greenmedinfo--2020-04-01--Ammi visnaga, parsley, barley, and camel's grass all display renoprotective effects.

BACKGROUND : The kidney is an essential organ required by the body to perform several important functions .
Nephrotoxicity is one of the most prevailing kidney complications that result from exposure to an extrinsic or intrinsic toxicant , which increase the need for the acquisition of proper remedies .
Recently , natural remedies are gaining great attention owed to the fact that they have fewer side effects than most conventional drugs .
METHODS : The current study recorded a new therapeutic role of the well-known medicinal plants for kidney stones [ Ammi visnaga ( AVE ) , Petroselinum crispum ( @ @ @ @ @ @ @ ) , and Cymbopogon schoenanthus ( CSE ) ] .
Hence , the aqueous extracts of these plants examined against CCl-induced toxicity in mammalian kidney ( Vero ) cells .
RESULTS : These extracts showed the presence of varying amounts of phenolic and triterpenoid compounds , as well as vitamin C. Owing to the antioxidant potential of these constituents , the extracts suppressed the CCl-induced oxidative stress significantly ( p < 0.05 ) by scavenging the reactive oxygen species and enhancing the cellular antioxidant indices .
In addition , these extracts significantly ( @ @ @ @ @ @ @ inflammation by inhibiting the gene expression of NF-кB , iNOS , and in turn the level of nitric oxide .
Consequently , the morphological appearance of Vero cells , cellular necrosis , and the gene expression of kidney injury molecule-1 ( a marker of renal injury ) after these treatments were improved .
The AVE improved CCl-induced oxidative and inflammatory stress in Vero cells and showed a more potent effect than the commonly used alpha-Ketoanalogue drug ( ketosteril ) in most of the studied assays .
CONCLUSION : Thus , the studied plant @ @ @ @ @ @ @ as promising extracts in the management of nephrotoxicity and other chronic diseases associated with oxidative stress and inflammation .

BACKGROUND: The kidney is an essential organ required by the body to perform several important functions. Nephrotoxicity is one of the most prevailing kidney complications that result from exposure to an extrinsic or intrinsic toxicant, which increase the need for the acquisition of proper remedies. Recently, natural remedies are gaining great attention owed to the fact that they have fewer side effects than most conventional drugs.
METHODS: The current study recorded a new therapeutic role of the well-known medicinal plants for kidney stones [Ammi visnaga (AVE), Petroselinum crispum (PCE), Hordeum vulgare (HVE), and Cymbopogon schoenanthus (CSE)]. Hence, the aqueous extracts of these plants examined against CCl-induced toxicity in mammalian kidney (Vero) cells.
RESULTS: These extracts showed the presence of varying amounts of phenolic and triterpenoid compounds, as well as vitamin C. Owing to the antioxidant potential of these constituents, the extracts suppressed the CCl-induced oxidative stress significantly (p<0.05) by scavenging the reactive oxygen species and enhancing the cellular antioxidant indices. In addition, these extracts significantly (p<0.05) reduced the CCl-induced inflammation by inhibiting the gene expression of NF-кB, iNOS, and in turn the level of nitric oxide. Consequently, the morphological appearance of Vero cells, cellular necrosis, and the gene expression of kidney injury molecule-1 (a marker of renal injury) after these treatments were improved. The AVE improved CCl-induced oxidative and inflammatory stress in Vero cells and showed a more potent effect than the commonly used alpha-Ketoanalogue drug (ketosteril) in most of the studied assays.
CONCLUSION: Thus, the studied plant extracts, especially AVE can be considered as promising extracts in the management of nephrotoxicity and other chronic diseases associated with oxidative stress and inflammation.


greenmedinfo--2020-04-01--Decreased vitamin C uptake mediated by SLC2A3 promotes leukaemia progression and impedes TET2 restor

Decreased vitamin C uptake mediated by SLC2A3 promotes leukaemia progression and impedes TET2 restoration.

BACKGROUND : Vitamin C suppresses leukaemogenesis by modulating Tet methylcytosine dioxygenase ( TET ) activity .
However , its beneficial effect in the treatment of patients with acute myeloid leukaemia ( AML ) remains controversial .
In this study , we aimed to identify a potential predictive biomarker for vitamin C treatment in AML .
METHODS : Gene expression patterns and their relevance to the survival of AML patients were analysed with The Cancer Genome Atlas ( TCGA ) and Therapeutically Applicable Research to Generate Effective Treatments ( TARGET ) database cases .
In vitro experiments were performed on AML @ @ @ @ @ @ @ and patient-derived primary AML cells .
RESULTS : SLC2A3 expression was significantly decreased in leukaemic blast cells .
Below-median SLC2A3 expression was associated with poor overall survival .
Low SLC2A3 expression was associated with less effective demethylation , and a diminished vitamin C effect in the AML and lymphoma cell lines .
SLC2A3 knockdown in the KG-1 cell line decreased the response of vitamin C. In patient-derived primary AML cells , vitamin C only restored TET2 activity when SLC2A3 was expressed .
CONCLUSION : SLC2A3 could be used as a potential biomarker to @ @ @ @ @ @ @ in AML .

BACKGROUND: Vitamin C suppresses leukaemogenesis by modulating Tet methylcytosine dioxygenase (TET) activity. However, its beneficial effect in the treatment of patients with acute myeloid leukaemia (AML) remains controversial. In this study, we aimed to identify a potential predictive biomarker for vitamin C treatment in AML.
METHODS: Gene expression patterns and their relevance to the survival of AML patients were analysed with The Cancer Genome Atlas (TCGA) and Therapeutically Applicable Research to Generate Effective Treatments (TARGET) database cases. In vitro experiments were performed on AML cell lines, a SLC2A3-knockdown cell line and patient-derived primary AML cells.
RESULTS: SLC2A3 expression was significantly decreased in leukaemic blast cells. Below-median SLC2A3 expression was associated with poor overall survival. Low SLC2A3 expression was associated with less effective demethylation, and a diminished vitamin C effect in the AML and lymphoma cell lines. SLC2A3 knockdown in the KG-1 cell line decreased the response of vitamin C. In patient-derived primary AML cells, vitamin C only restored TET2 activity when SLC2A3 was expressed.
CONCLUSION: SLC2A3 could be used as a potential biomarker to predict the effect of vitamin C treatment in AML.


greenmedinfo--2020-04-01--This study described the immunomodulatory effects of parsley.

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greenmedinfo--2020-04-01--Ascorbic acid can be used as an anti-biofilm agent to prevent biofilm formation of S. aureus and thu

Ascorbic acid can be used as an anti-biofilm agent to prevent biofilm formation of S. aureus and thus biofilm-related infections.

AIMS : ( ) is a life-threatening pathogen with high morbidity and mortality rates which causes nosocomial and community-acquired infections .
Biofilm , considered to be a common virulence factor for pathogens , plays a significant role in recurrent and untreatable infections .
Biofilm formation ofis mediated by synthesis of either poly-N-acetylglucosamine in an ica-dependent manner or surface proteins in an ica-independent manner .
In some cases treatment is impossible and recurrent .
In this study , -dependent biofilm-producingisolates were detected and the anti-biofilm effect of ascorbic acid against biofilm formation of isolates was investigated .
METHODS : A total @ @ @ @ @ @ @ isolates stored in our bacterial stock were used to detect-dependent biofilm-producing MSSA isolates .
The anti-biofilm study was undertaken with three-dependent biofilm-producing isolates ( MSSA2-4 ) and ATCC 29213 ( MSSA1 ) .
Biofilms and the anti-biofilm effect of ascorbic acid were detected using the microtitre plate ( MtP ) method .
16S-rRNA , A andD genes and expression levels ofA andD of isolates were detected by RT-PCR .
RESULTS : The minimum inhibitory concentrations ( MICs ) of ascorbic acid prevented biofilm formation of MSSA1 and MSSA3 .
Also , 1/2 MIC @ @ @ @ @ @ @ MSSA3 .
It was observed that biofilm formation decreased with increased concentration .
There was no significant increase ingene expression of MSSA1 and MSSA2 .
Expression ofA andD of MSSA3 decreased 13 % and 38 % , respectively .
Expression ofA in MSSA4 decreased 12 % .
CONCLUSION : The results of our study show that ascorbic acid can be used as an anti-biofilm agent to prevent biofilm formation ofand thus biofilm-related infections .

AIMS: () is a life-threatening pathogen with high morbidity and mortality rates which causes nosocomial and community-acquired infections. Biofilm, considered to be a common virulence factor for pathogens, plays a significant role in recurrent and untreatable infections. Biofilm formation ofis mediated by synthesis of either poly-N-acetylglucosamine in an ica-dependent manner or surface proteins in an ica-independent manner. In some cases treatment is impossible and recurrent. In this study,-dependent biofilm-producingisolates were detected and the anti-biofilm effect of ascorbic acid against biofilm formation of isolates was investigated.
METHODS: A total of 21 methicillin-sensitive(MSSA) clinical isolates stored in our bacterial stock were used to detect-dependent biofilm-producing MSSA isolates. The anti-biofilm study was undertaken with three-dependent biofilm-producing isolates (MSSA2-4) and ATCC 29213 (MSSA1). Biofilms and the anti-biofilm effect of ascorbic acid were detected using the microtitre plate (MtP) method. 16S-rRNA,A andD genes and expression levels ofA andD of isolates were detected by RT-PCR.
RESULTS: The minimum inhibitory concentrations (MICs) of ascorbic acid prevented biofilm formation of MSSA1 and MSSA3. Also, 1/2 MIC of ascorbic acid prevented biofilm formation of MSSA3. It was observed that biofilm formation decreased with increased concentration. There was no significant increase ingene expression of MSSA1 and MSSA2. Expression ofA andD of MSSA3 decreased 13% and 38%, respectively. Expression ofA in MSSA4 decreased 12%.
CONCLUSION: The results of our study show that ascorbic acid can be used as an anti-biofilm agent to prevent biofilm formation ofand thus biofilm-related infections.


greenmedinfo--2020-04-01--Ascorbic acid inhibits vascular remodeling induced by mental stress in overweight/obese men.

BACKGROUND : Mental stress ( MS ) is related to endothelial dysfunction in overweight/obese men .
It is believed that the pro-oxidant profile , associated with an imbalance in the vascular remodeling process , may contribute to deleterious effects of MS on endothelial function .
However , it is unknown whether administration of ascorbic acid ( AA ) , a potent antioxidant , can prevent oxidative and remodeling dysfunction during MS in these subjects .
METHODS : Fourteen overweight/obese grade I men ( 27 ± 7 years ; 29.7 ± 2.6 kg·m ) underwent the Stroop Color Word Test for @ @ @ @ @ @ @ ( 3 g ) or placebo ( PL , 0.9 % NaCl ) intravenous infusions .
Venous blood samples were collected at baseline and the last minute of MS to measure nitrite concentration ( chemiluminescence ) , protein carbonylation , thiobarbituric acid reactive substances ( TBARS ) and catalase activity ( colorimetric assays ) , superoxide dismutase ( SOD ; immunoenzymatic assay ) , activities of active/inactive ( pro ) forms of metalloproteinases-9 and -2 ( MMP ; zymography ) and its respective tissue inhibitors concentration ( TIMP-1 and TIMP-2 ; immunoenzymatic assays @ @ @ @ @ @ @ minimize the oxidative imbalance and vascular remodeling induced by MS .

BACKGROUND: Mental stress (MS) is related to endothelial dysfunction in overweight/obese men. It is believed that the pro-oxidant profile, associated with an imbalance in the vascular remodeling process, may contribute to deleterious effects of MS on endothelial function. However, it is unknown whether administration of ascorbic acid (AA), a potent antioxidant, can prevent oxidative and remodeling dysfunction during MS in these subjects.
METHODS: Fourteen overweight/obese grade I men (27 ± 7 years; 29.7 ± 2.6 kg·m) underwent the Stroop Color Word Test for 5 min to induce MS after AA (3 g) or placebo (PL, 0.9% NaCl) intravenous infusions. Venous blood samples were collected at baseline and the last minute of MS to measure nitrite concentration (chemiluminescence), protein carbonylation, thiobarbituric acid reactive substances (TBARS) and catalase activity (colorimetric assays), superoxide dismutase (SOD; immunoenzymatic assay), activities of active/inactive (pro) forms of metalloproteinases-9 and -2 (MMP; zymography) and its respective tissue inhibitors concentration (TIMP-1 and TIMP-2; immunoenzymatic assays).
RESULTS: At baseline, MMP-9 activity (p < 0.01), the MMP-9/proMMP-9 ratio (p = 0.02) and TIMP-1 concentration (p = 0.05) were reduced, whereas proMPP-9 activity was increased (p = 0.02) after AA compared to PL infusion. After PL infusion, MS increased protein carbonylation (p < 0.01), catalase (p < 0.01), and the MMP-9/proMMP-9 ratio (p = 0.04) when compared to baseline. AA infusion reduced protein carbonylation (p = 0.02), MMP-9 activity (p < 0.01), and MMP-9/pro-MMP-9 ratio (p < 0.01), while SOD (p = 0.04 vs baseline), proMPP-9 (p < 0.01 vs PL), MMP-2 (p < 0.01 vs PL) and TIMP-2 (p = 0.02 vs baseline) remained elevated during MS.
CONCLUSIONS: AA appears to minimize the oxidative imbalance and vascular remodeling induced by MS.


greenmedinfo--2020-04-01--Vitamin C regulates Schwann cell myelination by promoting DNA demethylation of pro-myelinating genes

Vitamin C regulates Schwann cell myelination by promoting DNA demethylation of pro-myelinating genes.

Ascorbic acid ( vitamin C ) is critical for Schwann cells to myelinate peripheral nerve axons during development and remyelination after injury .
However , its exact mechanism remains elusive .
Vitamin C is a dietary nutrient that was recently discovered to promote active DNA demethylation .
Schwann cell myelination is characterized by global DNA demethylation in vivo and may therefore be regulated by vitamin C. We found that vitamin C induces a massive transcriptomic shift ( n = 3,848 genes ) in primary cultured Schwann cells while simultaneously producing a global increase in genomic 5-hydroxymethylcytosine ( 5hmC ) , @ @ @ @ @ @ @ .
Vitamin C upregulates 10 pro-myelinating genes which exhibit elevated 5hmC content in both the promoter and gene body regions of these loci following treatment .
Using a mouse model of human vitamin C metabolism , we found that maternal dietary vitamin C deficiency causes peripheral nerve hypomyelination throughout early development in resulting offspring .
Additionally , dietary vitamin C intake regulates the expression of myelin-related proteins such as periaxin ( PRX ) and myelin basic protein ( MBP ) during development and remyelination after injury in mice .
Taken together , these @ @ @ @ @ @ @ myelination through 1 ) increased DNA demethylation and transcription of pro-myelinating genes , and 2 ) its known role in stabilizing collagen helices to form the basal lamina that is necessary for myelination .

Ascorbic acid (vitamin C) is critical for Schwann cells to myelinate peripheral nerve axons during development and remyelination after injury. However, its exact mechanism remains elusive. Vitamin C is a dietary nutrient that was recently discovered to promote active DNA demethylation. Schwann cell myelination is characterized by global DNA demethylation in vivo and may therefore be regulated by vitamin C. We found that vitamin C induces a massive transcriptomic shift (n = 3,848 genes) in primary cultured Schwann cells while simultaneously producing a global increase in genomic 5-hydroxymethylcytosine (5hmC), a DNA demethylation intermediate which regulates transcription. Vitamin C upregulates 10 pro-myelinating genes which exhibit elevated 5hmC content in both the promoter and gene body regions of these loci following treatment. Using a mouse model of human vitamin C metabolism, we found that maternal dietary vitamin C deficiency causes peripheral nerve hypomyelination throughout early development in resulting offspring. Additionally, dietary vitamin C intake regulates the expression of myelin-related proteins such as periaxin (PRX) and myelin basic protein (MBP) during development and remyelination after injury in mice. Taken together, these results suggest that vitamin C cooperatively promotes myelination through 1) increased DNA demethylation and transcription of pro-myelinating genes, and 2) its known role in stabilizing collagen helices to form the basal lamina that is necessary for myelination.


greenmedinfo--2020-04-02--Intake of vitamin C, vitamin E, selenium, zinc and polyunsaturated fatty acids and upper respiratory

Intake of vitamin C, vitamin E, selenium, zinc and polyunsaturated fatty acids and upper respiratory tract infection.

BACKGROUND/OBJECTIVES : Antioxidants and polyunsaturated fatty acids ( PUFAs ) have a role in the human immune defense and may affect the susceptibility to upper respiratory tract infection ( URTI ) .
To examine dietary intake of vitamin C , vitamin E , selenium , zinc and PUFAs in relation to URTI incidence in a prospective cohort study .
SUBJECTS/METHODS : A total of 1533 Swedish women and men aged 25-64 years were followed for nine months during 2011-2012 .
Information on dietary intake was assessed through a web-based food frequency questionnaire , and events of URTI were self-reported prospectively @ @ @ @ @ @ @ regression was applied to obtain incidence rate ratios with 95 % confidence intervals .
RESULTS : The mean number of URTI events was 0.9 among all participants , 1.0 among women and 0.7 among men .
In women , the incidence rate ratios ( 95 % confidence interval ) for high compared with low intake were 0.69 ( 0.55-0.88 ) for vitamin C , 0.77 ( 0.62-0.96 ) for vitamin E , 0.57 ( 0.39-0.83 ) for docosahexaenoic acid ( DHA ) and 0.80 ( 0.65-0.99 ) for arachidonic acid ( AA ) @ @ @ @ @ @ @ or zinc among women .
In men , an increased URTI incidence was seen with medium vitamin E intake ( 1.42 ( 1.09-1.85 ) ) and high zinc intake ( 1.50 ( 1.04-2.16 ) ) .
No association was found for vitamin C , selenium or PUFAs among men .
CONCLUSIONS : We found an inverse association of URTI incidence among women for vitamin C , vitamin E , DHA and AA intake and a positive association among men for vitamin E and zinc intake .
The observed gender differences warrant further investigation @

BACKGROUND/OBJECTIVES: Antioxidants and polyunsaturated fatty acids (PUFAs) have a role in the human immune defense and may affect the susceptibility to upper respiratory tract infection (URTI). To examine dietary intake of vitamin C, vitamin E, selenium, zinc and PUFAs in relation to URTI incidence in a prospective cohort study.
SUBJECTS/METHODS: A total of 1533 Swedish women and men aged 25-64 years were followed for nine months during 2011-2012. Information on dietary intake was assessed through a web-based food frequency questionnaire, and events of URTI were self-reported prospectively as they occurred. Cox proportional hazards regression was applied to obtain incidence rate ratios with 95% confidence intervals.
RESULTS: The mean number of URTI events was 0.9 among all participants, 1.0 among women and 0.7 among men. In women, the incidence rate ratios (95% confidence interval) for high compared with low intake were 0.69 (0.55-0.88) for vitamin C, 0.77 (0.62-0.96) for vitamin E, 0.57 (0.39-0.83) for docosahexaenoic acid (DHA) and 0.80 (0.65-0.99) for arachidonic acid (AA). No association was found for selenium or zinc among women. In men, an increased URTI incidence was seen with medium vitamin E intake (1.42 (1.09-1.85)) and high zinc intake (1.50 (1.04-2.16)). No association was found for vitamin C, selenium or PUFAs among men.
CONCLUSIONS: We found an inverse association of URTI incidence among women for vitamin C, vitamin E, DHA and AA intake and a positive association among men for vitamin E and zinc intake. The observed gender differences warrant further investigation.


greenmedinfo--2020-04-02--Immune modulatory and anti-oxidative effect of selenium against pulmonary tuberculosis.

Prevalence of pulmonary tuberculosis ( TB ) in Pakistan is due to poor living conditions , malnutrition and low immunity @ @ @ @ @ conducted to show the role of selenium complement to enhance the immune status against TB @ @ @ @ @ TB patients were divided into treatment ( selenium and anti-tuberculosis drug ) and control groups @ @ @ @ @ Levels of selenium , immunoglobulin and leukocyte count were determined before and after treatment .
@ @ @ @ @ levels of immunoglobulin and leukocyte count in patients as compared to control group .
The @ @ @ @ @ , glutathione and total antioxidants were remarkably lowered among control type group as compared to @ @ @ @ @ < 0.01 ) .
However , the values of lipid peroxidation products malondialdehyde ( MDA @ @ @ @ @ control group than treatment group .

Prevalence of pulmonary tuberculosis (TB) in Pakistan is due to poor living conditions, malnutrition and low immunity. The present project was conducted to show the role of selenium complement to enhance the immune status against TB. Total of 80 human TB patients were divided into treatment (selenium and anti-tuberculosis drug) and control groups (anti-tuberculosis drug). Levels of selenium, immunoglobulin and leukocyte count were determined before and after treatment. Selenium showed significant increase in levels of immunoglobulin and leukocyte count in patients as compared to control group. The level of SOD, catalase, glutathione and total antioxidants were remarkably lowered among control type group as compared to treatment type group (P<0.01). However, the values of lipid peroxidation products malondialdehyde (MDA) were notably higher in control group than treatment group.


greenmedinfo--2020-04-02--The insertion of functional groups in organic selenium compounds promote changes in mitochondrial pa

The insertion of functional groups in organic selenium compounds promote changes in mitochondrial parameters and raise the antibacterial activity.

Organic selenium compounds are widely associated with numerous pharmacological properties .
However , selenium compounds , such as Ebselen ( Ebs ) and Diphenyl Diselenide ( DPDS ) , could interact with mitochondrial respiratory complexes , especially with thiol groups .
The present study evaluated whether the insertion of functional groups , o-methoxy , and p-methyl on organic selenium compounds promotes changes in mitochondrial functioning parameters and whether this is related to antibacterial activity .
Here we tested some in vitro parameters after the exposure of mitochondria to different concentrations ofβ-selenoamines 1-phenyl-3- ( p-tolylselanyl ) propan-2-amine ( C1 ) and @ @ @ @ @ @ @ ) and analogs of DPDS 1,2-bis ( 2-methoxyphenyl ) diselenide ( C3 ) and 1,2-bisp-tolyldiselenide ( C4 ) .
We also evaluated the antibacterial activity of β-selenoamines and diselenides against Methicillin-resistant Staphylococcus aureus and Escherichia coli .
Our results showed that o-methoxy insertion increased the antioxidant properties , without affecting the mitochondrial membrane potential .
The compounds with a p-methyl insertion affected the mitochondrial membrane potential and significantly decreased the State III respiration and RCR .
Besides , the p-methyl compounds presented antibacterial activity at lower concentrations than those shown in o-methoxy , @ @ @ @ @ @ @ damage to thiol groups and better absorption in gram-positive bacteria due to their relationship with cell wall constituents .
Finally , our study confirms that structural modifications in organic selenium compounds provide changes in mitochondrial functioning but also raise their antibacterial effect .
This strategy can be used as a target for the development of new enough potent antibacterial to restrict the advance of resistant bacterial infections .

Organic selenium compounds are widely associated with numerous pharmacological properties. However, selenium compounds, such as Ebselen (Ebs) and Diphenyl Diselenide (DPDS), could interact with mitochondrial respiratory complexes, especially with thiol groups. The present study evaluated whether the insertion of functional groups, o-methoxy, and p-methyl on organic selenium compounds promotes changes in mitochondrial functioning parameters and whether this is related to antibacterial activity. Here we tested some in vitro parameters after the exposure of mitochondria to different concentrations ofβ-selenoamines 1-phenyl-3-(p-tolylselanyl)propan-2-amine (C1) and 1-(2-methoxyphenylselanyl)-3-phenylpropan-2-amine (C2) and analogs of DPDS 1,2-bis(2-methoxyphenyl)diselenide (C3) and 1,2-bisp-tolyldiselenide (C4). We also evaluated the antibacterial activity of β-selenoamines and diselenides against Methicillin-resistant Staphylococcus aureus and Escherichia coli. Our results showed that o-methoxy insertion increased the antioxidant properties, without affecting the mitochondrial membrane potential. The compounds with a p-methyl insertion affected the mitochondrial membrane potential and significantly decreased the State III respiration and RCR. Besides, the p-methyl compounds presented antibacterial activity at lower concentrations than those shown in o-methoxy, precisely by the same mechanism that promotes damage to thiol groups and better absorption in gram-positive bacteria due to their relationship with cell wall constituents. Finally, our study confirms that structural modifications in organic selenium compounds provide changes in mitochondrial functioning but also raise their antibacterial effect. This strategy can be used as a target for the development of new enough potent antibacterial to restrict the advance of resistant bacterial infections.


greenmedinfo--2020-04-02--Zinc supplementation ameliorates lung injury by reducing neutrophil recruitment and activity.

INTRODUCTION : Zinc is well known for its anti-inflammatory effects , including regulation of migration and activity of polymorphonuclear neutrophils ( PMN ) .
Zinc deficiency is associated with inflammatory diseases such as acute lung injury ( ALI ) .
As deregulated neutrophil recruitment and their hyper-activation are hallmarks of ALI , benefits of zinc supplementation on the development of lipopolysaccharides ( LPS ) -induced ALI were tested .
METHODS : 64 C57Bl/6 mice , split into eight groups , were injected with 30 µg zinc 24 hours before exposure to aerosolised LPS for 4 hours .
Zinc homoeostasis was @ @ @ @ @ @ @ as well as metallothionein-1 expression .
Recruitment of neutrophils to alveolar , interstitial and intravascular space was assessed using flow cytometry .
To determine the extent of lung damage , permeability and histological changes and the influx of protein into the bronchoalveolar lavage fluid were measured .
Inflammatory status and PMN activity were evaluated via tumour necrosis factor α levels and formation of neutrophil extracellular traps .
The effects of zinc supplementation prior to LPS stimulation on activation of primary human granulocytes and integrity of human lung cell monolayers were assessed as well @ @ @ @ @ @ @ prior to LPS-induced ALI indeed significantly decreased the recruitment of neutrophils to the lungs and prevented their hyperactivity and thus lung damage was decreased .
Results from in vitro investigations using human cells suggest the transferability of the finding to human disease , whichremains to be tested in more detail .
CONCLUSION : Zinc supplementation attenuated LPS-induced lung injury in a murine ALI model .
Thus , the usage of zinc-based strategies should be considered to prevent detrimental consequences of respiratory infection and lung damage in risk groups .

INTRODUCTION: Zinc is well known for its anti-inflammatory effects, including regulation of migration and activity of polymorphonuclear neutrophils (PMN). Zinc deficiency is associated with inflammatory diseases such as acute lung injury (ALI). As deregulated neutrophil recruitment and their hyper-activation are hallmarks of ALI, benefits of zinc supplementation on the development of lipopolysaccharides (LPS)-induced ALI were tested.
METHODS: 64 C57Bl/6 mice, split into eight groups, were injected with 30 µg zinc 24 hours before exposure to aerosolised LPS for 4 hours. Zinc homoeostasis was characterised measuring serum and lung zinc concentrations as well as metallothionein-1 expression. Recruitment of neutrophils to alveolar, interstitial and intravascular space was assessed using flow cytometry. To determine the extent of lung damage, permeability and histological changes and the influx of protein into the bronchoalveolar lavage fluid were measured. Inflammatory status and PMN activity were evaluated via tumour necrosis factor α levels and formation of neutrophil extracellular traps. The effects of zinc supplementation prior to LPS stimulation on activation of primary human granulocytes and integrity of human lung cell monolayers were assessed as well.
RESULTS: Injecting zinc 24 hours prior to LPS-induced ALI indeed significantly decreased the recruitment of neutrophils to the lungs and prevented their hyperactivity and thus lung damage was decreased. Results from in vitro investigations using human cells suggest the transferability of the finding to human disease, whichremains to be tested in more detail.
CONCLUSION: Zinc supplementation attenuated LPS-induced lung injury in a murine ALI model. Thus, the usage of zinc-based strategies should be considered to prevent detrimental consequences of respiratory infection and lung damage in risk groups.


greenmedinfo--2020-04-02--Prevention of infections of the upper respiratory tract.

Because of its high prevalence acute respiratory diseases have a significant impact on the population .
The focus of this @ @ @ @ @ of knowledge for the prophylactic efficacy of : zinc , vitamin C , Echinacea preparations @ @ @ @ @ physical measures .
Furthermore , the benefits of pneumococcal and influenza vaccine were elicited .
@ @ @ @ @ physical measures proved to be the most effective , cost-effective method to prevent infections .
@ @ @ @ @ Echinacea preparations ( for example : E. purpurea ) , vitamin C and garlic showed @ @ @ @ @ of infection and must be elicited individually .
Pneumococcal and annual influenza vaccines in family @ @ @ @ @ accordingly topical STIKO-recommendation .
Nevertheless , the prophylactic effect from influenza vaccines on usual cold @ @ @ @

Because of its high prevalence acute respiratory diseases have a significant impact on the population. The focus of this review was the current state of knowledge for the prophylactic efficacy of: zinc, vitamin C, Echinacea preparations, garlic and carrying out physical measures. Furthermore, the benefits of pneumococcal and influenza vaccine were elicited. In the synopsis, the physical measures proved to be the most effective, cost-effective method to prevent infections. The intake of zinc, Echinacea preparations (for example: E. purpurea), vitamin C and garlic showed moderate success in the prevention of infection and must be elicited individually. Pneumococcal and annual influenza vaccines in family practice should be given furthermore accordingly topical STIKO-recommendation. Nevertheless, the prophylactic effect from influenza vaccines on usual cold illnesses is unsettled.


greenmedinfo--2020-04-02--Why You Don't Want to Take Aspirin or Motrin for COVID-19


greenmedinfo--2020-04-02--Pharmacologic ascorbate as a pro-drug for hydrogen peroxide release to kill mycobacteria.

BACKGROUND AND PURPOSE : Tuberculosis is one of the most highly fatal diseases worldwide , and one-third of the world 's population has been infected with Mycobacterium tuberculosis ( M. tuberculosis ) .
A previous study showed that M. tuberculosis was highly susceptible to being killed by ascorbate ( i.e .
vitamin C , VC ) , but the molecular mechanisms of the bactericidal activity of VC against M. tuberculosis are still not well understood .
EXPERIMENTAL APPROACH : We assayed the effects of VC as an anti-tuberculosis drug against mycobacteria ( i.e .
M. bovis BCG or M. tuberculosis @ @ @ @ @ @ @ RAW 264.7 cells ) .
Relative global protein expression changes in 5 mM VC-treated and control samples of H37Rv were investigated by Tandem mass tag ( TMT ) -based quantitative proteomic analysis .
qRT-PCR was also used to measure the differential expression of six intracellular stress response mycobacteria genes .
KEY RESULTS : Quantitative proteomic analysis showed that 11 peptide components including rip3 , fdxA , Rv2028c , mtp , LH57_00670 , hspX , pfkB , Rv1824 , Rv1813c , LH57_08410 and Rv2030c were up-regulated and 17 peptide components were down-regulated in 5 @ @ @ @ @ @ @ samples .
qRT-PCR also verified that VC could induce the expression of six genes ( hsp , fdxD , furA , devR , hspX , and dnaB ) in BCG and H37Rv .
We also found that exosomes from RAW 264.7 cells treated with pharmacologic VC could kill M. bovis BCG in vitro .
CONCLUSION AND IMPLICATIONS : Our results demonstrated that the bactericidal activity of VC against mycobacteria , as a pro-drug for hydrogen peroxide formation ( HO ) , was dependent on reactive oxygen species production and the activated oxidative stress @ @ @ @ @ @ @ and exosomes from macrophages treated with VC could be used as potential anti-tuberculosis drugs .

BACKGROUND AND PURPOSE: Tuberculosis is one of the most highly fatal diseases worldwide, and one-third of the world's population has been infected with Mycobacterium tuberculosis (M. tuberculosis). A previous study showed that M. tuberculosis was highly susceptible to being killed by ascorbate (i.e. vitamin C, VC), but the molecular mechanisms of the bactericidal activity of VC against M. tuberculosis are still not well understood.
EXPERIMENTAL APPROACH: We assayed the effects of VC as an anti-tuberculosis drug against mycobacteria (i.e. M. bovis BCG or M. tuberculosis H37Rv) in macrophages (i.e. RAW 264.7 cells). Relative global protein expression changes in 5 mM VC-treated and control samples of H37Rv were investigated by Tandem mass tag (TMT)-based quantitative proteomic analysis. qRT-PCR was also used to measure the differential expression of six intracellular stress response mycobacteria genes.
KEY RESULTS: Quantitative proteomic analysis showed that 11 peptide components including rip3, fdxA, Rv2028c, mtp, LH57_00670, hspX, pfkB, Rv1824, Rv1813c, LH57_08410 and Rv2030c were up-regulated and 17 peptide components were down-regulated in 5 mM VC-treated H37Rv compared with the control samples. qRT-PCR also verified that VC could induce the expression of six genes (hsp, fdxD, furA, devR, hspX, and dnaB) in BCG and H37Rv. We also found that exosomes from RAW 264.7 cells treated with pharmacologic VC could kill M. bovis BCG in vitro.
CONCLUSION AND IMPLICATIONS: Our results demonstrated that the bactericidal activity of VC against mycobacteria, as a pro-drug for hydrogen peroxide formation (HO), was dependent on reactive oxygen species production and the activated oxidative stress pathway, which suggested that pharmaceutical VC and exosomes from macrophages treated with VC could be used as potential anti-tuberculosis drugs.


greenmedinfo--2020-04-02--Alternate pathway to ascorbate induced inhibition of Mycobacterium tuberculosis.

Ascorbate has been demonstrated to interfere with the growth of Mycobacterium tuberculosis .
It scavenges oxygen in the culture medium to induce dormancy of M. tuberculosis .
It kills the mycobacteria by generating reactive oxygen intermediates via iron mediated Fenton reactions .
In this study , we observed that ascorbate can inhibit M. tuberculosis isocitrate lyase ( MtbICL ) with an ICof 2.15 mΜ .
MtbICL is an essential enzyme for the survival of M. tuberculosis under dormancy .
We studied the effect of ascorbate on the growth of M. tuberculosis H37Rv metabolizing through citric acid cycle or glyoxylate cycle @ @ @ @ @ @ @ sole carbon source .
It was observed that 4 mM ascorbate inhibited ∼89 % of the growth in glucose medium , which was confirmed to be mediated by Fenton reaction , as the inhibition was significantly lesser ( 61 % ) under low iron condition .
On the other hand , in acetate medium , ∼97 % of the growth was inhibited and the inhibition wasuninfluenced by the iron levels .
3-nitropropionate , a known inhibitor of MtbICL , was seen to cause significantly higher inhibition in the acetate medium than in the @ @ @ @ @ @ @ to iron levels in either medium .
Molecular docking and dynamic simulation studies confirmedstable binding of ascorbate to MtbICL leading to its inhibition .
These observations suggest an additional pathway for ascorbate induced inhibition of M. tuberculosis through inhibition of glyoxylate cycle .
Since human immune cells can accumulate ascorbate in millimolar concentrations , the in vitroactivity range ( 1-4 mM ) of ascorbate against M. tuberculosis could be extrapolated in vivo .
Our result supports the possible benefits of adding high vitamin C diet in TB-treated patients .

Ascorbate has been demonstrated to interfere with the growth of Mycobacterium tuberculosis. It scavenges oxygen in the culture medium to induce dormancy of M. tuberculosis. It kills the mycobacteria by generating reactive oxygen intermediates via iron mediated Fenton reactions. In this study, we observed that ascorbate can inhibit M. tuberculosis isocitrate lyase (MtbICL) with an ICof 2.15 mΜ. MtbICL is an essential enzyme for the survival of M. tuberculosis under dormancy. We studied the effect of ascorbate on the growth of M. tuberculosis H37Rv metabolizing through citric acid cycle or glyoxylate cycle with glucose or acetate respectively as the sole carbon source. It was observed that 4 mM ascorbate inhibited ∼89% of the growth in glucose medium, which was confirmed to be mediated by Fenton reaction, as the inhibition was significantly lesser (61%) under low iron condition. On the other hand, in acetate medium, ∼97% of the growth was inhibited and the inhibition wasuninfluenced by the iron levels. 3-nitropropionate, a known inhibitor of MtbICL, was seen to cause significantly higher inhibition in the acetate medium than in the glucose medium; however it was indifferent to iron levels in either medium. Molecular docking and dynamic simulation studies confirmedstable binding of ascorbate to MtbICL leading to its inhibition. These observations suggest an additional pathway for ascorbate induced inhibition of M. tuberculosis through inhibition of glyoxylate cycle. Since human immune cells can accumulate ascorbate in millimolar concentrations, the in vitroactivity range (1-4 mM) of ascorbate against M. tuberculosis could be extrapolated in vivo. Our result supports the possible benefits of adding high vitamin C diet in TB-treated patients.


greenmedinfo--2020-04-02--New App Requires Reporting of People Sneezing or Coughing


greenmedinfo--2020-04-02--The role of physiological vitamin C concentrations on key functions of neutrophils isolated from hea

The role of physiological vitamin C concentrations on key functions of neutrophils isolated from healthy individuals.

Vitamin C ( ascorbate ) is important for neutrophil function and immune health .
Studies showing improved immune function have primarily used cells from scorbutic animals or from individuals with infectious conditions or immune cell disorders .
Few studies have focused on the requirements of neutrophils from healthy adults .
Therefore , we have investigated the role of vitamin C , at concentrations equivalent to those obtained in plasma from oral intakes ( i.e.
, 50-200µmol/L ) , on key functions of neutrophils isolated from healthy individuals .
Cells were either pre-loaded with dehydroascorbic acid , which is rapidly reduced @ @ @ @ @ @ @ were activated in the presence of extracellular ascorbate .
We measured the effects of enhanced ascorbate uptake on the essential functions of chemotaxis , oxidant production , programmed cell death and neutrophil extracellular trap ( NET ) formation .
We found that neutrophils isolated from healthy individuals already had replete ascorbate status ( 0.35 nmol/10cells ) , therefore they did not uptake additional ascorbate .
However , they readily took up dehydroascorbic acid , thus significantly increasing their intracellular ascorbate concentrations , although this was found to have no additional effect on superoxide @ @ @ @ @ @ @ ascorbate appeared to enhance directional mobilityin the presence of the chemoattractant formyl-methionyl-leucyl-phenylalanine ( fMLP ) .
Stimulation of the cells in the presence of ascorbate significantly increased intracellular ascorbate concentrations and , although this exhibited a non-significant increase in phosphatidylserine exposure , NET formation was significantly attenuated .
Our findings demonstrate the ability of neutrophils to regulate their uptake of ascorbate from the plasma of healthy humans to maintain an optimal level within the cell for proper functioning .
Higher oral intakes , however , may help reduce tissue damage and inflammatory pathologies @ @ @ @ @

Vitamin C (ascorbate) is important for neutrophil function and immune health. Studies showing improved immune function have primarily used cells from scorbutic animals or from individuals with infectious conditions or immune cell disorders. Few studies have focused on the requirements of neutrophils from healthy adults. Therefore, we have investigated the role of vitamin C, at concentrations equivalent to those obtained in plasma from oral intakes (i.e., 50-200µmol/L), on key functions of neutrophils isolated from healthy individuals. Cells were either pre-loaded with dehydroascorbic acid, which is rapidly reduced intracellularly to ascorbate, or the cells were activated in the presence of extracellular ascorbate. We measured the effects of enhanced ascorbate uptake on the essential functions of chemotaxis, oxidant production, programmed cell death and neutrophil extracellular trap (NET) formation. We found that neutrophils isolated from healthy individuals already had replete ascorbate status (0.35 nmol/10cells), therefore they did not uptake additional ascorbate. However, they readily took up dehydroascorbic acid, thus significantly increasing their intracellular ascorbate concentrations, although this was found to have no additional effect on superoxide production or chemotaxis. Interestingly, extracellular ascorbate appeared to enhance directional mobilityin the presence of the chemoattractant formyl-methionyl-leucyl-phenylalanine (fMLP). Stimulation of the cells in the presence of ascorbate significantly increased intracellular ascorbate concentrations and, although this exhibited a non-significant increase in phosphatidylserine exposure, NET formation was significantly attenuated. Our findings demonstrate the ability of neutrophils to regulate their uptake of ascorbate from the plasma of healthy humans to maintain an optimal level within the cell for proper functioning. Higher oral intakes, however, may help reduce tissue damage and inflammatory pathologies associated with NET formation.


greenmedinfo--2020-04-02--Schisandrae Chinensis Fructus inhibits behavioral deficits induced by sleep deprivation and chronic

Schisandrae Chinensis Fructus inhibits behavioral deficits induced by sleep deprivation and chronic unpredictable mild stress.

The present study was undertaken to explore the interactions between sleep deprivation ( SD ) and Schisandrae Chinensis Fructus ( SCF ) treatment in the antidepressant-like effects .
We observed that SD aggravated the anxiety-like behavior induced by chronic unpredictable mild stress ( CUMS ) in the elevated plus maze test .
However , the forced swimming test and sucrose preference test showed that SD ( 12 hr ) alleviated the depressive symptoms and SD ( 72 hr ) has the opposite effects .
Administration of SCF showed a promising therapeutic effect on depression and anxiety induced by CUMS and @ @ @ @ @ @ @ strengthen the antidepressant-like effects of SD ( 12 hr ) according to the behavioral tests .
In addition , the BDNF level in hippocampus was elevated by SD ( 12 hr ) and SCF treatment and together with the upregulation of TrkB/CREB/ERK and PI3K/AKT/GSK3β/mTOR signaling pathways .
Besides , the protein levels of p70S6K and PSD95 , which are downstream targets of mTOR , also increased by the treatment .
These results indicated that the antidepressant-like effect of SCF in the CUMS depends on the activation of BDNF and the modulation of TrkB/CREB/ERK @ @ @ @ @ @ @ 12 hr ) shared a common etiology consisting of complex bidirectional interactions with SCF .

The present study was undertaken to explore the interactions between sleep deprivation (SD) and Schisandrae Chinensis Fructus (SCF) treatment in the antidepressant-like effects. We observed that SD aggravated the anxiety-like behavior induced by chronic unpredictable mild stress (CUMS) in the elevated plus maze test. However, the forced swimming test and sucrose preference test showed that SD (12 hr) alleviated the depressive symptoms and SD (72 hr) has the opposite effects. Administration of SCF showed a promising therapeutic effect on depression and anxiety induced by CUMS and SD. Moreover, SCF could potential strengthen the antidepressant-like effects of SD (12 hr) according to the behavioral tests. In addition, the BDNF level in hippocampus was elevated by SD (12 hr) and SCF treatment and together with the upregulation of TrkB/CREB/ERK and PI3K/AKT/GSK3β/mTOR signaling pathways. Besides, the protein levels of p70S6K and PSD95, which are downstream targets of mTOR, also increased by the treatment. These results indicated that the antidepressant-like effect of SCF in the CUMS depends on the activation of BDNF and the modulation of TrkB/CREB/ERK andPI3K/AKT/GSK3β/mTOR signaling cascades, and SD (12 hr) shared a common etiology consisting of complex bidirectional interactions with SCF.


greenmedinfo--2020-04-02--Op-Ed: COVID: It's Not One Thing, It's Not One Disease


greenmedinfo--2020-04-02--S. chinensis fruit extract is a potential herbal drug candidate for the amelioration and prevention

S. chinensis fruit extract is a potential herbal drug candidate for the amelioration and prevention of Parkinson's disease.

( Turcz . )
Baill .
( ) is a well-known botanical medicine and nutritional supplement that has been shown to have potential effects on neurodegeneration .
To investigate the potential neuroprotective effect offruit extract , 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine ( MPTP ) was used to induce behavioral disorders and dopaminergic neuronal damage in mice , and biochemical indicators were examined .
Male C57BL/6 mice were used to establish the MPTP-induced parkinsonian syndrome model .
Open field and rotarod tests were performed to evaluate the overall manifestation of motor deficits and rodent motor coordination .
The mice were divided into 8 groups as @ @ @ @ @ @ @ ( 25 mg/kg , i.p . )
; extract pretreatment ( 0.5 , 1.5 , 5 g/kg , p.o . )
; andextract treatment ( 0.5 , 1.5 , 5 g/kg , p.o. )
.
Liquid chromatography coupled to electrochemical detection was used to monitor neurochemicals in the striatum .
Tyrosine hydroxylase content was measured by immunohistochemistry , and biochemical antioxidative indicators were used to evaluate the potential neuroprotective effects offruit extract .
The results demonstrated that treatment withfruit extract ameliorated MPTP-induced deficits in behavior , exercise balance , dopamine level , dopaminergic @ @ @ @ @ @ @ the striatum of mice .
Among the pretreated and treatment groups , a high dose offruit extract was the most effective treatment .
In conclusion , fruit extract is a potential herbal drug candidate for the amelioration and prevention of Parkinson 's disease .

(Turcz.) Baill. () is a well-known botanical medicine and nutritional supplement that has been shown to have potential effects on neurodegeneration. To investigate the potential neuroprotective effect offruit extract, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was used to induce behavioral disorders and dopaminergic neuronal damage in mice, and biochemical indicators were examined. Male C57BL/6 mice were used to establish the MPTP-induced parkinsonian syndrome model. Open field and rotarod tests were performed to evaluate the overall manifestation of motor deficits and rodent motor coordination. The mice were divided into 8 groups as follows: normal control; MPTP alone (25 mg/kg, i.p.);extract pretreatment (0.5, 1.5, 5 g/kg, p.o.); andextract treatment (0.5, 1.5, 5 g/kg, p.o.). Liquid chromatography coupled to electrochemical detection was used to monitor neurochemicals in the striatum. Tyrosine hydroxylase content was measured by immunohistochemistry, and biochemical antioxidative indicators were used to evaluate the potential neuroprotective effects offruit extract. The results demonstrated that treatment withfruit extract ameliorated MPTP-induced deficits in behavior, exercise balance, dopamine level, dopaminergic neurons, and tyrosine hydroxylase-positive cells in the striatum of mice. Among the pretreated and treatment groups, a high dose offruit extract was the most effective treatment. In conclusion,fruit extract is a potential herbal drug candidate for the amelioration and prevention of Parkinson's disease.


greenmedinfo--2020-04-02--Schisandra chinensis acidic polysaccharide partialy reverses acetaminophen-induced liver injury.

Schisandra chinensis is a hepatoprotective herb that has been used for centuries in China .
Polysaccharide is one of the major active components in S. chinensis , which has been reported to improve liver injuries induced by carbon tetrachloride , alcohol , or high-fat diet .
In this study , we observed the effects and corresponding mechanisms of the secondary component of Schisandra polysaccharide ( acidic polysaccharide , SCAP ) on a murine model of severe acute liver injury induced by acetaminophen ( APAP ) .
SCAP significantly decreased the serum alanine aminotransferase ( ALT ) , aspartate aminotransferas ( @ @ @ @ @ @ @ TNF-α ) , and interleukin-1β ( IL-1β ) levels , and was found to alleviate hepatic pathological alterations in the mouse model .
Meanwhile , SCAP revealed a protective effects on the liver injury-related enzymes and factors , such as significantly diminished malondialdehyde ( MDA ) levels and glutathione ( GSH ) depletion , reduced ratio of B-cell lymphoma-2 ( Bcl-2 ) -associated X protein ( Bax ) /Bcl-2 , prohibited cleaved caspase-3 expression , and elevated the expression of p-AMPK , p-Akt , p-glycogen synthase kinase 3β ( GSK 3β ) , @ @ @ @ @ @ @ 2 ) and heme oxygenase-1 ( HO-1 ) proteins in the liver tissues of the mouse model .
In conclusion , we speculated that the protective activities of SCAP on the APAP-induced mouse model of acute liver injury might be related to its antioxidation , anti-inflammation and anti-apoptosis properties .

Schisandra chinensis is a hepatoprotective herb that has been used for centuries in China. Polysaccharide is one of the major active components in S. chinensis, which has been reported to improve liver injuries induced by carbon tetrachloride, alcohol, or high-fat diet. In this study, we observed the effects and corresponding mechanisms of the secondary component of Schisandra polysaccharide (acidic polysaccharide, SCAP) on a murine model of severe acute liver injury induced by acetaminophen (APAP). SCAP significantly decreased the serum alanine aminotransferase (ALT), aspartate aminotransferas (AST), tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β) levels, and was found to alleviate hepatic pathological alterations in the mouse model. Meanwhile, SCAP revealed a protective effects on the liver injury-related enzymes and factors, such as significantly diminished malondialdehyde (MDA) levels and glutathione (GSH) depletion, reduced ratio of B-cell lymphoma-2 (Bcl-2)-associated X protein (Bax)/Bcl-2, prohibited cleaved caspase-3 expression, and elevated the expression of p-AMPK, p-Akt, p-glycogen synthase kinase 3β (GSK 3β), nuclear factor erythroid 2-derived-like 2 (Nrf 2) and heme oxygenase-1 (HO-1) proteins in the liver tissues of the mouse model. In conclusion, we speculated that the protective activities of SCAP on the APAP-induced mouse model of acute liver injury might be related to its antioxidation, anti-inflammation and anti-apoptosis properties.


greenmedinfo--2020-04-02--A review of Schisandra chinensis and its phytotherapeutical applications.

Schisandra ( Schisandra chinensis ) has been used for centuries as a plant of traditional Chinese medicine .
Its biological @ @ @ @ @ associated with dibenzocyclooctadiene lignans , while specific polysaccharides may also be involved .
The lignans @ @ @ @ @ Their activity has been investigated in hundreds of studies that have confirmed adaptogenic effects , @ @ @ @ @ hepatoprotective effects and potential anticancer potential .
This summary review of the literature synthesizes the @ @ @ @ @ bioactivities of schisandra constituents , description of folk use ofextracts , overview of clinical studies @ @ @ @ @ vitro tests bringing insight into mechanisms of action .

Schisandra (Schisandra chinensis) has been used for centuries as a plant of traditional Chinese medicine. Its biological activity and pharmacological use are associated with dibenzocyclooctadiene lignans, while specific polysaccharides may also be involved. The lignans of schisandra are genus-specific. Their activity has been investigated in hundreds of studies that have confirmed adaptogenic effects, central nervous system stimulation, hepatoprotective effects and potential anticancer potential. This summary review of the literature synthesizes the current state-of-the-art in research on bioactivities of schisandra constituents, description of folk use ofextracts, overview of clinical studies and additional information on in vitro tests bringing insight into mechanisms of action.


greenmedinfo--2020-04-02--These results suggest that schisandrol B can alleviate the severity of asthma.

The aim of this paper was to investigate the active components of Schisandra chinensis in the treatment of asthma and the related mechanisms by a network pharmacology approach .
The active components of Schisandra chinensis and the corresponding targets were obtained from the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform ( TCMSP ) .
Eight active components in Schisandra chinensis and 56 related targets were screened out according to two indicators , oral bioavailability ( OB ) and drug-likeness ( DL ) .
A total of 132 targets related to asthma were screened out through Therapeutic Target Database @ @ @ @ @ @ @ database and Cytoscape software were used to build the '' drug-active compound-target '' network and protein-protein interaction ( PPI ) network .
The key targets were further predicted by the analysis of related biological processes and the pathway-enrichment .
A total of 10 intersection targets between Schisandra chinensis and asthma were obtained by building Venn diagrams , and lignans in Schisandra chinensis were found to be associated with asthma .
The key targets Ptgs2 and Nos2 were further screened out , and schisandrol B ( SCB ) was predicted as the most related @ @ @ @ @ @ @ asthma model was established with ovalbumin and aluminum hydroxide for verifying the effect of SCB and related mechanisms .
The results showed that SCB could inhibit the gene expression of proinflammatory factors to play a therapeutic role in asthma by reducing the expression of Nos2 and Ptgs2 and regulating the NF-κB signaling pathway to intervene in the process of cell metabolism in mice .
These results suggest that SCB can alleviate the severity of asthma through the mechanisms predicted by network pharmacology , and provide a basis for further understanding of the application @ @ @ @ @ @ @ .

The aim of this paper was to investigate the active components of Schisandra chinensis in the treatment of asthma and the related mechanisms by a network pharmacology approach. The active components of Schisandra chinensis and the corresponding targets were obtained from the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP). Eight active components in Schisandra chinensis and 56 related targets were screened out according to two indicators, oral bioavailability (OB) and drug-likeness (DL). A total of 132 targets related to asthma were screened out through Therapeutic Target Database (TTD) data. The String database and Cytoscape software were used to build the"drug-active compound-target"network and protein-protein interaction (PPI) network. The key targets were further predicted by the analysis of related biological processes and the pathway-enrichment. A total of 10 intersection targets between Schisandra chinensis and asthma were obtained by building Venn diagrams, and lignans in Schisandra chinensis were found to be associated with asthma. The key targets Ptgs2 and Nos2 were further screened out, and schisandrol B (SCB) was predicted as the most related key component to asthma. A mouse asthma model was established with ovalbumin and aluminum hydroxide for verifying the effect of SCB and related mechanisms. The results showed that SCB could inhibit the gene expression of proinflammatory factors to play a therapeutic role in asthma by reducing the expression of Nos2 and Ptgs2 and regulating the NF-κB signaling pathway to intervene in the process of cell metabolism in mice. These results suggest that SCB can alleviate the severity of asthma through the mechanisms predicted by network pharmacology, and provide a basis for further understanding of the application of Schisandra chinensis in thetreatment of asthma.


greenmedinfo--2020-04-02--Schisandrin A protects against lipopolysaccharide-induced mastitis.

Schisandrin A ( Sch A ) , a dibenzocyclooctadiene lignan extracted from Schisandra chinensis ( Turcz . )
Baill.
, has anti-oxidant and anti-inflammatory effects , but the effect on masitits has not been studied .
Therefore , we investigated the effect of Sch A in cell and mouse models of lipopolysaccharide ( LPS ) -induced mastitis .
Studies in vivo showed that Sch A reduced LPS-induced mammary injury and the production of pro-inflammatory mediators .
Sch A also decreased the levels of pro-inflammatory mediators and activated nuclear factor-E2 associated factor 2 ( Nrf2 ) signaling pathway in mouse mammary @ @ @ @ @ @ @ Nrf2 inhibitor partially abrogated the downregulation of Sch A on LPS-induced inflammatory response .
In addition , LPS stimulation suppressed autophagy , while both Sch A and the autophagy inducer rapamycin activated autophagy in mMECs , which down-regulated inflammatory response .
Sch A also restrained LPS-induced phosphorylation of mammalian target of rapamycin ( mTOR ) and activated AMP-activated protein kinase ( AMPK ) and unc-51 like kinase 1 ( ULK1 ) .
In summary , these results suggest that Sch A exerts protective effects in LPS-induced mastitis models by activating Nrf2 signaling pathway @ @ @ @ @ @ @ initiated by suppressing mTOR signaling pathway and activating AMPK-ULK1 signaling pathway .

Schisandrin A (Sch A), a dibenzocyclooctadiene lignan extracted from Schisandra chinensis (Turcz.) Baill., has anti-oxidant and anti-inflammatory effects, but the effect on masitits has not been studied. Therefore, we investigated the effect of Sch A in cell and mouse models of lipopolysaccharide (LPS)-induced mastitis. Studies in vivo showed that Sch A reduced LPS-induced mammary injury and the production of pro-inflammatory mediators. Sch A also decreased the levels of pro-inflammatory mediators and activated nuclear factor-E2 associated factor 2 (Nrf2) signaling pathway in mouse mammary epithelial cells (mMECs). The Nrf2 inhibitor partially abrogated the downregulation of Sch A on LPS-induced inflammatory response. In addition, LPS stimulation suppressed autophagy, while both Sch A and the autophagy inducer rapamycin activated autophagy in mMECs, which down-regulated inflammatory response. Sch A also restrained LPS-induced phosphorylation of mammalian target of rapamycin (mTOR) and activated AMP-activated protein kinase (AMPK) and unc-51 like kinase 1 (ULK1). In summary, these results suggest that Sch A exerts protective effects in LPS-induced mastitis models by activating Nrf2 signaling pathway and inducing autophagy and the autophagy is initiated by suppressing mTOR signaling pathway and activating AMPK-ULK1 signaling pathway.


greenmedinfo--2020-04-02--Anti-fatigue effect of anwulignan via the NRF2 and PGC-1α signaling pathway in mice.

OBJECTIVE : To examine the anti-fatigue function of anwulignan from Schisandra and its underlying mechanism .
METHODS : After an excessive fatigue mouse model was created , anwulignan was administered to the mice , and its effect on exercise tolerance was studied by the weight-bearing swimming test , rotarod test , grip strength test , and tail suspension test .
The biochemical indicators closely related to fatigue , including blood urea nitrogen ( BUN ) , lactic acid ( LD ) , lactate dehydrogenase ( LDH ) , and creatine kinase ( CK ) in the serum ; liver glycogen @ @ @ @ @ @ @ ; muscle glycogen ( MG ) ; inorganic phosphate ( Pi ) and Annexin V in the gastrocnemius ; superoxide dismutase ( SOD ) and glutathione peroxidase ( GSH-Px ) activities ; malondialdehyde ( MDA ) , catalase ( CAT ) , and thiobarbituric acid reactive substances ( TBARS ) ; and the 8-hydroxy-2-deoxyguanosine ( 8-OHdG ) and reactive oxygen species ( ROS ) content in both serum and the gastrocnemius were detected .
Morphological changes were also observed .
The anti-fatigue-related proteins of the NRF2/ARE , Bcl2 , and PGC-1α pathways in @ @ @ @ @ @ @ by western blot .
RESULTS : Anwulignan significantly increased the exercise tolerance by decreasing BUN , LD , LDH , CK , Pi , MDA , TBARS , 8-OHdG , ROS , and Annexin V levels and increasing LG , MG , SOD , CAT , and GSH-Px levels , significantly upregulated the expression of NRF2 and Bcl2 proteins , which are anti-oxidation and anti-apoptosis regulators , and also activated the p38MAPK-PGC-1α pathway .
CONCLUSION : Anwulignan can increase exercise tolerance and relieve fatigue in an excessive fatigue mouse model .
The underlying @ @ @ @ @ @ @ on the NRF2 and PGC-1α signaling pathway .
This study will provide scientific data for anwulignan to be developed as a novel and efficient component in anti-oxidant or anti-fatigue health food .

OBJECTIVE: To examine the anti-fatigue function of anwulignan from Schisandra and its underlying mechanism.
METHODS: After an excessive fatigue mouse model was created, anwulignan was administered to the mice, and its effect on exercise tolerance was studied by the weight-bearing swimming test, rotarod test, grip strength test, and tail suspension test. The biochemical indicators closely related to fatigue, including blood urea nitrogen (BUN), lactic acid (LD), lactate dehydrogenase (LDH), and creatine kinase (CK) in the serum; liver glycogen (LG) in the liver tissue; muscle glycogen (MG); inorganic phosphate (Pi) and Annexin V in the gastrocnemius; superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities; malondialdehyde (MDA), catalase (CAT), and thiobarbituric acid reactive substances (TBARS); and the 8-hydroxy-2-deoxyguanosine (8-OHdG) and reactive oxygen species (ROS) content in both serum and the gastrocnemius were detected. Morphological changes were also observed. The anti-fatigue-related proteins of the NRF2/ARE, Bcl2, and PGC-1α pathways in the gastrocnemius of the mice were detected by western blot.
RESULTS: Anwulignan significantly increased the exercise tolerance by decreasing BUN, LD, LDH, CK, Pi, MDA, TBARS, 8-OHdG, ROS, and Annexin V levels and increasing LG, MG, SOD, CAT, and GSH-Px levels, significantly upregulated the expression of NRF2 and Bcl2 proteins, which are anti-oxidation and anti-apoptosis regulators, and also activated the p38MAPK-PGC-1α pathway.
CONCLUSION: Anwulignan can increase exercise tolerance and relieve fatigue in an excessive fatigue mouse model. The underlying mechanism may be through its regulatory effect on the NRF2 and PGC-1α signaling pathway. This study will provide scientific data for anwulignan to be developed as a novel and efficient component in anti-oxidant or anti-fatigue health food.


greenmedinfo--2020-04-02--Effect of methanol extract of Schisandrae Fructus on high fat diet induced hyperlipidemia.

OBJECTIVE : To investigate the effects and molecular targets of Schisandrae Fructus ( SF ) methanol extract ( SFme ) @ @ @ @ @ by high fat diet .
METHODS : We observed changes in body weight , blood @ @ @ @ @ , high-density lipoprotein ( HDL ) -cholesterol , and triglyceride .
The extent of accumulation @ @ @ @ @ lipid metabolism disorder also evaluated by measuring malondialdehyde ( MDA ) level .
In addition @ @ @ @ @ in hepatic tissues , target protein of SFme was identified using a protein interaction database @ @ @ @ @ decreased total cholesterol and triglyceride levels without alteration of body weight in mice , and @ @ @ @ @ was statistically decreased by SFme .
And expression changes of cyclin- dependent kinase 1 ( @ @ @ @ @ kinase 2 ( Lrrk2 ) were restored by SFme .
CONCLUSION : The effect of @ @ @ @ @ induced hyperlipidemia via decreasing total cholesterol and triglyceride levels may involve the expression of Cdk1 @ @ @ @

OBJECTIVE: To investigate the effects and molecular targets of Schisandrae Fructus (SF) methanol extract (SFme) in mice with hyperlipidemia induced by high fat diet.
METHODS: We observed changes in body weight, blood serum content of total cholesterol, high-density lipoprotein (HDL)-cholesterol, and triglyceride. The extent of accumulation of lipid peroxide due to lipid metabolism disorder also evaluated by measuring malondialdehyde (MDA) level. In addition, after getting gene expression in hepatic tissues, target protein of SFme was identified using a protein interaction database.
RESULTS: SFme significantly decreased total cholesterol and triglyceride levels without alteration of body weight in mice, and the liver content of MDA was statistically decreased by SFme. And expression changes of cyclin- dependent kinase 1 (Cdk1) and leucine-rich repeat kinase 2 (Lrrk2) were restored by SFme.
CONCLUSION: The effect of SFme on the high- fat-diet induced hyperlipidemia via decreasing total cholesterol and triglyceride levels may involve the expression of Cdk1 and Lrrk2 proteins.


greenmedinfo--2020-04-02--These results suggest that S. chinensis acidic polysaccharide improves the insulin resistance in T2D

These results suggest that S. chinensis acidic polysaccharide improves the insulin resistance in T2D by inhibiting inflammation.

Polysaccharide fromhas the effect of lowering blood glucose and improving insulin resistance ( IR ) .
However , its underlying mechanism remains unclear .
In this study , a rat model of type 2 diabetes ( T2D ) was created to explore whetheracidic polysaccharide ( SCAP ) would improve the IR in T2D rats by inhibiting inflammation .
A combination of a high-fat diet and low dose of streptozotocin ( STZ , 30 mg/kg , intraperitoneally ) were administered to rats for establishing the T2D model .
Then , these T2D rats were orally administered with SCAP ( 25 , @ @ @ @ @ @ @ 8 weeks .
The results indicated that SCAP significantly lowered the fasting blood glucose , elevated the fasting insulin , and improved glucose tolerance .
SCAP also decreased the serum interleukin-1 ( IL-1 ) , interleukin-6 ( IL-6 ) , tumor necrosis factor- ( TNF- ) , C-reactive protein ( CRP ) , and nuclear factor-B ( NF-B ) levels , as well as their mRNA expression in the liver tissue .
Further , SCAP significantly inhibited the upregulation of phosphorylated c-Jun N-terminal kinase ( p-JNK ) and NF-B protein , and it @ @ @ @ @ @ @ ) , phosphorylated phosphatidylinositol 3-kinase ( p-PI3K ) , and phosphorylated protein kinase B ( p-AKT ) protein expression levels significantly .
These results suggest that SCAP improves the IR in T2D rats by inhibiting inflammation .

Polysaccharide fromhas the effect of lowering blood glucose and improving insulin resistance (IR). However, its underlying mechanism remains unclear. In this study, a rat model of type 2 diabetes (T2D) was created to explore whetheracidic polysaccharide (SCAP) would improve the IR in T2D rats by inhibiting inflammation. A combination of a high-fat diet and low dose of streptozotocin (STZ, 30 mg/kg, intraperitoneally) were administered to rats for establishing the T2D model. Then, these T2D rats were orally administered with SCAP (25, 50, or 100 mg/kg) for 8 weeks. The results indicated that SCAP significantly lowered the fasting blood glucose, elevated the fasting insulin, and improved glucose tolerance. SCAP also decreased the serum interleukin-1(IL-1), interleukin-6 (IL-6), tumor necrosis factor-(TNF-), C-reactive protein (CRP), and nuclear factor-B (NF-B) levels, as well as their mRNA expression in the liver tissue. Further, SCAP significantly inhibited the upregulation of phosphorylated c-Jun N-terminal kinase (p-JNK) and NF-B protein, and it increased phosphorylated insulin receptor substrate-1 (p-IRS-1), phosphorylated phosphatidylinositol 3-kinase (p-PI3K), and phosphorylated protein kinase B (p-AKT) protein expression levels significantly. These results suggest that SCAP improves the IR in T2D rats by inhibiting inflammation.


greenmedinfo--2020-04-02--Schisandra extract and ascorbic acid synergistically enhance cognition.

Cognitive decline is observed in aging and neurodegenerative diseases , including Alzheimer 's disease ( AD ) and dementia .
Intracellular energy produced via mitochondrial respiration is used in the regulation of synaptic plasticity and structure , including dendritic spine length and density , as well as for the release of neurotrophic factors involved in learning and memory .
To date , a few synthetic agents for improving mitochondrial function have been developed for overcoming cognitive impairment .
However , no natural compounds that modulate synaptic plasticity by directly targeting mitochondria have been developed .
Here , we demonstrate that @ @ @ @ @ @ @ ascorbic acid ( AA ) improved cognitive function and induced synaptic plasticity-regulating proteins by enhancing mitochondrial respiration .
Treatment of embryonic mouse hippocampal mHippoE-14 cells with a 4:1 mixture of SCE and AA increased basal oxygen consumption rate .
We found that mice injected with the SCE-AA mixture showed enhanced learning and memory and recognition ability .
We further observed that injection of the SCE-AA mixture in mice significantly increased expression of postsynaptic density protein 95 ( PSD95 ) , an increase that was correlated with enhanced brain-derived neurotrophic factor ( BDNF ) @ @ @ @ @ @ @ mixture of SCE and AA improves mitochondrial function and memory , suggesting that this natural compound mixture could be used to alleviate AD and aging-associated memory decline .

Cognitive decline is observed in aging and neurodegenerative diseases, including Alzheimer's disease (AD) and dementia. Intracellular energy produced via mitochondrial respiration is used in the regulation of synaptic plasticity and structure, including dendritic spine length and density, as well as for the release of neurotrophic factors involved in learning and memory. To date, a few synthetic agents for improving mitochondrial function have been developed for overcoming cognitive impairment. However, no natural compounds that modulate synaptic plasticity by directly targeting mitochondria have been developed. Here, we demonstrate that a mixture ofextract (SCE) and ascorbic acid (AA) improved cognitive function and induced synaptic plasticity-regulating proteins by enhancing mitochondrial respiration. Treatment of embryonic mouse hippocampal mHippoE-14 cells with a 4:1 mixture of SCE and AA increased basal oxygen consumption rate. We found that mice injected with the SCE-AA mixture showed enhanced learning and memory and recognition ability. We further observed that injection of the SCE-AA mixture in mice significantly increased expression of postsynaptic density protein 95 (PSD95), an increase that was correlated with enhanced brain-derived neurotrophic factor (BDNF) expression. These results demonstrate that a mixture of SCE and AA improves mitochondrial function and memory, suggesting that this natural compound mixture could be used to alleviate AD and aging-associated memory decline.


greenmedinfo--2020-04-02--The bioflavonoid galangin suppresses the growth of ehrlich ascites carcinoma.

Bioflavonoids are plant compounds touted for their potential to treat or prevent several diseases including cancer caused by various stress conditions .
Galangin ( 4H-1-Benzopyran-4-one , 3 , 5 , 7-trihydroxy-2-phenyl- ) , a flavonoid , is a polyphenolic compound found primarily in medicinal herb , Alpinia galanga .
This study aims to demonstrate the galangin as a pharmacological lead compound using in vitro , in vivo , and in silico model targeting specific cancer condition and proteins .
The proliferation of MCF-7 and Ehrlich ascites carcinoma ( EAC ) cells was significantly inhibited with an IC₅₀ of 34.11 and @ @ @ @ @ @ @ animal model system , galangin has inhibited the tumor growth by 73.51 % ± 4.742 in EAC-induced Swiss Albino mice with no evidences of mortality as compared to standard drug , 5-fluorouracil .
The effectiveness of galangin is proven in an animalsystem suggesting its pharmacokinetics behavior in an animal model which is also complemented by outcome of in silico analysis with more than 88 % of human intestinal absorption and significant Caco-2 cell , MDCK cell , and skin permeability as predicted by in silico methods .
Galangin was docked against 19 different @ @ @ @ @ @ @ the energetic analysis indicates that it exhibits higher predicted binding free energy of -12.7 kcal/mol with Bcl-xL protein .

Bioflavonoids are plant compounds touted for their potential to treat or prevent several diseases including cancer caused by various stress conditions. Galangin (4H-1-Benzopyran-4-one, 3, 5, 7-trihydroxy-2-phenyl-), a flavonoid, is a polyphenolic compound found primarily in medicinal herb, Alpinia galanga. This study aims to demonstrate the galangin as a pharmacological lead compound using in vitro, in vivo, and in silico model targeting specific cancer condition and proteins. The proliferation of MCF-7 and Ehrlich ascites carcinoma (EAC) cells was significantly inhibited with an IC₅₀ of 34.11 and 22.29 μg/ml, respectively. In an animal model system, galangin has inhibited the tumor growth by 73.51% ± 4.742 in EAC-induced Swiss Albino mice with no evidences of mortality as compared to standard drug, 5-fluorouracil. The effectiveness of galangin is proven in an animalsystem suggesting its pharmacokinetics behavior in an animal model which is also complemented by outcome of in silico analysis with more than 88 % of human intestinal absorption and significant Caco-2 cell, MDCK cell, and skin permeability as predicted by in silico methods. Galangin was docked against 19 different proteins involved in tumorogenesis and apoptosis; the energetic analysis indicates that it exhibits higher predicted binding free energy of -12.7 kcal/mol with Bcl-xL protein.


greenmedinfo--2020-04-02--Galangin induces autophagy through upregulation of p53 in HepG2 cells.

AIM : To investigate the mechanism by which galangin , a polyphenolic compound derived from medicinal herbs , induces autophagy of HepG2 cells .
METHODS : The MTT [ 3- ( 4,5-dimethyl-thiazol-2-yl ) 2,5-diphenyl-tetrazolium bromide ] assay was used to measure cell viability .
Apoptosis was evaluated by TUNEL assay with flow cytometry , and PARP cleavage was detected by Western blotting .
Autophagy was measured by fluorescence microscopy and transmission electron microscopy .
Protein expressions were detected by Western blotting .
Pifithrin- was used for pretreatment and siRNA was used to knock down p53 expression to explore the pathway @ @ @ @ @ @ @ Furthermore , Hep3B cells were used to express the exogenous wild-type p53 .
RESULTS : Galangin treatment inhibited cell proliferation and induced autophagy ( 130μ mol/l ) and apoptosis ( 370 μ mol/l ) .
In particular , galangin treatment in HepG2 cells caused ( 1 ) an accumulation of autophagosomes , ( 2 ) elevated levels of microtubule-associated protein light chain 3 , and ( 3 ) an increased percentage of cells with vacuoles .
p53 expression was also increased .
The galangin-induced autophagy was attenuated by the inhibition of p53 in @ @ @ @ @ @ @ in Hep3B cells restored the galangin-induced higher percentage of cells with vacuoles to normal level .
CONCLUSION : Our results indicate that galangin not only induced apoptosis but also prompted cell autophagy indifferent concentrations .
Galangin mediates autophagy through a p53-dependent pathway in HepG2 cells .
Our findings may help in the discovery of a chemotherapeutic drug with the novel pattern of inhibiting cell proliferation for the treatment of hepatocellular carcinoma cells .

AIM: To investigate the mechanism by which galangin, a polyphenolic compound derived from medicinal herbs,induces autophagy of HepG2 cells.
METHODS: The MTT[3-(4,5-dimethyl-thiazol-2-yl)2,5-diphenyl-tetrazolium bromide]assay was used to measure cell viability. Apoptosis was evaluated by TUNEL assay with flow cytometry, and PARP cleavage was detected by Western blotting. Autophagy was measured by fluorescence microscopy and transmission electron microscopy. Protein expressions were detected by Western blotting. Pifithrin- was used for pretreatment and siRNA was used to knock down p53 expression to explore the pathway mediated by galangin in HepG2 cells. Furthermore, Hep3B cells were used to express the exogenous wild-type p53.
RESULTS: Galangin treatment inhibited cell proliferation and induced autophagy (130μ mol/l) and apoptosis (370 μ mol/l). In particular, galangin treatment in HepG2 cells caused (1) an accumulation of autophagosomes, (2) elevated levels of microtubule-associated protein light chain 3, and (3) an increased percentage of cells with vacuoles. p53 expression was also increased. The galangin-induced autophagy was attenuated by the inhibition of p53 in HepG2 cells, and overexpression of p53 in Hep3B cells restored the galangin-induced higher percentage of cells with vacuoles to normal level.
CONCLUSION: Our results indicate that galangin not only induced apoptosis but also prompted cell autophagy indifferent concentrations. Galangin mediates autophagy through a p53-dependent pathway in HepG2 cells. Our findings may help in the discovery of a chemotherapeutic drug with the novel pattern of inhibiting cell proliferation for the treatment of hepatocellular carcinoma cells.


greenmedinfo--2020-04-02--Galangin induces apoptosis in hepatocellular carcinoma cells.

This study has investigated whether galangin , a flavonol derived from Alpinia officinarum Hance and used as food additives in southern China , induces apoptosis in hepatocellular carcinoma cells ( HCCs ) by activation of the caspase-8 and Bid pathway .
The apoptosis of HCCs was evaluated by in situ uptake of propidium iodide and Hoechst 33258 .
Protein expressions were detected by Western blotting .
Caspase-8 activity was measured using colorimetric method .
To confirm the galangin-induced apoptotic pathway , inhibition of caspase-8 activity by Z-IETD-FMK , knockdown of Bid expression with siRNA , and overexpression of Bcl-2 in @ @ @ @ @ @ @ The results show that galangin has significantly induced apoptosis in HCC lines .
The caspase-8 is activated , and the cleavage of Bid results in the increase in tBid .
The galangin-induced apoptosis is attenuated by Z-IETD-FMK , Bid siRNA , and Bcl-2 overexpression , respectively .
However , Bcl-2 fails to suppress caspase-8 activation and the cleavage of Bid .
This study has demonstrated that galangin induces apoptosis in HCCs by activating caspase 8/t-Bid mitochondrial pathway .
Although Bcl-2 overexpression attenuates galangin-mediated apoptosis of HCCs , it is not mediated by the @ @ @ @ @ @ @ .

This study has investigated whether galangin, a flavonol derived from Alpinia officinarum Hance and used as food additives in southern China, induces apoptosis in hepatocellular carcinoma cells (HCCs) by activation of the caspase-8 and Bid pathway. The apoptosis of HCCs was evaluated by in situ uptake of propidium iodide and Hoechst 33258. Protein expressions were detected by Western blotting. Caspase-8 activity was measured using colorimetric method. To confirm the galangin-induced apoptotic pathway, inhibition of caspase-8 activity by Z-IETD-FMK, knockdown of Bid expression with siRNA, and overexpression of Bcl-2 in cells were carried out, respectively. The results show that galangin has significantly induced apoptosis in HCC lines. The caspase-8 is activated, and the cleavage of Bid results in the increase in tBid. The galangin-induced apoptosis is attenuated by Z-IETD-FMK, Bid siRNA, and Bcl-2 overexpression, respectively. However, Bcl-2 fails to suppress caspase-8 activation and the cleavage of Bid. This study has demonstrated that galangin induces apoptosis in HCCs by activating caspase 8/t-Bid mitochondrial pathway. Although Bcl-2 overexpression attenuates galangin-mediated apoptosis of HCCs, it is not mediated by the inhibition of tBid generation and caspase-8 activation.


greenmedinfo--2020-04-02--Galangin inhibits tumor growth and metastasis of B16F10 melanoma.

Galangin , an active flavonoid extracted from the root of the Alpinia officinarum Hance , showed a cytotoxic effect on several cancer cell lines in vitro .
However , there is no information available concerning its antimetastatic effect .
Focal adhesion kinase ( FAK ) , a cytoplasmic tyrosine kinase , is involved in many aspects of cellular processes such as proliferation , adhesion , and invasion .
Studies have shown that FAK is a promising target for therapeutic intervention in melanoma .
In the present study , proliferation of B16F10 cells was suppressed when exposed to various doses of @ @ @ @ @ @ @ was also detected by clonogenic survival assay .
The capabilities of cell adhesion , cell spreading , and cell motility were impaired by galangin , reinforced by F-actin rearrangement .
Molecular data showed that both FAK mRNA level and protein level were reduced dose-dependently .
Additionally , galangin reduced phosphorylation of FAK ( Tyr397 ) protein .
Transient transfection reporter assays showed that galangin suppressed the transcription of FAK gene , indicating FAK expression is a candidate target of galangin .
The antimetastatic function of galangin is further supported by the fact that @ @ @ @ @ @ @ colonies in the lung tissue on C57BL/6J mouse lung metastatic model using B16F10 melanoma cells .
Immunochemical analyses showed that galangin decreased FAK expression in vivo .
These data add to our new understanding that galangin can inhibit B16F10 melanoma metastasis both in vivo and in vitro , and that FAK is a valid therapeutic target against melanoma .

Galangin, an active flavonoid extracted from the root of the Alpinia officinarum Hance, showed a cytotoxic effect on several cancer cell lines in vitro. However, there is no information available concerning its antimetastatic effect. Focal adhesion kinase (FAK), a cytoplasmic tyrosine kinase, is involved in many aspects of cellular processes such as proliferation, adhesion, and invasion. Studies have shown that FAK is a promising target for therapeutic intervention in melanoma. In the present study, proliferation of B16F10 cells was suppressed when exposed to various doses of galangin. Inhibition on proliferation by galangin was also detected by clonogenic survival assay. The capabilities of cell adhesion, cell spreading, and cell motility were impaired by galangin, reinforced by F-actin rearrangement. Molecular data showed that both FAK mRNA level and protein level were reduced dose-dependently. Additionally, galangin reduced phosphorylation of FAK (Tyr397) protein. Transient transfection reporter assays showed that galangin suppressed the transcription of FAK gene, indicating FAK expression is a candidate target of galangin. The antimetastatic function of galangin is further supported by the fact that it could inhibit the formation of tumor colonies in the lung tissue on C57BL/6J mouse lung metastatic model using B16F10 melanoma cells. Immunochemical analyses showed that galangin decreased FAK expression in vivo. These data add to our new understanding that galangin can inhibit B16F10 melanoma metastasis both in vivo and in vitro, and that FAK is a valid therapeutic target against melanoma.


greenmedinfo--2020-04-02--Galangin inhibits osteoclastic bone destruction and osteoclastogenesis.

We investigated the effect of galangin , a natural flavonoid , on osteoclastic bone destruction in collagen-induced arthritis and examined the molecular mechanisms by which galangin affects osteoclastogenesis in bone marrow derived macrophages .
In mice with collagen-induced arthritis , administration of galangin significantly reduced the arthritis clinical score , edema and severity of disease without toxicity .
Interestingly , galangin treatment during a later stage of collagen-induced arthritis , using mice with a higher clinical arthritis score , still significantly slowed the progression of the disease .
Extensive cartilage and bone erosive changes as well as synovial inflammation , @ @ @ @ @ @ @ inhibited in arthritic mice treated with galangin .
Furthermore , galangin-treated arthritic mice showed a significant reduction in the concentrations of IL-1β , TNF-α and IL-17 .
We found that galangin inhibited osteoclastogenic factors and osteoclast formation in bone marrow-derived macrophages and osteoblast co-cultured cells , and increased osteoprotegerin ( OPG ) levels in osteoblasts .
Galangin and NF-κB siRNA suppressed RANKL-induced phosphorylationof the c-jun N-terminal kinase ( JNK ) and p38 mitogen-activated protein kinase ( MAPK ) , but not AKT and extracellular signal-regulated kinase 1/2 ( ERK1/2 ) .
Also , @ @ @ @ @ @ @ SB203580 reduced RANKL-induced expressions of phospho-c-Jun , c-fos and NFATc1 genes during osteoclast development .
In addition , galangin suppressed RANKL-induced phosphorylation of NF-κB , phospho-IκBα , inflammatory cytokines and osteoclast formation in bone marrow-derived macrophages .
Our data suggest that galangin prevented osteoclastic bone destruction and osteoclastogenesis in osteoclast precursors as well as in collagen-induced arthritis mice without toxicity via attenuation of RANKL-induced activation of JNK , p38 and NF-κB pathways .

We investigated the effect of galangin, a natural flavonoid, on osteoclastic bone destruction in collagen-induced arthritis and examined the molecular mechanisms by which galangin affects osteoclastogenesis in bone marrow derived macrophages. In mice with collagen-induced arthritis, administration of galangin significantly reduced the arthritis clinical score, edema and severity of disease without toxicity. Interestingly, galangin treatment during a later stage of collagen-induced arthritis, using mice with a higher clinical arthritis score, still significantly slowed the progression of the disease. Extensive cartilage and bone erosive changes as well as synovial inflammation, synovial hyperplasia and pannus formation were dramatically inhibited in arthritic mice treated with galangin. Furthermore, galangin-treated arthritic mice showed a significant reduction in the concentrations of IL-1β, TNF-α and IL-17. We found that galangin inhibited osteoclastogenic factors and osteoclast formation in bone marrow-derived macrophages and osteoblast co-cultured cells, and increased osteoprotegerin (OPG) levels in osteoblasts. Galangin and NF-κB siRNA suppressed RANKL-induced phosphorylationof the c-jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK), but not AKT and extracellular signal-regulated kinase 1/2 (ERK1/2). Also, the JNK inhibitor SP600125 and p38 inhibitor SB203580 reduced RANKL-induced expressions of phospho-c-Jun, c-fos and NFATc1 genes during osteoclast development. In addition, galangin suppressed RANKL-induced phosphorylation of NF-κB, phospho-IκBα, inflammatory cytokines and osteoclast formation in bone marrow-derived macrophages. Our data suggest that galangin prevented osteoclastic bone destruction and osteoclastogenesis in osteoclast precursors as well as in collagen-induced arthritis mice without toxicity via attenuation of RANKL-induced activation of JNK, p38 and NF-κB pathways.


greenmedinfo--2020-04-02--Galangin has the potential to be a promising agent for melanoma treatment.

Galangin , an active flavonoid present at high concentration in Alpinia officinarum Hance and propolis , shows cytotoxicity towards several @ @ @ @ @ melanoma .
However , the specific cellular targets of galangin-induced cytotoxicity in melanoma are still @ @ @ @ @ investigated the effects of galangin in B16F10 melanoma cells and explored the possible molecular mechanisms @ @ @ @ @ viability of B16F10 cells , and also induced cell apoptosis shown by Hoechst 33342 staining @ @ @ @ @ flow cytometric assay .
Furthermore , upon galangin treatment , disruption of mitochondrial membrane potential @ @ @ @ @ .
Western blotting analysis indicated that galangin activated apoptosis signaling cascades by cleavage of procaspase-9 @ @ @ @ @ B16F10 cells .
Moreover , galangin significantly induced activation of phosphor-p38 MAPK in a time @ @ @ @ @ SB203580 , an inhibitor of p38 , partially attenuated galangin-induced apoptosis in B16F10 cells .
@ @ @ @ @ suggests that galangin has the potential to be a promising agent for melanoma treatment and @ @ @ @ @ a chemotherapeutic agent .

Galangin, an active flavonoid present at high concentration in Alpinia officinarum Hance and propolis, shows cytotoxicity towards several cancer cell lines, including melanoma. However, the specific cellular targets of galangin-induced cytotoxicity in melanoma are still unknown. Here, we investigated the effects of galangin in B16F10 melanoma cells and explored the possible molecular mechanisms. Galangin significantly decreased cell viability of B16F10 cells, and also induced cell apoptosis shown by Hoechst 33342 staining and Annexin V-PI double staining flow cytometric assay. Furthermore, upon galangin treatment, disruption of mitochondrial membrane potential was observed by JC-1 staining. Western blotting analysis indicated that galangin activated apoptosis signaling cascades by cleavage of procaspase-9, procaspase-3 and PARP in B16F10 cells. Moreover, galangin significantly induced activation of phosphor-p38 MAPK in a time and dose dependent manner. SB203580, an inhibitor of p38, partially attenuated galangin-induced apoptosis in B16F10 cells. Taken together, this work suggests that galangin has the potential to be a promising agent for melanoma treatment and may be further evaluated as a chemotherapeutic agent.


greenmedinfo--2020-04-03--Regulatory role of vitamin E in the immune system and inflammation.

Vitamin E , a potent lipid-soluble antioxidant , found in higher concentration in immune cells compared to other cells in blood , is one of the most effective nutrients known to modulate immune function .
Vitamin E deficiency has been demonstrated to impair normal functions of the immune system in animals and humans , which can be corrected by vitamin E repletion .
Although deficiency is rare , vitamin E supplementation above current dietary recommendations has been shown to enhance the function of the immune system and reduce risk of infection , particularly in older individuals .
The mechanisms responsible @ @ @ @ @ @ @ the immune system and inflammation have been explored in cell-based , pre-clinical and clinical intervention studies .
Vitamin E modulates T cell function through directly impacting T cell membrane integrity , signal transduction , and cell division , and also indirectly by affecting inflammatory mediators generated from other immune cells .
Modulation of immune function by vitamin E has clinical relevance as it affects host susceptibility to infectious diseases such as respiratory infections , in addition to allergic diseases such as asthma .
Studies examining the role of vitamin E in the immune @ @ @ @ @ @ @ , emerging evidence suggests that other forms of vitamin E , including other tocopherols as well as tocotrienols , may also have potent immunomodulatory functions .
Future research should continue to identify and confirm the optimal doses for individuals at different life stage , health condition , nutritional status , and genetic heterogeneity .
Future research should also characterize the effects of non-α-alpha-tocopherol vitamin E on immune cell function as well as their potential clinical application .
© 2018 IUBMB Life , 71 ( 4 ) :487-494 , 2019 .

Vitamin E, a potent lipid-soluble antioxidant, found in higher concentration in immune cells compared to other cells in blood, is one of the most effective nutrients known to modulate immune function. Vitamin E deficiency has been demonstrated to impair normal functions of the immune system in animals and humans, which can be corrected by vitamin E repletion. Although deficiency is rare, vitamin E supplementation above current dietary recommendations has been shown to enhance the function of the immune system and reduce risk of infection, particularly in older individuals. The mechanisms responsible for the effect of vitamin E on the immune system and inflammation have been explored in cell-based, pre-clinical and clinical intervention studies. Vitamin E modulates T cell function through directly impacting T cell membrane integrity, signal transduction, and cell division, and also indirectly by affecting inflammatory mediators generated from other immune cells. Modulation of immune function by vitamin E has clinical relevance as it affects host susceptibility to infectious diseases such as respiratory infections, in addition to allergic diseases such as asthma. Studies examining the role of vitamin E in the immune system have typically focused onα-tocopherol; however, emerging evidence suggests that other forms of vitamin E, including other tocopherols as well as tocotrienols, may also have potent immunomodulatory functions. Future research should continue to identify and confirm the optimal doses for individuals at different life stage, health condition, nutritional status, and genetic heterogeneity. Future research should also characterize the effects of non-α-alpha-tocopherol vitamin E on immune cell function as well as their potential clinical application. © 2018 IUBMB Life, 71(4):487-494, 2019.


greenmedinfo--2020-04-03--This review will summarize the immunological changes observed with vitamin E intervention in animals

This review will summarize the immunological changes observed with vitamin E intervention in animals and humans.

Vitamin E is a fat-soluble antioxidant that can protect the polyunsaturated fatty acids ( PUFAs ) in the membrane from @ @ @ @ @ of reactive oxygen species ( ROS ) and reactive nitrogen species ( RNS ) , @ @ @ @ @ Immunomodulatory effects of vitamin E have been observed in animal and human models under normal @ @ @ @ @ advances in understating of the development , function , and regulation of dendritic cells ( @ @ @ @ @ natural killer ( NK ) cells , T cells , and B cells , recent @ @ @ @ @ E 's effects on specific immune cells .
This review will summarize the immunological changes @ @ @ @ @ in animals and humans , and then describe the cell-specific effects of vitamin E in @ @ @ @ @ of immunomodulation and implications of vitamin E for immunological diseases .

Vitamin E is a fat-soluble antioxidant that can protect the polyunsaturated fatty acids (PUFAs) in the membrane from oxidation, regulate the production of reactive oxygen species (ROS) and reactive nitrogen species (RNS), and modulate signal transduction. Immunomodulatory effects of vitamin E have been observed in animal and human models under normal and disease conditions. With advances in understating of the development, function, and regulation of dendritic cells (DCs), macrophages, natural killer (NK) cells, T cells, and B cells, recent studies have focused on vitamin E's effects on specific immune cells. This review will summarize the immunological changes observed with vitamin E intervention in animals and humans, and then describe the cell-specific effects of vitamin E in order to understand the mechanisms of immunomodulation and implications of vitamin E for immunological diseases.