbial metabolism in diverse environments were found both up- and down-regulated in LEO-piperacillin combinatory treatment. Our study provides new information concerning the transcriptional changes that occur during the LEO and piperacillin interaction against the multidrug-resistant bacteria and contributes to unravel the mechanisms underlying this synergism.


greenmedinfo--2020-07-31--Anti-psoriatic effect of Lavandula angustifolia essential oil and its major components linalool and

Anti-psoriatic effect of Lavandula angustifolia essential oil and its major components linalool and linalyl acetate.

ETHNO-PHARMACOLOGICAL RELEVANCE : Lavender oil ( LO ) is an aromatic/essential oil extracted from Lavandula angustifolia and traditionally used as an aromatherapy massage oil due to its anti-inflammatory and wound healing property and also for providing the relief in other skin conditions such as psoriasis , dermatitis and eczema .
However , LO has not been evaluated scientifically for psoriasis like skin inflammation .
AIM OF THE STUDY : This study aimed to investigate the LO and its major components linalool ( L ) and linalyl acetate ( LA ) against psoriasis like skin inflammation .
MATERIALS AND METHODS : @ @ @ @ @ @ @ IMQ ) induced psoriasis like skin inflammation in BALB/c mice .
Assessment of anti-psoriatic effect of LO , L and LA was done on the basis of change in ear thickness , psoriasis area severity index ( PASI ) scoring at alternative day , CosCam scoring using skin analyzer equipped with SkinSys software , biochemical , immunohistochemical and histological investigations .
Level of effectiveness against psoriasis was investigated by percent reduction in PASI scores , skin analysis scores and level of Th-1 and Th-17 cell expressing cytokines , as compared to the diseased @ @ @ @ @ @ @ LO 10 % showed 73.67 % recovery in PASI and 87 % in Th-17 cell-specific cytokines towards normal as compared to disease group .
L and LA were identified as the major components of LO and favoured ligands for selected psoriasis targets .
At 2 % topical dose , L and LA showed 64 % and 47.61 % recovery in PASI scores , respectively .
Both , L and LA showed significant recovery in Th-1specific TNF-α and IL-1β however , only L showed significant recovery of Th-17 cytokines ( IL-17 and IL-22 ) @ @ @ @ @ @ @ restored granulosis ) , L restored epidermal hyperplasia and parakeratosis toward the normal condition .
On the other hand , L also reduced the expression of NF-κβ , ccr6 and IL-17 , while LA reduced the expression of NF-κβ only .
At 10 % topical dose , LO was observed to be slight irritant while at 2 % topical dose , L and LA were found non-irritant to the skin .
CONCLUSION : This study proves the effectiveness of LO and its major phytoconstituents linalool and linalyl acetate against IMQ induced psoriasis like @ @ @ @ @ @ @ for topical use of lavender oil .

ETHNO-PHARMACOLOGICAL RELEVANCE: Lavender oil (LO) is an aromatic/essential oil extracted from Lavandula angustifolia and traditionally used as an aromatherapy massage oil due to its anti-inflammatory and wound healing property and also for providing the relief in other skin conditions such as psoriasis, dermatitis and eczema. However, LO has not been evaluated scientifically for psoriasis like skin inflammation.
AIM OF THE STUDY: This study aimed to investigate the LO and its major components linalool (L) and linalyl acetate (LA) against psoriasis like skin inflammation.
MATERIALS AND METHODS: Anti-psoriatic activity was done using Imiquimod (IMQ) induced psoriasis like skin inflammation in BALB/c mice. Assessment of anti-psoriatic effect of LO, L and LA was done on the basis of change in ear thickness, psoriasis area severity index (PASI) scoring at alternative day, CosCam scoring using skin analyzer equipped with SkinSys software, biochemical, immunohistochemical and histological investigations. Level of effectiveness against psoriasis was investigated by percent reduction in PASI scores, skin analysis scores and level of Th-1 and Th-17 cell expressing cytokines, as compared to the diseased mice.
RESULTS: Topical application of LO 10% showed 73.67% recovery in PASI and 87% in Th-17 cell-specific cytokines towards normal as compared to disease group. L and LA were identified as the major components of LO and favoured ligands for selected psoriasis targets. At 2% topical dose, L and LA showed 64% and 47.61% recovery in PASI scores, respectively. Both, L and LA showed significant recovery in Th-1specific TNF-α and IL-1β however, only L showed significant recovery of Th-17 cytokines (IL-17 and IL-22). In contrast to LA (which restored granulosis), L restored epidermal hyperplasia and parakeratosis toward the normal condition. On the other hand, L also reduced the expression of NF-κβ, ccr6 and IL-17,while LA reduced the expression of NF-κβ only. At 10% topical dose, LO was observed to be slight irritant while at 2% topical dose, L and LA were found non-irritant to the skin.
CONCLUSION: This study proves the effectiveness of LO and its major phytoconstituents linalool and linalyl acetate against IMQ induced psoriasis like skin inflammation and provides the scientific evidence for topical use of lavender oil.


greenmedinfo--2020-07-31--Chemical characterization of Lavandula dentata essential oil cultivated in Chile and its antibiofilm

Chemical characterization of Lavandula dentata essential oil cultivated in Chile and its antibiofilm effect against candida albicans.

is the most common human fungal pathogen , and with the increase in resistance rates worldwide , it is necessary to search for new pharmacological alternatives.L .
essential oil is recognized as having antimicrobial properties .
However , its effect against fungal biofilms has been poorly described.-related infections involve the development of biofilms , which are highly resistant to conventional antifungals .
In this work , we evaluated the antibiofilm effect ofL .
essential oil againstFirst , we characterized the essential oil by gas chromatography-mass spectrometry .
The antifungal effect onreference strains was evaluated by a disk diffusion assay and @ @ @ @ @ @ @ a microdilution assay .
The effect of the essential oil on the adhesion ability ofwas determined through a crystal violet assay , and morphogenesis inhibition was assessed by light microscopy .
The effect of the essential oil on the microarchitecture of biofilms was evaluated through scanning electron microscopy .
Finally , the antibiofilm effect was evaluated through an adapted biofilm scratch assay and XTT viability assay .
The main constituent of the essential oil was the monoterpenoid eucalyptol ( 60 % ) .
The essential oil presented minimal inhibitory concentrations of 156 and @ @ @ @ @ @ @ This minimal inhibitory concentration inhibited adhesion , morphogenesis , biofilm formation , altered microarchitecture , and decreased the viability of established biofilms formed on abiotic surfaces for both strains assayed .
This study demonstrates that the essential oil fromcould be a promising treatment againstbiofilms .

is the most common human fungal pathogen, and with the increase in resistance rates worldwide, it is necessary to search for new pharmacological alternatives.L. essential oil is recognized as having antimicrobial properties. However, its effect against fungal biofilms has been poorly described.-related infections involve the development of biofilms, which are highly resistant to conventional antifungals. In this work, we evaluated the antibiofilm effect ofL. essential oil againstFirst, we characterized the essential oil by gas chromatography-mass spectrometry. The antifungal effect onreference strains was evaluated by a disk diffusion assay and the minimal inhibitory concentration was obtained through a microdilution assay. The effect of the essential oil on the adhesion ability ofwas determined through a crystal violet assay, and morphogenesis inhibition was assessed by light microscopy. The effect of the essential oil on the microarchitecture of biofilms was evaluated through scanning electron microscopy. Finally, the antibiofilm effect was evaluated through an adapted biofilm scratch assay and XTT viability assay. The main constituent of the essential oil was the monoterpenoid eucalyptol (60%). The essential oil presented minimal inhibitory concentrations of 156 and 130 µg/mL against two strains assayed. This minimal inhibitory concentration inhibited adhesion, morphogenesis, biofilm formation, altered microarchitecture, and decreased the viability of established biofilms formed on abiotic surfaces for both strains assayed. This study demonstrates that the essential oil fromcould be a promising treatment againstbiofilms.


greenmedinfo--2020-07-31--M. officinalis and L. angustifolia effect is similar to fluoxetine in mild to moderate depression.

BACKGROUND : Depression has rapidly progressed worldwide , and the need for an efficient treatment with low side effect has risen .
Melissa officinalis L and Lavandula angustifolia Mill have been traditionally used in Asia for the treatment of depression .
Many textbooks of traditional Persian medicine refer to these herbs for the treatment of depression while there are no adequate clinical trials to support this claim .
The present study aimed to evaluate the efficacy of M. officinalis and L. angustifolia compared to fluoxetine for the treatment of mild to moderate depression in an 8-week randomized , double-blind clinical @ @ @ @ @ @ @ who met the Diagnostic and Statistical Manual of Mental Disorders , 5th edition ( DSM-5 ) for major depression , were randomly assigned to 3 groups to daily receive either M. officinalis ( 2 g ) or L. angustifolia ( 2 g ) or fluoxetine ( 20 mg ) and were assessed in weeks 0 , 2 , 4 and 8 by the Hamilton Rating Scale for Depression ( HAM-D ) including 17 items .
RESULTS : Our study showed that M. officinalis and L. angustifolia effect similar to fluoxetine in mild to @ @ @ @ @ @ @ , df = 2,42 , p = 0.877 ) .
CONCLUSION : Due to some restrictions in this study including absence of placebo group , large-scale trials are needed to investigate the anti-depressant effect of these two herbs with more details .

BACKGROUND: Depression has rapidly progressed worldwide, and the need for an efficient treatment with low side effect has risen. Melissa officinalis L and Lavandula angustifolia Mill have been traditionally used in Asia for the treatment of depression. Many textbooks of traditional Persian medicine refer to these herbs for the treatment of depression while there are no adequate clinical trials to support this claim. The present study aimed to evaluate the efficacy of M. officinalis and L. angustifolia compared to fluoxetine for the treatment of mild to moderate depression in an 8-week randomized, double-blind clinical trial.
METHODS: Forty-five adult outpatients who met the Diagnostic and Statistical Manual of Mental Disorders, 5th edition (DSM-5) for major depression, were randomly assigned to 3 groups to daily receive either M. officinalis (2 g) or L. angustifolia (2 g) or fluoxetine (20 mg) and were assessed in weeks 0, 2, 4 and 8 by the Hamilton Rating Scale for Depression (HAM-D) including 17 items.
RESULTS: Our study showed that M. officinalis and L. angustifolia effect similar to fluoxetine in mild to moderate depression. (F = 0.131, df = 2,42, p = 0.877).
CONCLUSION: Due to some restrictions in this study including absence of placebo group, large-scale trials are needed to investigate the anti-depressant effect of these two herbs with more details.
TRIAL REGISTRATION: IRCT2014061718126N1 . Registration date: 2015-06-04-"Retrospectively registered".


greenmedinfo--2020-07-31--These data support the potential uses of M. officinalis in the treatment of heart ischemia- reperfus

These data support the potential uses of M. officinalis in the treatment of heart ischemia- reperfusion disorders.

has antioxidant and anti-inflammatory activities and is used in various diseases .
Aim of the studyWe investigated the role ofextract ( MOE ) against ischemia-induced arrhythmia and heart injury after five days of reperfusion in anrat model of regional heart ischemia .
The leaf extract ofwas standardized through HPLC analysis .
Adult male Sprague-Dawley rats ( n = 32 ) were subjected to 30 min of ischemia by occlusion of the left anterior descending coronary artery followed by 5 days of reperfusion .
The rats ( n = 8 in each group ) were randomized to receive vehicle oras follows @ @ @ @ @ @ @ with ischemia , groups II , III and IV received different doses of MOE- ( 25 , 50 and 100 mg/kg , respectively ) , by oral gavage daily for 14 days prior to ischemia .
Administration ofsignificantly improved ischemia/reperfusion ( I/R ) -induced myocardial dysfunction by reduction of infarct size , also , during the ischemic period , ventricular tachycardia , and ventricular ectopic beats episodes decreased as compared with that of the control group .
Stabilized ST segment changes and QTc shortening increased the R and T wave amplitudes and the @ @ @ @ @ @ @ also caused significant elevations in serum superoxide dismutase ( SOD ) activity as well as a significant decrease in serum cardiac troponin I ( CTnI ) , lactate dehydrogenase ( LDH ) , and malondialdehyde ( MDA ) levels , 5 days after reperfusion .
MOE-100mg/kg was the effective dose .
Cinamic acid ( 21.81± 1.26 mg/gr ) was the main phenolic compound of plant sample .
The ethanol extract ofwas observed to exhibit cardioprotective effects against I/R injury , probably due to antioxidant properties .
The results indicate that MOE has antioxidant @ @ @ @ @ @ @ ischemia-reperfusion induced injury as was reflected by reduction of infarct size and cardiac injury biomarkers .
These data support the potential uses of M. officinalis in the treatment of heart ischemia- reperfusion disorders and even developing new anti- arrhythmias drugs after further investigations .

has antioxidant and anti-inflammatory activities and is used in various diseases. Aim of the studyWe investigated the role ofextract (MOE) against ischemia-induced arrhythmia and heart injury after five days of reperfusion in anrat model of regional heart ischemia. The leaf extract ofwas standardized through HPLC analysis. Adult male Sprague-Dawley rats (n = 32) were subjected to 30 min of ischemia by occlusion of the left anterior descending coronary artery followed by 5 days of reperfusion. The rats (n = 8 in each group) were randomized to receive vehicle oras follows: group I served as saline control with ischemia, groups II, III and IV received different doses of MOE- (25, 50 and 100 mg/kg, respectively), by oral gavage daily for 14 days prior to ischemia. Administration ofsignificantly improved ischemia/reperfusion (I/R)-induced myocardial dysfunction by reduction of infarct size, also, during the ischemic period, ventricular tachycardia, and ventricular ectopic beats episodes decreased as compared with that of the control group. Stabilized ST segment changes and QTc shortening increased the R and T wave amplitudes and the heart rate during ischemia. The extract also caused significant elevations in serum superoxide dismutase (SOD) activity as well as a significant decrease in serum cardiac troponin I (CTnI), lactate dehydrogenase (LDH), and malondialdehyde (MDA) levels, 5 days after reperfusion. MOE-100mg/kg was the effective dose. Cinamic acid (21.81± 1.26 mg/gr) was the main phenolic compound of plant sample. The ethanol extract ofwas observed to exhibit cardioprotective effects against I/R injury, probably due to antioxidant properties. The results indicate that MOE has antioxidant and cardio-protective effects against ischemia-induced arrhythmias and ischemia-reperfusion induced injury as was reflected by reduction of infarct size and cardiac injury biomarkers. These data support the potential uses of M. officinalis in the treatment of heart ischemia- reperfusion disorders and even developing new anti- arrhythmias drugs after further investigations.


greenmedinfo--2020-07-31--L-theanine, Magnolia officinalis, and Melissa officinalis may represent a useful and safe candidate

L-theanine, Magnolia officinalis, and Melissa officinalis may represent a useful and safe candidate for the management of mood disorders.

Mood disorders represent one of the most prevalent and costly psychiatric diseases worldwide .
The current therapies are generally characterized by several well-known side effects which limit their prolonged use .
The use of herbal medicine for the management of several psychiatric conditions is becoming more established , as it is considered a safer support to conventional pharmacotherapy .
The aim of this study was to investigate the possible anxiolytic and antidepressant activity of a fixed combination of L-theanine , , and ( TMM ) in an attempt to evaluate how the multiple modulations of different physiological systems may contribute @ @ @ @ @ @ @ an anxiolytic-like and antidepressant-like activity in vivo , which was related to a neuroprotective effect in an in vitro model of excitotoxicity .
The effect of TMM was not altered by the presence of flumazenil , thus suggesting a non-benzodiazepine-like mechanism of action .
On the contrary , a significant reduction in the effect was observed in animals and neuronal cells co-treated with AM251 , a cannabinoid receptor type 1 ( CB1 ) antagonist , suggesting that the endocannabinoid system may be involved in the TMM mechanism of action .
In conclusion , @ @ @ @ @ @ @ candidate for the management of mood disorders with an innovative mechanism of action , particularly as an adjuvant to conventional therapies .

Mood disorders represent one of the most prevalent and costly psychiatric diseases worldwide. The current therapies are generally characterized by several well-known side effects which limit their prolonged use. The use of herbal medicine for the management of several psychiatric conditions is becoming more established, as it is considered a safer support to conventional pharmacotherapy. The aim of this study was to investigate the possible anxiolytic and antidepressant activity of a fixed combination of L-theanine,, and(TMM) in an attempt to evaluate how the multiple modulations of different physiological systems may contribute to reducing mood disorders. TMM showed an anxiolytic-like and antidepressant-like activity in vivo, which was related to a neuroprotective effect in an in vitro model of excitotoxicity. The effect of TMM was not altered by the presence of flumazenil, thus suggesting a non-benzodiazepine-like mechanism of action. On the contrary, a significant reduction in the effect was observed in animals and neuronal cells co-treated with AM251, a cannabinoid receptor type 1 (CB1) antagonist, suggesting that the endocannabinoid system may be involved in the TMM mechanism of action. In conclusion, TMM may represent a useful and safe candidate for the management of mood disorders with an innovative mechanism of action, particularly as an adjuvant to conventional therapies.


greenmedinfo--2020-07-31--l-Theanine attenuates liver aging by inhibiting advanced glycation end products.

Redox and inflammation imbalances are associated with increased levels of advanced glycation end products ( AGEs ) , leading to the degeneration of body function .
l-Theanine , derived from tea , reportedly inhibits AGE formation in vitro .
We investigated the effects on AGE content , oxidative stress , and inflammatory factors in d-galactose-induced aging rats for prevention and treatment of age-related liver dysfunction .
l-Theanine increased activities of antioxidant enzymes such as superoxide dismutase , catalase , and glutathione peroxidase , thus enhancing total antioxidant capacity , and decreasing malondialdehyde and nitric oxide synthase levels in serum and @ @ @ @ @ @ @ , interleukin ( IL ) -1β , tumour necrosis factor-alpha , and IL-6 were decreased in serum and liver , whereas those of anti-inflammatory factors , IL-4 and IL-10 , were increased in the serum .
Further , l-theanine inhibited AGE production and decreased the levels of the liver function markers , alanine aminotransaminase and aspartate aminotransferase .
It also significantly increased the mRNA expression levels of FoxO1 and downregulated NF-κB ( p65 ) but suppressed the phosphorylation of both FOXO1 and NF-κB ( p65 ) .
Moreover , l-theanine effectively attenuated d-galactose-induced @ @ @ @ @ @ @ liver .
Overall , l-theanine reversed the d-galactose-induced imbalance in oxidative stress and inflammatory responses , reduced AGEs content in aging rats , maintained homeostasis in the body , and ameliorated liver aging .

Redox and inflammation imbalances are associated with increased levels of advanced glycation end products (AGEs), leading to the degeneration of body function. l-Theanine, derived from tea, reportedly inhibits AGE formation in vitro. We investigated the effects on AGE content, oxidative stress, and inflammatory factors in d-galactose-induced aging rats for prevention and treatment of age-related liver dysfunction. l-Theanine increased activities of antioxidant enzymes such as superoxide dismutase, catalase, and glutathione peroxidase, thus enhancing total antioxidant capacity, and decreasing malondialdehyde and nitric oxide synthase levels in serum and liver. Levels of the pro-inflammatory factors, interleukin (IL)-1β, tumour necrosis factor-alpha, and IL-6 were decreased in serum and liver, whereas those of anti-inflammatory factors, IL-4 and IL-10, were increased in the serum. Further, l-theanine inhibited AGE production and decreased the levels of the liver function markers, alanine aminotransaminase and aspartate aminotransferase. It also significantly increased the mRNA expression levels of FoxO1 and downregulated NF-κB(p65) but suppressed the phosphorylation of both FOXO1 and NF-κB (p65). Moreover, l-theanine effectively attenuated d-galactose-induced oedema and vacuole formation, thus protectingthe liver. Overall, l-theanine reversed the d-galactose-induced imbalance in oxidative stress and inflammatory responses, reduced AGEs content in aging rats, maintained homeostasis in the body, and ameliorated liver aging.


greenmedinfo--2020-08-01--Combination of pomegranate extract and curcumin ameliorates thioacetamide-induced liver fibrosis.

Protection against liver injury and its consequences is considered an essential issue to minimize the number of annual deaths caused by liver diseases .
The present study was designed to evaluate the potential role of pomegranate extract ( PE ) and/or curcumin in regression of thioacetamide ( TAA ) -induced liver fibrosis , focusing on their modulatory effects on Nrf2/HO-1 , NF-κB , and TGF-β/Smad3 signaling pathways .
Liver fibrosis was induced in male Wistar rats by intraperitoneal injection of TAA ( 100 mg/kg ) three times a week , for 8 weeks .
To assess the protective effects of @ @ @ @ @ @ @ , rats were treated on a daily basis with oral doses of PE ( 200 mg/kg ) and/or curcumin ( 200 mg/kg ) for 8 weeks .
The results indicated that PE and/or curcumin attenuated TAA-induced liver fibrogenesis , as evidenced by significant improvement in the liver function tests ( AST , ALT , ALP , and albumin ) , oxidative stress biomarkers ( MDA , SOD , and GSH ) , and inflammatory biomarkers ( NF-ĸB , TNF-α , IL-1β , iNOS , TGF-β , and MPO ) , compared to TAA @ @ @ @ @ @ @ and/or curcumin exerted a significant upregulation of Nrf2/HO-1 gene expressions along with significant downregulation of NF-ĸB , TGF-β , and phospho-Smad3 protein expressions , as well as α-SMA and collagen-1 gene expressions .
The histopathological examination has corroborated these findings .
In conclusion , hepatoprotective activities of PE and/or curcumin could be linked to their abilities to modulate Nrf2/HO-1 , NF-κB , and TGF-β/Smad3 signaling pathways .
It is worth noting that the combination of PE and curcumin exerted superior hepatoprotective effects against TAA-induced liver fibrosis , as compared to monotherapy .

Protection against liver injury and its consequences is considered an essential issue to minimize the number of annual deaths caused by liver diseases. The present study was designed to evaluate the potential role of pomegranate extract (PE) and/or curcumin in regression of thioacetamide (TAA)-induced liver fibrosis, focusing on their modulatory effects on Nrf2/HO-1, NF-κB, and TGF-β/Smad3 signaling pathways. Liver fibrosis was induced in male Wistar rats by intraperitoneal injection of TAA (100 mg/kg) three times a week, for 8 weeks. To assess the protective effects of PE and/or curcumin against TAA-induced liver fibrosis, rats were treated on a daily basis with oral doses of PE (200 mg/kg) and/or curcumin (200 mg/kg) for 8 weeks. The results indicated that PE and/or curcumin attenuated TAA-induced liver fibrogenesis, as evidenced by significant improvement in the liver function tests (AST, ALT, ALP, and albumin), oxidative stress biomarkers (MDA, SOD, and GSH), and inflammatory biomarkers (NF-ĸB, TNF-α, IL-1β, iNOS, TGF-β, and MPO), compared to TAA group. Moreover, treatment with PE and/or curcumin exerted a significant upregulation of Nrf2/HO-1 gene expressions along with significant downregulation of NF-ĸB, TGF-β, and phospho-Smad3 protein expressions, as well as α-SMA and collagen-1 gene expressions. The histopathological examination has corroborated these findings. In conclusion, hepatoprotective activities of PE and/or curcumin could be linked to their abilities to modulate Nrf2/HO-1, NF-κB, and TGF-β/Smad3 signaling pathways. It is worth noting that the combination of PE and curcumin exerted superior hepatoprotective effects against TAA-induced liver fibrosis, as compared to monotherapy.


greenmedinfo--2020-08-01--Pomegranate mesocarp preparations could represent a complementary approach to conventional therapies

Pomegranate mesocarp preparations could represent a complementary approach to conventional therapies for promoting abdominal pain relief.

The management of chronic visceral pain related to Inflammatory Bowel Diseases or Irritable Bowel Syndrome is still a clinical problem and new therapeutic strategies continue to be investigated .
In the present study , the efficacy of a pomegranate decoction and of its polysaccharide and ellagitannin components in preventing the development of colitis-induced abdominal pain in rats was evaluated .
After colitis induction by 2,4-dinitrobenzenesulfonic acid ( DNBS ) , the pomegranate decoction ( 300 mg kg ) , polysaccharides ( 300 mg kg ) , and ellagitannins ( 45 mg kg ) were orally administered for 14 days .
@ @ @ @ @ @ @ in the colitic animals both at 7 and 14 days .
Similar efficacy was shown by polysaccharides , but with lower potency .
Ellagitannins administered at dose equivalent to decoction content showed higher efficacy in reducing the development of visceral pain .
Macroscopic and microscopic evaluations performed on the colon 14 days after the damage showed that all three preparations reduced the overall amount of mast cells , the number of degranulated mast cells , and the density of collagen fibers in the mucosal stroma .
Although ellagitannins seem to be responsible for @ @ @ @ @ @ @ on DNBS-induced colitis , the polysaccharides support and enhance its effect .
Therefore , pomegranate mesocarp preparations could represent a complementary approach to conventional therapies for promoting abdominal pain relief .

The management of chronic visceral pain related to Inflammatory Bowel Diseases or Irritable Bowel Syndrome is still a clinical problem and new therapeutic strategies continue to be investigated. In the present study, the efficacy of a pomegranate decoction and of its polysaccharide and ellagitannin components in preventing the development of colitis-induced abdominal pain in rats was evaluated. After colitis induction by 2,4-dinitrobenzenesulfonic acid (DNBS), the pomegranate decoction (300 mg kg), polysaccharides (300 mg kg), and ellagitannins (45 mg kg) were orally administered for 14 days. Repeated treatment with decoction reduced visceral hypersensitivity in the colitic animals both at 7 and 14 days. Similar efficacy was shown by polysaccharides, but with lower potency. Ellagitannins administered at dose equivalent to decoction content showed higher efficacy in reducing the development of visceral pain. Macroscopic and microscopic evaluations performed on the colon 14 days after the damage showed that all three preparations reduced the overall amount of mast cells, the number of degranulated mast cells, and the density of collagen fibers in the mucosal stroma. Although ellagitannins seem to be responsible for most of the beneficial effects of pomegranate on DNBS-induced colitis, the polysaccharides support and enhance its effect. Therefore, pomegranate mesocarp preparations could represent a complementary approach to conventional therapies for promoting abdominal pain relief.


greenmedinfo--2020-08-01--Antifungal activity of punicalagin-nystatin combinations against Candida albicans.

OBJECTIVES : Oral candidiasis is the most common opportunistic fungal infection of oral mucosa and results from an overgrowth of Candida , especially Candida albicans .
The potential anti-C. albicans and cytotoxicity of punicalagin ( PCG ) , isolated from Punica granatum , alone or with nystatin ( NYS ) were evaluated .
METHODS : Activity of compounds alone or in combinations was determined against two C. albicans strains ( ATCC 90028 and SC5314 ) .
Minimal inhibitory concentration ( MIC ) -50 and Minimum Fungicidal Concentration ( MFC ) were assessed by XTT assay and CFU counts , respectively @ @ @ @ @ @ @ inhibitory concentration index was performed .
Ergosterol pathway was investigated as a possible PCG antifungal mechanism .
Cytotoxicity assays were undertaken on human primary oral keratinocytes and gingival fibroblasts incubated with antifungal concentrations of PCG and/or NYS for 24 hr .
RESULTS : Combination of NYS and PCG increased antifungal efficacy , compared with compounds tested alone .
Combinations 4 ( PCG-6.25 μg/ml ; NYS-3.9 μg/ml ) and 5 ( PCG-12.5 μg/ml ; NYS-1.95 μg/ml ) were more effective since they reduced the MIC-50 of PCG ( 50 μg/ml ) by 8 and @ @ @ @ @ @ @ candidal inhibition and nullified the PCG cytotoxicity for keratinocytes .
PCG antifungal mechanism did not involve ergosterol biosynthesis pathway .
CONCLUSIONS : The favorable outcomes for combination of PCG and NYS encourage further testing this therapeutic strategy against C. albicans .

OBJECTIVES: Oral candidiasis is the most common opportunistic fungal infection of oral mucosa and results from an overgrowth of Candida, especially Candida albicans. The potential anti-C. albicans and cytotoxicity of punicalagin (PCG), isolated from Punica granatum, alone or with nystatin (NYS) were evaluated.
METHODS: Activity of compounds alone or in combinations was determined against two C. albicans strains (ATCC 90028 and SC5314). Minimal inhibitory concentration (MIC)-50 and Minimum Fungicidal Concentration (MFC) were assessed by XTT assay and CFU counts, respectively. For combinations, determination of fractional inhibitory concentration index was performed. Ergosterol pathway was investigated as a possible PCG antifungal mechanism. Cytotoxicity assays were undertaken on human primary oral keratinocytes and gingival fibroblasts incubated with antifungal concentrations of PCG and/or NYS for 24 hr.
RESULTS: Combination of NYS and PCG increased antifungal efficacy, compared with compounds tested alone. Combinations 4 (PCG-6.25 μg/ml; NYS-3.9 μg/ml) and 5 (PCG-12.5 μg/ml; NYS-1.95 μg/ml) were more effective since they reduced the MIC-50 of PCG (50 μg/ml) by 8 and 4 times, respectively, increased the candidal inhibition and nullified the PCG cytotoxicity for keratinocytes. PCG antifungal mechanism did not involve ergosterol biosynthesis pathway.
CONCLUSIONS: The favorable outcomes for combination of PCG and NYS encourage further testing this therapeutic strategy against C. albicans.