greenmedinfo--2020-11-26--Bioactive compounds of Rheum ribes L. and its anticancerogenic effect via induction of apoptosis and

Bioactive compounds of Rheum ribes L. and its anticancerogenic effect via induction of apoptosis and miR-200 family expression in human colorectal cancer cells.

L. is a widespread plant species in the eastern part of our country and is consumed as a vegateble by @ @ @ @ @ our study , we investigated whetherhas anti-cancerogenic effect on colorectal cancer cell lines .
Six @ @ @ @ @ .
Total phenolic , flavonoid contents , antioxidant activities , and cytotoxic effects of all @ @ @ @ @ were determined .
Differences in expression levels of the miR-200 family and target genes were @ @ @ @ @ cells .
Antiproliferative effect was determined by TUNEL , Annexin V , cell cycle , @ @ @ @ @ of BCL-2 , ZEB1 , GATA4 and FAS/CD95 proteins were determined by ELISA .
According @ @ @ @ @ expression analysis , the only dose group with a significant increase (

L. is a widespread plant species in the eastern part of our country and is consumed as a vegateble by the folk people. In our study, we investigated whetherhas anti-cancerogenic effect on colorectal cancer cell lines. Six different extracts were obtained from. Total phenolic, flavonoid contents, antioxidant activities, and cytotoxic effects of all extracts on colorectal cancer cells were determined. Differences in expression levels of the miR-200 family and target genes were assessed by real-time qPCR in cells. Antiproliferative effect was determined by TUNEL, Annexin V, cell cycle, invasion analysis; and levels of BCL-2, ZEB1, GATA4 and FAS/CD95 proteins were determined by ELISA. According to the results of miRNA expression analysis, the only dose group with a significant increase ( < 0,05) in the expression level of all of miRNAs in both cell lines was RM (Root methanol) extract alone. Our results showed that, RM caused a significant increase in the expressions of miR-200a/b/c and miR-141, and it suppressed BCL-2, ZEB1, GATA4 expressions, with this way. Thus, it has been suggested that the treatment of RM alone, or combined treatment of RM with 5-FU result in a better response than cancer cells treated with 5-FU alone.


greenmedinfo--2020-11-26--The effect of Rheum ribes L. on oxidative stress in diabetic rats.

Objectives Rheum ribes L. is a perennial plant that belongs to the family of Polygonaceae , which is often used in traditional therapy because it possesses many bioactivities , such as antioxidant and antibacterial ones .
Here we examined the effect of different R. ribes L. extracts on oxidative stress in experimental diabetic rats .
Methods Thirty-six rats were divided into six groups as follows : group I , control group ; group II , diabetic rats ; group III , diabetic rats treated with the aqueous extract of R. ribes L. by gavage at 50 mg/kg for 15 days @ @ @ @ @ @ @ by gavage with the ethanolic extract of R. ribes L. at 50 mg/kg for 15 days ; group V , nondiabetic rats treated by gavage with the aqueous extract of R. ribes L. at 50 mg/kg for 15 days ; group VI , nondiabetic rats treated by gavage with the ethanol extract of R. ribes L. at 50 mg/kg for 15 days .
After 15 days , the animals were sacrificed and the liver and kidney tissues of each animal were isolated .
Superoxide dismutase ( SOD ) , catalase ( CAT ) @ @ @ @ @ @ @ peroxidase ( GSH-Px ) activities in the tissue samples were measured , and histopathologic examination was carried out .
Results R. ribes L. was effective in reducing the oxidative stress and increasing the levels of the antioxidant enzymes .
Increased levels of MDA and decreased levels of SOD , CAT and GSH-Px were observed in both the liver and kidney tissues in group II .
Decreased levels of MDA and increased levels of SOD , CAT and GSH-Px were observed in group III compared with group II .
In group IV , decreased @ @ @ @ @ @ @ SOD , CAT and GSH-Px were observed in comparison with group II .
Conclusions Diabetes increases oxidative stress and causes a decrease in antioxidant enzyme levels .
Both aqueous and ethanolic extracts of R. ribes L. decrease oxidative stress activity and increase the levels of antioxidant enzymes .
The ethanol extract of R. ribes L. has a higher antioxidant effect than the aqueous extract .

Objectives Rheum ribes L. is a perennial plant that belongs to the family of Polygonaceae, which is often used in traditional therapy because it possesses many bioactivities, such as antioxidant and antibacterial ones. Here we examined the effect of different R. ribes L. extracts on oxidative stress in experimental diabetic rats. Methods Thirty-six rats were divided into six groups as follows: group I, control group; group II, diabetic rats; group III, diabetic rats treated with the aqueous extract of R. ribes L. by gavage at 50 mg/kg for 15 days; group IV, diabetic rats treated by gavage with the ethanolic extract of R. ribes L. at 50 mg/kg for 15 days; group V, nondiabetic rats treated by gavage with the aqueous extract of R. ribes L. at 50 mg/kg for 15 days; group VI, nondiabetic rats treated by gavage with the ethanol extract of R. ribes L. at 50 mg/kg for 15 days. After 15 days, the animals were sacrificed and the liver and kidney tissues of each animal were isolated. Superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA) and glutathione peroxidase (GSH-Px) activities in the tissue samples were measured, and histopathologic examination was carried out. Results R. ribes L. was effective in reducing the oxidative stress and increasing the levels of the antioxidant enzymes. Increased levels of MDA and decreased levels of SOD, CAT and GSH-Px were observed in both the liver and kidney tissues in group II. Decreased levels of MDA and increased levels of SOD, CAT and GSH-Px were observed in group III compared with group II. In group IV, decreased levels of MDA and increased levels of SOD, CAT and GSH-Px were observed in comparison with group II. Conclusions Diabetes increases oxidative stress and causes a decrease in antioxidant enzyme levels. Both aqueous and ethanolic extracts of R. ribes L. decrease oxidative stress activity and increase the levels of antioxidant enzymes. The ethanol extract of R. ribes L. has a higher antioxidant effect than the aqueous extract.


greenmedinfo--2020-11-26--Effect of isgin ( Rheum ribes L.) on biochemical parameters, antioxidant activity and DNA damage in

Effect of isgin ( Rheum ribes L.) on biochemical parameters, antioxidant activity and DNA damage in rats with obesity induced with high-calorie diet.

The present study was designed to investigate the effects ofL .
plant root extracts on DNA damage , biochemical and @ @ @ @ @ experimental obesity induced with a high-calorie diet .
The study groups were divided as '' @ @ @ @ @ '' , '' obese control ( OC ) '' , '' obese + ( OR1 @ @ @ @ @ '' and '' obese + ( OR2 ) ( 400 mg/kg ) '' .
At @ @ @ @ @ , rats were sacrificed and blood and tissue samples were obtained .
According to the @ @ @ @ @ of DNA damage in tissues of 8-OHdG was determined to be significantly reduced in brain @ @ @ @ @ OR2 groups compared to the NC group .
However , fluctuations were identified in the @ @ @ @ @ system elements and serum biomarkers in tissues .
In conclusion , plant root extract ensured @ @ @ @ @ brain tissues and MDA levels and showed positive effects on antioxidant parameter activities in different @ @

The present study was designed to investigate the effects ofL. plant root extracts on DNA damage, biochemical and antioxidant parameters in rats with experimental obesity induced with a high-calorie diet. The study groups were divided as"normal control(NC)","obese control(OC)","obese +(OR1)(200 mg/kg)"and"obese +(OR2)(400 mg/kg)". At the end of the application, rats were sacrificed and blood and tissue samples were obtained. According to the results obtained, the marker of DNA damage in tissues of 8-OHdG was determined to be significantly reduced in brain tissue of the OR1 and OR2 groups compared to the NC group. However, fluctuations were identified in the MDA activity, antioxidant defense system elements and serum biomarkers in tissues. In conclusion,plant root extract ensured improvements in DNA damage in brain tissues and MDA levels and showed positive effects on antioxidant parameter activities in different tissues.


greenmedinfo--2020-11-26--In vitro and ex vivo antiparasitic effect of Rheum ribes L. extract against the hydatid cyst protosc

In vitro and ex vivo antiparasitic effect of Rheum ribes L. extract against the hydatid cyst protoscoleces.

BACKGROUND : Cystic echinococcosis is a zoonotic infection in humans and herbivorous animals with worldwide distribution which caused by larva stage of Echinococcus granulosus .
Rhubarb ( Rheum ribes L. ) as an herbal medicines has various therapeutics properties such as the antioxidant , anticancer , and antimicrobial ones .
With respect to the potential of the biological activities of this plant in traditional and modern medicine , we aim to examine its protoscolicidal effects against E. granulosus protoscolecess in vitro and ex vivo .
METHODS : Collected protoscoleces from liver hydatid cysts of infected sheep were exposed to the @ @ @ @ @ @ @ , 450 , 900 mg/mL ) for 5-60 min in vitro and ex vivo .
Then using the eosin exclusion assay the viability of protoscoleces was studied .
RESULTS : R. ribes extract had a potent protoscolicidal activity in vitro so that at the 450 and 900 mg/ml killed 56.3 and 100 % of protoscoleces after 10 min exposure .
Ex vivo assay , the extract needed more time to kill the protoscoleces than the in vitro ; so that at the concentration of 900 mg/mL , all protoscoleces were killed after 15 @ @ @ @ @ @ @ exhibited the potent protoscolicidal effects of R. ribes extract particularly at the concentration of 900 mg/ml which completely killed the parasite after < 15 min exposure .
However , more and supplementary studies are required to verify these findings through assessing in animal models and clinical subjects .

BACKGROUND: Cystic echinococcosis is a zoonotic infection in humans and herbivorous animals with worldwide distribution which caused by larva stage of Echinococcus granulosus. Rhubarb (Rheum ribes L.) as an herbal medicines has various therapeutics properties such as the antioxidant, anticancer, and antimicrobial ones. With respect to the potential of the biological activities of this plant in traditional and modern medicine, we aim to examine its protoscolicidal effects against E. granulosus protoscolecess in vitro and ex vivo.
METHODS: Collected protoscoleces from liver hydatid cysts of infected sheep were exposed to the different concentrations of the extract (225, 450, 900 mg/mL) for 5-60 min in vitro and ex vivo. Then using the eosin exclusion assay the viability of protoscoleces was studied.
RESULTS: R. ribes extract had a potent protoscolicidal activity in vitro so that at the 450 and 900 mg/ml killed 56.3 and 100% of protoscoleces after 10 min exposure. Ex vivo assay, the extract needed more time to kill the protoscoleces than the in vitro; so that at the concentration of 900 mg/mL, all protoscoleces were killed after 15 minutes.
CONCLUSION: The obtained results exhibited the potent protoscolicidal effects of R. ribes extract particularly at the concentration of 900 mg/ml which completely killed the parasite after<15 min exposure. However, more and supplementary studies are required to verify these findings through assessing in animal models and clinical subjects.


greenmedinfo--2020-11-27--Potentiation of the effect of lonidamine by quercetin in MCF-7 human breast cancer cells.

Combination therapies are becoming increasingly important to develop an effective treatment in cancer .
Lonidamine is frequently used in cancer treatment , but it 's often preferred to be used in combination with other drugs because of its side effects .
In the present study , the efficacy of the combination of lonidamine with quercetin , a flavonoid of natural origin , on human MCF-7 breast cancer cells was evaluated .
The results showed that the combined use of the compounds significantly increased cytotoxicity compared to administration alone ( p < 0.0001 ) .
In addition , while lonidamine induced @ @ @ @ @ @ @ phase , administration of quercetin and its combination with lonidamine arrested the cell division at S point , indicating the synergistic strength of quercetin on cytotoxicity .
The combination of quercetin and lonidamine significantly induced apoptosis of MCF-7 cells ( p < 0.0001 ) and increased caspase levels ( p < 0.0001 ) .
In this study , the combination of quercetin and lonidamine has been evaluated for the first time and the combination treatment decreased MMP-2/-9 mRNA expression more potently than the effects of the compounds alone .
The results showed that @ @ @ @ @ @ @ quercetin , and their combination may be a candidate for a novel strategy of treatment for breast cancer .

Combination therapies are becoming increasingly important to develop an effective treatment in cancer. Lonidamine is frequently used in cancer treatment, but it's often preferred to be used in combination with other drugs because of its side effects. In the present study, the efficacy of the combination of lonidamine with quercetin, a flavonoid of natural origin, on human MCF-7 breast cancer cells was evaluated. The results showed that the combined use of the compounds significantly increased cytotoxicity compared to administration alone (p<0.0001). In addition, while lonidamine induced a cell cycle arrest in the G2/M phase, administration of quercetin and its combination with lonidamine arrested the cell division at S point, indicating the synergistic strength of quercetin on cytotoxicity. The combination of quercetin and lonidamine significantly induced apoptosis of MCF-7 cells (p<0.0001) and increased caspase levels (p<0.0001). In this study, the combination of quercetin and lonidamine has been evaluated for the first time and the combination treatment decreased MMP-2/-9 mRNA expression more potently than the effects of the compounds alone. The results showed that lonidamine was more effective when combined with quercetin, and their combination may be a candidate for a novel strategy of treatment for breast cancer.


greenmedinfo--2020-11-27--Effects of berberine hydrochloride on methamphetamine-induced anxiety behaviors and relapse in rats.

Objectives : This research aimed at evaluating the effect of berberine hydrochloride on anxiety-related behaviors induced by methamphetamine ( METH ) in rats , assessing relapse and neuroprotective effects .
Materials and Methods : 27 male Wistar rats were randomly assigned into groups of Control , METH-withdrawal ( METH addiction and subsequent withdrawal ) , and METH addiction with berberine hydrochloride oral treatment ( 100 mg/kg/per day ) during the three weeks of withdrawal .
Two groups received inhaled METH self-administration for two weeks ( up to 10 mg/kg ) .
The elevated plus maze ( EPM ) test and @ @ @ @ @ @ @ carried out one day after the last berberine treatment and relapse was assessed by conditional place preference ( CPP ) test .
TUNEL assay and immunofluorescence staining for NF-κB , TLR4 , Sirt1 , and α-actin expression in the hippocampus were tested .
Results : After 3 weeks withdrawal , berberine hydrochloride decreased locomotor activity and reduced anxiety-related behaviors in comparison with the METH-withdrawal group ( < 0.001 ) .
The obtained results from CPP showed that berberine significantly reduced relapse ( < 0.01 ) .
Significantly decrease in activation of TLR4 , @ @ @ @ @ @ @ found and the percentage of TLR4 , Sirt1 , and α-actin improved in berberine-treated group ( < 0.001 ) .
A significant activity rise of NF-κB of cells in the METH-withdrawal group was detected compared to berberine-treated and control groups ( < 0.001 ) .
Conclusion : Treatment with berberine hydrochloride via modulating neuroinflammation may be considered as a potential new medication for the treatment of METH addiction and relapse .
The histological assays supported the neuroprotective effects of berberine in the hippocampus .

Objectives: This research aimed at evaluating the effect of berberine hydrochloride on anxiety-related behaviors induced by methamphetamine (METH) in rats, assessing relapse and neuroprotective effects.
Materials and Methods: 27 male Wistar rats were randomly assigned into groups of Control, METH-withdrawal (METH addiction and subsequent withdrawal), and METH addiction with berberine hydrochloride oral treatment (100 mg/kg/per day) during the three weeks of withdrawal. Two groups received inhaled METH self-administration for two weeks (up to 10 mg/kg). The elevated plus maze (EPM) test and open field test (OFT) were carried out one day after the last berberine treatment and relapse was assessed by conditional place preference (CPP) test. TUNEL assay and immunofluorescence staining for NF-κB, TLR4, Sirt1, and α-actin expression in the hippocampus were tested.
Results: After 3 weeks withdrawal, berberine hydrochloride decreased locomotor activity and reduced anxiety-related behaviors in comparison with the METH-withdrawal group (<0.001). The obtained results from CPP showed that berberine significantly reduced relapse (<0.01). Significantly decrease in activation of TLR4, Sirt1, andα-actin in METH-withdrawal group was found and the percentage of TLR4, Sirt1, and α-actin improved in berberine-treated group (<0.001). A significant activity rise of NF-κB of cells in the METH-withdrawal group was detected compared to berberine-treated and control groups (<0.001).
Conclusion: Treatment with berberine hydrochloride via modulating neuroinflammation may be considered as a potential new medication for the treatment of METH addiction and relapse. The histological assays supported the neuroprotective effects of berberine in the hippocampus.


greenmedinfo--2020-11-27--Protective effects of flavonoids in acute models of light-induced retinal degeneration.

Degeneration of photoreceptors caused by excessive illumination , inherited mutations or aging are the principal pathology of blinding diseases .
Pharmacological compounds that stabilize the visual receptor , rhodopsin , and modulate the cellular pathways triggering death of photoreceptors could avert this pathology .
Interestingly , flavonoids can modulate the cellular processes such as oxidative stress , inflammatory responses , and apoptosis that are activated during retinal degeneration .
As we found previously , flavonoids also bind directly to unliganded rod opsin , enhancing its folding , stability , and regeneration .
In addition , flavonoids stimulate rhodopsin gene expression @ @ @ @ @ @ @ of two main dietary flavonoids , quercetin and myricetin inand WT BALB/c mice susceptible to light-induced photoreceptors ' degeneration .
Usingimaging such as optical coherence tomography , scanning laser ophthalmoscopy and histological assessment of retinal morphology , we found that treatment with these flavonoids prior to light insult remarkably protected retina from deterioration and preserved its function .
Using HPLC-MS analysis , we detected these flavonoids in the eye upon their intraperitoneal administration .
The molecular events associated with the protective effect of quercetin and myricetin were related to the elevated expression of @ @ @ @ @ @ @ , decreased expression of the specific inflammatory markers , and the shift of the equilibrium between BAX/BCL-2 towards an anti-apoptotic profile .
These results were confirmed in photoreceptor-derived 661W cells treated with either HOor all -- retinal stressors implicated in the mechanism of retinal degeneration .
Altogether , flavonoids could have significant prophylactic value for retinal degenerative diseases.Flavonoids commonly present in food exhibit advantageous effects in blinding diseases .
They bind to , and stabilize unliganded rod opsin , which in excess accelerate degenerative processes in the retina .
Additionally , flavonoids enhance @ @ @ @ @ @ @ rod and cone opsins , inhibit the inflammatory reactions and induce the expression of anti-apoptotic markers in the retina , preventing the degenerationThus , flavonoids could have a prophylactic value for retinal degenerative diseases .

Degeneration of photoreceptors caused by excessive illumination, inherited mutations or aging are the principal pathology of blinding diseases. Pharmacological compounds that stabilize the visual receptor, rhodopsin, and modulate the cellular pathways triggering death of photoreceptors could avert this pathology. Interestingly, flavonoids can modulate the cellular processes such as oxidative stress, inflammatory responses, and apoptosis that are activated during retinal degeneration. As we found previously, flavonoids also bind directly to unliganded rod opsin, enhancing its folding, stability, and regeneration. In addition, flavonoids stimulate rhodopsin gene expression. Thus, we evaluated the effect of two main dietary flavonoids, quercetin and myricetin inand WT BALB/c mice susceptible to light-induced photoreceptors' degeneration. Usingimaging such as optical coherence tomography, scanning laser ophthalmoscopy and histological assessment of retinal morphology, we found that treatment with these flavonoids prior to light insult remarkably protected retina from deterioration and preserved its function. Using HPLC-MS analysis, we detected these flavonoids in the eye upon their intraperitoneal administration. The molecular events associated with the protective effect of quercetin and myricetin were related to the elevated expression of photoreceptor-specific proteins, rhodopsin and cone opsins, decreased expression of the specific inflammatory markers, and the shift of the equilibrium between BAX/BCL-2 towards an anti-apoptotic profile. These results were confirmed in photoreceptor-derived 661W cells treated with either HOor all--retinal stressors implicated in the mechanism of retinal degeneration. Altogether, flavonoids could have significant prophylactic value for retinal degenerative diseases.Flavonoids commonly present in food exhibit advantageous effects in blinding diseases. They bind to, and stabilize unliganded rod opsin, which in excess accelerate degenerative processes in the retina. Additionally, flavonoids enhance the expression of the visual receptors, rod and cone opsins, inhibit the inflammatory reactions and induce the expression of anti-apoptotic markers in the retina, preventing the degenerationThus, flavonoids could have a prophylactic value for retinal degenerative diseases.


greenmedinfo--2020-11-27--Molecular level insight into the benefit of myricetin and dihydromyricetin uptake in patients with A

Molecular level insight into the benefit of myricetin and dihydromyricetin uptake in patients with Alzheimer's diseases.

Alzheimer 's disease ( AD ) is a neurodegenerative disease with a high incidence rate and complicated pathogenesis .
Currently @ @ @ @ @ the symptoms of the disease , and with currently no cure for AD .
Flavonoid @ @ @ @ @ ( MYR ) and Dihydromyricetin ( DMY ) , are abundant in fruits and vegetables @ @ @ @ @ as food supplements in some countries .
Interestingly , MYR and DMY have been reported @ @ @ @ @ However , the underlying anti-AD mechanism of action of MYR and DMY is complex with @ @ @ @ @ In this review , we explore the benefit of MYR and DMY in AD patients @ @ @ @ @ Their mechanism of action are discussed from various aspects including amyloidβ-protein ( Aβ ) imbalance @ @ @ @ @ metal ions , autophagy disorder , and oxidative stress .

Alzheimer's disease (AD) is a neurodegenerative disease with a high incidence rate and complicated pathogenesis. Currently, all anti-AD drugs treat the symptoms of the disease, and with currently no cure for AD. Flavonoid containing natural products, Myricetin (MYR) and Dihydromyricetin (DMY), are abundant in fruits and vegetables, and have been approved as food supplements in some countries. Interestingly, MYR and DMY have been reported to have anti-AD effects. However, the underlying anti-AD mechanism of action of MYR and DMY is complex with many facets being identified. In this review, we explore the benefit of MYR and DMY in AD patients from a molecular level. Their mechanism of action are discussed from various aspects including amyloidβ-protein (Aβ) imbalance, neuroinflammation, dyshomeostasis of metal ions, autophagy disorder, and oxidative stress.


greenmedinfo--2020-11-27--Natural products: A rich source of antiviral drug lead candidates for the management of COVID-19.

Today , the world is suffering from the pandemic of a novel coronavirus disease ( COVID-19 ) , a respiratory illness caused by severe acute respiratory syndrome coronavirus 2 ( SARS-CoV-2 ) .
This pandemic is the third fatal coronavirus outbreak that has already occurred in the 21st century .
Even six months after its emergence , hundreds of thousands of people are still being infected with SARS-CoV-2 , and thousands of lives are lost every day across the world .
No effective therapy has been approved to date for the prevention or treatment of this disease , suggesting the @ @ @ @ @ @ @ search for effective treatments .
Throughout history , folk medicine has been successfully used to treat various ailments in humans and Traditional Chinese Medicine has been instrumental in the containment of a number of viral diseases .
Owing to their high chemical diversity and safety profiles , natural products offer great promises as potentially effective antiviral drugs .
In recent years , a large number of anti-coronaviral phytochemicals with different mechanisms of action have been identified .
Among them , tetra-O-galloyl-β-D-glucose , caffeic acid , and saikosaponin B2 block viral entry .
A @ @ @ @ @ @ @ Silvestrol inhibits protein synthesis .
Myricetin and scutellarein inhibit viral replication .
Emodin , luteolin , and quercetin demonstrate anti-coronaviral activity by inhibiting multipleprocesses in the virus life cycle .
In this review , we critically evaluate the findings of the natural product-based anti-coronaviral research that has been published during last two decades , and attempt to provide a comprehensive description about their utility as potential broad-spectrum anti-coronaviral drugs , examining leads that may guide/facilitate anti-SARS-CoV-2 drug development studies .

Today, the world is suffering from the pandemic of a novel coronavirus disease (COVID-19), a respiratory illness caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). This pandemic is the third fatal coronavirus outbreak that has already occurred in the 21st century. Even six months after its emergence, hundreds of thousands of people are still being infected with SARS-CoV-2, and thousands of lives are lost every day across the world. No effective therapy has been approved to date for the prevention or treatment of this disease, suggesting the need to broaden the scope in the search for effective treatments. Throughout history, folk medicine has been successfully used to treat various ailments in humans and Traditional Chinese Medicine has been instrumental in the containment of a number of viral diseases. Owing to their high chemical diversity and safety profiles, natural products offer great promises as potentially effective antiviral drugs. In recent years, a large number of anti-coronaviral phytochemicals with different mechanisms of action have been identified. Among them, tetra-O-galloyl-β-D-glucose, caffeic acid, and saikosaponin B2 block viral entry. A number of flavonoids inhibit viral proteases. Silvestrol inhibits protein synthesis. Myricetin and scutellarein inhibit viral replication. Emodin, luteolin, and quercetin demonstrate anti-coronaviral activity by inhibiting multipleprocesses in the virus life cycle. In this review, we critically evaluate the findings of the natural product-based anti-coronaviral research that has been published during last two decades, and attempt to provide a comprehensive description about their utility as potential broad-spectrum anti-coronaviral drugs, examining leads that may guide/facilitate anti-SARS-CoV-2 drug development studies.


greenmedinfo--2020-11-27--Emodin prevented the hydrogen peroxide-induced mitochondrial dysfunction and pro-inflammatory state

Emodin prevented the hydrogen peroxide-induced mitochondrial dysfunction and pro-inflammatory state in the SH-SY5Y cells.

Emodin ( EM ; 1,3,8-trihydroxy-6-methylanthracene-9,10-dione ; CHO ) is an anthraquinone and exerts cytoprotective effects , as observed in both in vitro and in vivo experimental models .
Mitochondrial dysfunction induced by reactive species plays a central role in the onset and progression of different human diseases .
Thus , we have tested here whether a pretreatment ( for 4 h ) with EM ( at 40 µM ) would be able to promote mitochondrial protection in the human neuroblastoma SH-SY5Y cells exposed to the pro-oxidant agent hydrogen peroxide ( HO ) .
We found that the pretreatment with EM @ @ @ @ @ @ @ of the mitochondrial complexes I and V , as well as on the production of adenosine triphosphate ( ATP ) and on the mitochondrial membrane potential ( MMP ) .
EM also prevented the HO-induced collapse in the tricarboxylic acid cycle ( TCA ) function .
An anti-inflammatory role for EM was also observed in this experimental model , since this anthraquinone decreased the secretion of interleukin-1β ( IL-1β ) and tumor necrosis factor-α ( TNF-α ) by the HO-challenged cells .
Inhibition of the adenosine monophosphate-activated protein kinase ( AMPK ) or @ @ @ @ @ @ @ erythroid 2-related factor 2 ( Nrf2 ) abolished the protection induced by EM in the HO-treated cells .
Therefore , EM prevented the HO-induced mitochondrial dysfunction and pro-inflammatory state in the SH-SY5Y cells by an AMPK/Nrf2-dependent manner .

Emodin (EM; 1,3,8-trihydroxy-6-methylanthracene-9,10-dione; CHO) is an anthraquinone and exerts cytoprotective effects, as observed in both in vitro and in vivo experimental models. Mitochondrial dysfunction induced by reactive species plays a central role in the onset and progression of different human diseases. Thus, we have tested here whether a pretreatment (for 4 h) with EM (at 40 µM) would be able to promote mitochondrial protection in the human neuroblastoma SH-SY5Y cells exposed to the pro-oxidant agent hydrogen peroxide (HO). We found that the pretreatment with EM suppressed the effects of HOon the activity of the mitochondrial complexes I and V, as well as on the production of adenosine triphosphate (ATP) and on the mitochondrial membrane potential (MMP). EM also prevented the HO-induced collapse in the tricarboxylic acid cycle (TCA) function. An anti-inflammatory role for EM was also observed in this experimental model, since this anthraquinone decreased the secretion of interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) by the HO-challenged cells. Inhibition of the adenosine monophosphate-activated protein kinase (AMPK) or silencing of the transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) abolished the protection induced by EM in the HO-treated cells. Therefore, EM prevented the HO-induced mitochondrial dysfunction and pro-inflammatory state in the SH-SY5Y cells by an AMPK/Nrf2-dependent manner.


greenmedinfo--2020-11-27--Synergistic antibacterial activity of berberine in combination with amylmetacresol against Enterococ

Synergistic antibacterial activity of berberine in combination with amylmetacresol against Enterococcus faecalis.

Objective : To study the antibacterial effect of berberine combined with amylmetacresol on .
Methods : Both dilution method and live bacteria CFU were used to determine the minimum inhibitory concentration ( MIC ) of berberine and amylmetacresol on .
The killing effect of berberine and amylmetacresol on planktonicwas detected by suspension quantitative germicidal test and live/dead bacteria staining .
The effects of berberine and amylmetacresol on the structure of mature biofilm ofwas observed by scanning electron microscopy ( SEM ) .
The toxicity of berberine and amylmetacresol on human oral keratinocytes ( HOK ) was determined by CCK-8 cell @ @ @ @ @ @ @ assay .
Results : The MIC of berberine was 512μg/mL , and the MIC of amylmetacresol was 0.023 3 % .
512 μg/mL berberine and 0.002 33 % amylmetacresol had a weak killing effect on planktonicalone , while they showed a synergistic antibacterial effect in combination .
Cell survival in the biofilm was only slightly changed by berberine and amylmetacresol .
The structure of biofilm was obviously changed by berberine and amylmetacresol .
512μg/mL berberine and 0.002 33 % amylmetacresol alone or in combination showed the survival rate was much higher than the @ @ @ @ @ @ @ had a low cytotoxicity .
Conclusion : Berberine and amylmetacresol had synergism against , and the biological safety of the combination use was better .

Objective: To study the antibacterial effect of berberine combined with amylmetacresol on.
Methods: Both dilution method and live bacteria CFU were used to determine the minimum inhibitory concentration (MIC) of berberine and amylmetacresol on. The killing effect of berberine and amylmetacresol on planktonicwas detected by suspension quantitative germicidal test and live/dead bacteria staining. The effects of berberine and amylmetacresol on the structure of mature biofilm ofwas observed by scanning electron microscopy (SEM). The toxicity of berberine and amylmetacresol on human oral keratinocytes (HOK) was determined by CCK-8 cell proliferation and cytotoxicity assay and cytotoxicity LDH assay.
Results: The MIC of berberine was 512μg/mL, and the MIC of amylmetacresol was 0.023 3%. 512 μg/mL berberine and 0.002 33% amylmetacresol had a weak killing effect on planktonicalone, while they showed a synergistic antibacterial effect in combination. Cell survival in the biofilm was only slightly changed by berberine and amylmetacresol. The structure of biofilm was obviously changed by berberine and amylmetacresol. 512μg/mL berberine and 0.002 33% amylmetacresol alone or in combination showed the survival rate was much higher than the injury rate, suggesting berberine and amylmetacresol had a low cytotoxicity.
Conclusion: Berberine and amylmetacresol had synergism against, and the biological safety of the combination use was better.


greenmedinfo--2020-11-27--Effect of dietary inclusion of pumpkin seed on nephrotoxicity occasioned by cisplatin in experimenta

Effect of dietary inclusion of pumpkin seed on nephrotoxicity occasioned by cisplatin in experimental rats.

The study evaluated the effect of dietary inclusion of pumpkin ( Cucurbita pepo L ) seed ( raw and roasted ) on nephrotoxicity caused by cisplatin in rats .
Rats were divided into control group , cisplatin-induced nephrotoxic untreated group , nephrotoxic-treated groups with Methimazole , dietary regimen containing raw pumpkin seed ( 5 % and 10 % ) and roasted pumpkin seed ( 5 % and 10 % ) for 14 days .
Results acquired uncovered that cisplatin intoxication significantly increased ( p ≤ .05 ) the levels of renal biomarkers , arginase activity , 8-hydroxy-2-deoxy guanosine ( 8-OHdG @ @ @ @ @ @ @ and reactive oxygen species ( ROS ) levels as well as significant decrease in functional sulfhydryl groups , nitric oxide levels , and antioxidant enzyme activities in rats ' kidney when compared to the control group .
These adverse changes , due to cisplatin inebriation in rodents , were in any case , forestalled by pre-treatment with pumpkin seed inclusive diet .
This holds promise for the use of pumpkin seed as a food supplement in the management of nephrotoxic-related disorders .
PRACTICAL APPLICATIONS : These results suggest that roasted pumpkin seed appears @ @ @ @ @ @ @ pumpkin seed through regulations of arginase activity , enhancement in the antioxidant system , suppression of renal markers and lipid peroxidation .
This holds p-omise for the use of roasted pumpkin seed as a food supplement in the management nephrotoxic-related disorders .

The study evaluated the effect of dietary inclusion of pumpkin (Cucurbita pepo L) seed (raw and roasted) on nephrotoxicity caused by cisplatin in rats. Rats were divided into control group, cisplatin-induced nephrotoxic untreated group, nephrotoxic-treated groups with Methimazole, dietary regimen containing raw pumpkin seed (5% and 10%) and roasted pumpkin seed (5% and 10%) for 14 days. Results acquired uncovered that cisplatin intoxication significantly increased (p ≤ .05) the levels of renal biomarkers, arginase activity, 8-hydroxy-2-deoxy guanosine (8-OHdG), malondialdehyde (MDA), and reactive oxygen species (ROS) levels as well as significant decrease in functional sulfhydryl groups, nitric oxide levels, and antioxidant enzyme activities in rats' kidney when compared to the control group. These adverse changes, due to cisplatin inebriation in rodents, were in any case, forestalled by pre-treatment with pumpkin seed inclusive diet. This holds promise for the use of pumpkin seed as a food supplement in the management of nephrotoxic-related disorders. PRACTICAL APPLICATIONS: These results suggest that roasted pumpkin seed appears to be more nephroprotective than the raw pumpkin seed through regulations of arginase activity, enhancement in the antioxidant system, suppression of renal markers and lipid peroxidation. This holds p-omise for the use of roasted pumpkin seed as a food supplement in the management nephrotoxic-related disorders.


greenmedinfo--2020-11-27--Monoterpenes from the leaves of Hydrangea paniculata and their hepatoprotective activities.

Three new monoterpenes , hydrangines A-C ( 1-3 ) , together with four known compounds , were isolated from the @ @ @ @ @ of Hydrangea paniculata .
The structures of new isolates were elucidated on the basis of @ @ @ @ @ analyses , and their absolute configurations were determined by comparison of experimental and calculated electronic @ @ @ @ @ in vitro bioassays at 10 μM , compounds 1-6 showed hepatoprotective activities against dl-galactosamine-induced toxicity @ @ @ @

Three new monoterpenes, hydrangines A-C (1-3), together with four known compounds, were isolated from the ethanol extract of the leaves of Hydrangea paniculata. The structures of new isolates were elucidated on the basis of extensive 1D and 2D NMR analyses, and their absolute configurations were determined by comparison of experimental and calculated electronic circular dichroism spectra. In in vitro bioassays at 10 μM, compounds 1-6 showed hepatoprotective activities against dl-galactosamine-induced toxicity in HL-7702 cells.


greenmedinfo--2020-11-27--Total coumarins from Hydrangea paniculata protect against cisplatin-induced acute kidney damage.

Hydrangea paniculata ( HP ) Sieb .
is a medical herb which is widely distributed in southern China , and current study is to evaluate renal protective effect of aqueous extract of HP by cisplatin-induced acute kidney injury ( AKI ) in animal model and its underlying mechanisms.HP extract was prepared and the major ingredients were coumarin glycosides .
AKI mouse models were established by single i.p .
injection of 20 mg/kg cisplatin , and HP was orally administrated for total five times .
The renal biochemical functions , pathological staining , kidney oxidative stress , and inflammatory status were @ @ @ @ @ @ @ infiltration of macrophages and neutrophils were also tested.HP administration could improve the renal function by decreasing concentration of blood urea nitrogen ( BUN ) and creatinine and attenuates renal oxidative stress and tubular pathological injury and apoptosis ; further research demonstrated that HP could inhibit the overproduction of proinflammatory cytokines and regulate caspase and BCL-2 family proteins .
HP also reduced renal infiltration of macrophages and neutrophils , and its effect might be by downregulating phosphorylation of ERK1/2 and stat3 signaling pathway.This present study suggests that HP could ameliorate cisplatin induced kidney damage @ @ @ @ @ @ @ tubular cell apoptosis .

Hydrangea paniculata (HP) Sieb. is a medical herb which is widely distributed in southern China, and current study is to evaluate renal protective effect of aqueous extract of HP by cisplatin-induced acute kidney injury (AKI) in animal model and its underlying mechanisms.HP extract was prepared and the major ingredients were coumarin glycosides. AKI mouse models were established by single i.p. injection of 20 mg/kg cisplatin, and HP was orally administrated for total five times. The renal biochemical functions, pathological staining, kidney oxidative stress, and inflammatory status were measured. Apoptosis of tubular cells and infiltration of macrophages and neutrophils were also tested.HP administration could improve the renal function by decreasing concentration of blood urea nitrogen (BUN) and creatinine and attenuates renal oxidative stress and tubular pathological injury and apoptosis; further research demonstrated that HP could inhibit the overproduction of proinflammatory cytokines and regulate caspase and BCL-2 family proteins. HP also reduced renal infiltration of macrophages and neutrophils, and its effect might be by downregulating phosphorylation of ERK1/2 and stat3 signaling pathway.This present study suggests that HP could ameliorate cisplatin induced kidney damage by antioxidation and suppressing renal inflammation and tubular cell apoptosis.


greenmedinfo--2020-11-28--Protective effects of Astragalin on spermatogenesis in streptozotocin-induced diabetes in male mice.

Spermatogenic dysfunction is a common complication in men with diabetes and is the most important manifestation of diabetes-related male reproduction damage .
Astragalin ( AG ) is one of the main flavonoids from Cuscuta chinensis , which has rich pharmacological activities .
This study aimed to establish whether AG may contribute to the recovery from spermatogenic dysfunction .
AG ( 3.3 , 10 and 30 mg/kg ) and Clomiphene ( 5 mg/kg ) were orally administered to streptozotocin-induced diabetic male mice for 8 weeks .
After the experiments performed , reproductive organs , sperm parameters and histomorphological changes were analysed @ @ @ @ @ @ @ in testicular tissues .
The results revealed that AG significantly improved the reproductive organs , sperm parameters and testicular morphology to different degrees in diabetic mice .
Nitric oxide ( NO ) and malondialdehyde ( MDA ) levels were significantly reduced , and the activities of superoxide dismutase ( SOD ) , glutathione peroxidase ( GSH-Px ) and catalase ( CAT ) , markedly increased in the testicular tissue after AG was administered .
Interestingly , AG also downregulated the protein expressions of tumour necrosis factor-α ( TNF-α ) and inducible nitric oxide @ @ @ @ @ @ @ In conclusion , AG is a potential beneficial agent to protect diabetic-induced spermatogenic dysfunction in male mice by increasing antioxidant enzymes activities and inhibiting inflammation .

Spermatogenic dysfunction is a common complication in men with diabetes and is the most important manifestation of diabetes-related male reproduction damage. Astragalin (AG) is one of the main flavonoids from Cuscuta chinensis, which has rich pharmacological activities. This study aimed to establish whether AG may contribute to the recovery from spermatogenic dysfunction. AG (3.3, 10 and 30 mg/kg) and Clomiphene (5 mg/kg) were orally administered to streptozotocin-induced diabetic male mice for 8 weeks. After the experiments performed, reproductive organs, sperm parameters and histomorphological changes were analysed. Antioxidant and anti-inflammatory capacity were estimated in testicular tissues. The results revealed that AG significantly improved the reproductive organs, sperm parameters and testicular morphology to different degrees in diabetic mice. Nitric oxide (NO) and malondialdehyde (MDA) levels were significantly reduced, and the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT), markedly increased in the testicular tissue after AG was administered. Interestingly, AG also downregulated the protein expressions of tumour necrosis factor-α (TNF-α) and inducible nitric oxide synthase (iNOS) in testes. In conclusion, AG is a potential beneficial agent to protect diabetic-induced spermatogenic dysfunction in male mice by increasing antioxidant enzymes activities and inhibiting inflammation.


greenmedinfo--2020-11-27--Astragalin suppresses inflammatory responses and bone destruction in mice with collagen-induced arth

Astragalin suppresses inflammatory responses and bone destruction in mice with collagen-induced arthritis.

Astragalin , as a bioactive flavonoid with anti-inflammatory , antioxidant , and protective properties , provides a potential agent for rheumatoid arthritis ( RA ) .
In this study , its therapeutic efficacy and the underlying mechanisms were explored using DBA/1J mice with collagen-induced arthritis ( CIA ) .
It was demonstrated that astragalin could significantly attenuate inflammation of CIA mice .
The effects were associated with decreased severity of arthritis ( based on the arthritis index ) , joint swelling and reduced bone erosion and destruction .
Furthermore , astragalin treatment suppressed the production of pro-inflammatory cytokines ( TNF-α @ @ @ @ @ @ @ ) , and inhibited the expression of matrix metalloproteinases ( MMP-1 , MMP-3 , and MMP-13 ) in chondrocytes and synovial cells of CIA mice .
Fibroblast-like synoviocytes derived from RA patients ( MH7A cells ) were applied to verify these effects.
, astragalin inhibited the expression of matrix metalloproteinases ( MMP-1 , MMP-3 , and MMP-13 ) dose-dependently in TNF-α-induced MH7A cells , with no apparent cytotoxicity .
Furthermore , astragalin suppressed the phosphorylation of p38 , JNK , and the activation of c-Jun/AP-1 in TNF-α-induced MH7A cells .
In conclusion , @ @ @ @ @ @ @ synovial inflammation and joint destruction in RA at least partially by restraining the phosphorylation of MAPKs and the activating of c-Jun/AP-1 .
Therefore , astragalin can be a potential therapeutic agent for RA .

Astragalin, as a bioactive flavonoid with anti-inflammatory, antioxidant, and protective properties, provides a potential agent for rheumatoid arthritis (RA). In this study, its therapeutic efficacy and the underlying mechanisms were explored using DBA/1J mice with collagen-induced arthritis (CIA). It was demonstrated that astragalin could significantly attenuate inflammation of CIA mice. The effects were associated with decreased severity of arthritis (based on the arthritis index), joint swelling and reduced bone erosion and destruction. Furthermore, astragalin treatment suppressed the production of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6, and IL-8), and inhibited the expression of matrix metalloproteinases (MMP-1, MMP-3, and MMP-13) in chondrocytes and synovial cells of CIA mice. Fibroblast-like synoviocytes derived from RA patients (MH7A cells) were applied to verify these effects., astragalin inhibited the expression of matrix metalloproteinases (MMP-1, MMP-3, and MMP-13) dose-dependently in TNF-α-induced MH7A cells, with no apparent cytotoxicity. Furthermore, astragalin suppressed the phosphorylation of p38, JNK, and the activation of c-Jun/AP-1 in TNF-α-induced MH7A cells. In conclusion, it has proven that astragalin could attenuate synovial inflammation and joint destruction in RA at least partially by restraining the phosphorylation of MAPKs and the activating of c-Jun/AP-1. Therefore, astragalin can be a potential therapeutic agent for RA.


greenmedinfo--2020-11-27--Astragalin promotes osteoblastic differentiation in MC3T3-E1 cells and bone formation in vivo.

Astragalin ( AG ) is a biologically active flavonoid compound that can be extracted from a number of medicinal plants .
However , the effects of AG on osteoblastic differentiation in mouse MC3T3-E1 cells and on bone formationhave not been studied fully .
In this study , we found that the activities of alkaline phosphatase ( ALP ) and mineralized nodules in MC3T3-E1 cells were both significantly increased after treatment with AG ( 5 , 10 , and 20μM ) .
Meanwhile , the mRNA and protein levels of osteoblastic marker genes in MC3T3-E1 cells after AG treatment were markedly @ @ @ @ @ @ @ In addition , the levels of BMP-2 , p-Smad1/5/9 , and Runx2 were significantly elevated in AG-treated MC3T3-E1 cells .
Moreover , we foundthat the protein levels of Erk1/2 , p-Erk1/2 , p38 , p-p38 , and p-JNK were also significantly increased in AG-treated MC3T3-E1 cells compared to those in the control group .
Finally , experiments demonstrated that AG significantly promoted bone formation in an ovariectomized ( OVX ) -induced osteoporotic mouse model .
This was evidenced by significant increases in the values of osteoblast-related parameters ( BFR/BS , MAR , Ob.S/BS @ @ @ @ @ @ @ parameters ( BMD , BV/TV , Tb.Th , and Tb.N . )
in OVX mice after AG treatment ( 5 , 10 , and 20 mg/kg ) .
Collectively , these results demonstrated that AG may promote osteoblastic differentiation in MC3T3-E1 cells via the activation of the BMP and MAPK pathways and promote bone formation .
These novel findings indicated that AG may be a useful bone anabolic agent for the prevention and treatment of osteoporosis .

Astragalin (AG) is a biologically active flavonoid compound that can be extracted from a number of medicinal plants. However, the effects of AG on osteoblastic differentiation in mouse MC3T3-E1 cells and on bone formationhave not been studied fully. In this study, we found that the activities of alkaline phosphatase (ALP) and mineralized nodules in MC3T3-E1 cells were both significantly increased after treatment with AG (5, 10, and 20μM). Meanwhile, the mRNA and protein levels of osteoblastic marker genes in MC3T3-E1 cells after AG treatment were markedly increased compared with a control group. In addition, the levels of BMP-2, p-Smad1/5/9, and Runx2 were significantly elevated in AG-treated MC3T3-E1 cells. Moreover, we foundthat the protein levels of Erk1/2, p-Erk1/2, p38, p-p38, and p-JNK were also significantly increased in AG-treated MC3T3-E1 cells compared to those in the control group. Finally,experiments demonstrated that AG significantly promoted bone formation in an ovariectomized (OVX)-induced osteoporotic mouse model. This was evidenced by significant increases in the values of osteoblast-related parameters (BFR/BS, MAR, Ob.S/BS, and Ob.N/B.Pm) and bone histomorphometric parameters (BMD, BV/TV, Tb.Th, and Tb.N.) in OVX mice after AG treatment (5, 10, and 20 mg/kg). Collectively, these results demonstrated that AG may promote osteoblastic differentiation in MC3T3-E1 cells via the activation of the BMP and MAPK pathways and promote bone formation. These novel findings indicated that AG may be a useful bone anabolic agent for the prevention and treatment of osteoporosis.


greenmedinfo--2020-11-27--Astragalin reduces lipopolysaccharide-induced acute lung injury in rats via induction of heme oxygen

Astragalin reduces lipopolysaccharide-induced acute lung injury in rats via induction of heme oxygenase-1.

Astragalin , a bioactive component of medicinal plants such as Rosa agrestis , has anti-inflammatory and antioxidant features .
Induction of heme oxygenase ( HO ) -1 is an effective strategy to reduce excessive generated oxidants during the pathogenesis of acute lung injury ( ALI ) .
The aim of the present study is to investigate that whether the anti-inflammatory and antioxidant features of astragalin is HO-1 dependent in lipopolysaccharide ( LPS ) -induced ALI .
Sprague-Dawley rats were used in animal study .
Intratracheal LPS was performed to induce experimental ALI model .
Astragalin was administrated 1 h after @ @ @ @ @ @ @ were used in cell study .
Samples from rats were harvested at 24 h post LPS challenge .
Astragalin treatment inhibited LPS-induced inflammatory cells infiltration in the lung and pulmonary edema .
Astragalin treatment markedly enhanced the activityof HO-1 compared with vehicle-treated group at 24 h post LPS challenge .
Levels of lipid hydroperoxide , a marker for oxidative stress , were decreased in astragalin-treated animals compared with vehicle-treated group .
However , the protective effect of astragalin on LPS-induced ALI was abolished in aninhibitor of HO-1-treated animals .
Moreover , the astragalin-induced @ @ @ @ @ @ @ epithelial cells was inhibited when nuclear factor erythroid-2-related factor 2 ( Nrf2 ) was silenced by small interfering RNA .
Astragalin reduces LPS-induced ALI via activation of Nrf2/HO-1 pathway .

Astragalin, a bioactive component of medicinal plants such as Rosa agrestis, has anti-inflammatory and antioxidant features. Induction of heme oxygenase (HO)-1 is an effective strategy to reduce excessive generated oxidants during the pathogenesis of acute lung injury (ALI). The aim of the present study is to investigate that whether the anti-inflammatory and antioxidant features of astragalin is HO-1 dependent in lipopolysaccharide (LPS)-induced ALI. Sprague-Dawley rats were used in animal study. Intratracheal LPS was performed to induce experimental ALI model. Astragalin was administrated 1 h after LPS challenge. Human lung epithelial cells were used in cell study. Samples from rats were harvested at 24 h post LPS challenge. Astragalin treatment inhibited LPS-induced inflammatory cells infiltration in the lung and pulmonary edema. Astragalin treatment markedly enhanced the activityof HO-1 compared with vehicle-treated group at 24 h post LPS challenge. Levels of lipid hydroperoxide, a marker for oxidative stress, were decreased in astragalin-treated animals compared with vehicle-treated group. However, the protective effect of astragalin on LPS-induced ALI was abolished in aninhibitor of HO-1-treated animals. Moreover, the astragalin-induced the upregulation of HO-1 in human lung epithelial cells was inhibited when nuclear factor erythroid-2-related factor 2 (Nrf2) was silenced by small interfering RNA. Astragalin reduces LPS-induced ALI via activation of Nrf2/HO-1 pathway.


greenmedinfo--2020-11-27--Astragalin induced selective kidney cancer cell death.

PURPOSE : Kidney cancer is responsible for a significant number of deaths worldwide .
This cancer is often diagnosed at advanced stages and there are frequent relapses following chemotherapy .
Target therapies are used now for kidney cancer , while the use of chemotherapy declines .
The currently used chemotherapeutic drugs have a number of adverse effects .
Herein , we examined the anticancer effects of Astragalin against a panel of kidney cancer cells .
METHODS : CellTiter-Glo Luminescent Cell Viability Assay Kit was used to examine the anti-proliferative effects of Astragalin .
Acridine orange ( AO ) /ethidium bromide @ @ @ @ @ @ @ V/promidium iodide ( PI ) staining assays were used to examine the apoptotic cell death .
Cell cycle analysis was performed by flow cytometry .
The mRNA expression was checked by qRT-PCR and protein expression was examined by western blotting .
RESULTS : Astragalin inhibited the growth of the all kidney cancer cell lines with IC50 ranging between 20 to 50µM .
Of note , Astragalin had low cytotoxic effects on the normal kidney cells with an IC50 of 110 µM .
The experiments have shown that Astragalin exerts antiproliferative effects on the @ @ @ @ @ @ @ death .
This effect was concomitant with upregulation of apoptotic proteins such as caspase 3 and 9 and Bax .
Astragalin also induced arrest of the A498 cells at the G2/M checkpoint of the cell cycle .
Also , Astragalin could upregulate the expression of tumor-suppressive microRNAs .
CONCLUSIONS : These results suggest that Astragalin exerts potent anticancer effects on kidney cancer cells and could pave the way in the management of kidney cancer provided clinical studies are carried out .

PURPOSE: Kidney cancer is responsible for a significant number of deaths worldwide. This cancer is often diagnosed at advanced stages and there are frequent relapses following chemotherapy. Target therapies are used now for kidney cancer, while the use of chemotherapy declines. The currently used chemotherapeutic drugs have a number of adverse effects. Herein, we examined the anticancer effects of Astragalin against a panel of kidney cancer cells.
METHODS: CellTiter-Glo Luminescent Cell Viability Assay Kit was used to examine the anti-proliferative effects of Astragalin. Acridine orange (AO)/ethidium bromide (EB), DAPI and annexin V/promidium iodide (PI) staining assays were used to examine the apoptotic cell death. Cell cycle analysis was performed by flow cytometry. The mRNA expression was checked by qRT-PCR and protein expression was examined by western blotting.
RESULTS: Astragalin inhibited the growth of the all kidney cancer cell lines with IC50 ranging between 20 to 50µM. Of note, Astragalin had low cytotoxic effects on the normal kidney cells with an IC50 of 110 µM. The experiments have shown that Astragalin exerts antiproliferative effects on the A498 kidney cancer cells by apoptotic cell death. This effect was concomitant with upregulation of apoptotic proteins such as caspase 3 and 9 and Bax. Astragalin also induced arrest of the A498 cells at the G2/M checkpoint of the cell cycle. Also, Astragalin could upregulate the expression of tumor-suppressive microRNAs.
CONCLUSIONS: These results suggest that Astragalin exerts potent anticancer effects on kidney cancer cells and could pave the way in the management of kidney cancer provided clinical studies are carried out.


greenmedinfo--2020-11-27--Chlorogenic acid inhibits forming of diabetes mellitus in rats induced by high-fat high-sucrose and

Chlorogenic acid inhibits forming of diabetes mellitus in rats induced by high-fat high-sucrose and streptozotocin.

To evaluate the inhibitory effect of chlorogenic acid on the forming of type 2 diabetes mellitus ( T2DM ) , @ @ @ @ @ ) rats , a recognized T2DM model induced by high-fat high-sucrose diet ( HFSD ) @ @ @ @ @ .
Thirty female SD rats were assigned equally to three groups randomly : normal control @ @ @ @ @ ) , chlorogenic acid treatment with HFSD and chlorogenic acid ( 90mg/kg , CA ) @ @ @ @ @ HFSD ( DM ) .
Upon treatment with chlorogenic acid , suppression of the onset @ @ @ @ @ glucose and insulin concentrations , improved glucose tolerance and increased body weight and visceral fat @ @ @ @ @ triglyceride , total cholesterol , low density lipoprotein levels , and kidney and pancreas morphology @ @ @ @ @ acid also inhibited the mRNA levels of hepatic G-6-Pase and up-regulated the mRNA levels of @ @ @ @ @ results indicated that before the onset of diabetes , chlorogenic acid had an inhibitory effect @ @ @ @ @ induced by HFSD and STZ through regulating the glucose and lipid metabolism .

To evaluate the inhibitory effect of chlorogenic acid on the forming of type 2 diabetes mellitus (T2DM), using Sprague Dawley (SD) rats, a recognized T2DM model induced by high-fat high-sucrose diet (HFSD) and streptozotocin (STZ). Thirty female SD rats were assigned equally to three groups randomly: normal control with standard commercial (NC), chlorogenic acid treatment with HFSD and chlorogenic acid (90mg/kg, CA), and diabetes model with HFSD (DM). Upon treatment with chlorogenic acid, suppression of the onset of diabetes, reduced serum glucose and insulin concentrations, improved glucose tolerance and increased body weight and visceral fat weight were observed. Serum triglyceride, total cholesterol, low density lipoprotein levels, and kidney and pancreas morphology were significantly ameliorated. Chlorogenic acid also inhibited the mRNA levels of hepatic G-6-Pase and up-regulated the mRNA levels of skeletal muscle GLUT4. Our results indicated that before the onset of diabetes, chlorogenic acid had an inhibitory effect against the forming of T2DM induced by HFSD and STZ through regulating the glucose and lipid metabolism.


greenmedinfo--2020-11-27--Chlorogenic acid alleviates hyperglycemia-induced cardiac fibrosis.

SCOPE : Hyperglycemia-induced cardiac fibrosis is one of the main causes of diabetic cardiomyopathy ( DM ) .
Chlorogenic acid ( CGA ) found in many foods has excellent hypoglycemic effectiveness , but it is not known whether CGA can improve DM by inhibiting cardiac fibrosis caused by hyperglycemia .
METHODS AND RESULTS : Type I diabetic mice were induced by streptozotocin , and after treatment with CGA for 12 weeks , cardiac functions and fibrosis were determined .
CGA significantly attenuated hyperglycemia-induced cardiac fibrosis and improved cardiac functions .
The mechanism of CGA on fibrotic inhibition was further studied @ @ @ @ @ @ @ interference technology in vivo and in vitro .
The results showed CGA exerted its anti-fibrotic effects through activating the cyclic GMP/protein kinase G pathway ( cGMP/PKG ) to block hyperglycemia-induced nuclear translocation of p-Smad2/3 , and then inhibiting pro-fibrotic gene expression in cardiac fibroblasts without depending on its hypoglycemic function .
Moreover , the data also revealed that CGA increased cGMP level and activated PKG in cardiac fibroblasts by enhancing endothelial nitric oxide synthase activity and NO production .
CONCLUSION : Besides lowering blood glucose , CGA also has an independent ability to @ @ @ @ @ @ @ consumption of foods rich in CGA for diabetic patients will have great benefits to improve diabetic cardiomyopathy .
This article is protected by copyright .
All rights reserved .

SCOPE: Hyperglycemia-induced cardiac fibrosis is one of the main causes of diabetic cardiomyopathy (DM). Chlorogenic acid (CGA) found in many foods has excellent hypoglycemic effectiveness, but it is not known whether CGA can improve DM by inhibiting cardiac fibrosis caused by hyperglycemia.
METHODS AND RESULTS: Type I diabetic mice were induced by streptozotocin, and after treatment with CGA for 12 weeks, cardiac functions and fibrosis were determined. CGA significantly attenuated hyperglycemia-induced cardiac fibrosis and improved cardiac functions. The mechanism of CGA on fibrotic inhibition was further studied by immunofluorescence, western blot and RNA interference technology in vivo and in vitro. The results showed CGA exerted its anti-fibrotic effects through activating the cyclic GMP/protein kinase G pathway (cGMP/PKG) to block hyperglycemia-induced nuclear translocation of p-Smad2/3, and then inhibiting pro-fibrotic gene expression in cardiac fibroblasts without depending on its hypoglycemic function. Moreover, the data also revealed that CGA increased cGMP level and activated PKG in cardiac fibroblasts by enhancing endothelial nitric oxide synthase activity and NO production.
CONCLUSION: Besides lowering blood glucose, CGA also has an independent ability to inhibit cardiac fibrosis. Therefore, long-term consumption of foods rich in CGA for diabetic patients will have great benefits to improve diabetic cardiomyopathy. This article is protected by copyright. All rights reserved.


greenmedinfo--2020-11-27--Synergistic effect of chlorogenic acid and levofloxacin against Klebsiella pneumonia infection.

The study aimed to investigate the antibacterial effect and potential mechanisms of chlorogenic acid ( CA ) in Klebsiella pneumonia ( KPN ) induced infection in vitro and in vivo .
62 KPN strains were collected from the First People 's Hospital of Yunnan Province .
CA and CA combined Levofloxacin ( LFX ) were detected for KPN biofilm ( BF ) formation in vitro .
The lung infection mice model were established by KPN .
The effect of CA ( 500 mg/kg ) , LFX ( 50 mg/kg ) and CA combined LFX ( 250 mg/kg + 25 mg/kg @ @ @ @ @ @ @ mice , the changes of inflammation factors of tumor necrosis factor-alpha ( TNF-α ) , interleukin ( IL ) -1β and IL-6 in serum , the histopathological analysis of lung and the protein expression of NLRP3 signaling pathway in vivo .
A total of 62 KPNs were isolated and identified , of which 13 ( 21 % ) strains were BF positive .
8 ( 13 % ) strains were extended spectrum β-lactamase strains ( ESBLs ) , and 20 ( 32 % ) strains are ESBLs biofilm positive .
In vitro study @ @ @ @ @ @ @ effect on KPN biofilm formation .
In vivo mice experiment , CA , especially CA + LFX treated group significantly decreased the serum levels of TNF-α , IL-1β and IL-6 , improved the survival ratio and lung pathology changes , and also reduced the protein expression of ASC , caspase 1 p20 , IL-1β and phosphor NF-κB p65 .
CA could effectively alleviate lung infection of KPN infected mice , and the antibacterial effection is strengthened by combined with LFX .
The study provide a theroy basis for making rational and scientific antibacterial @ @ @ @ @

The study aimed to investigate the antibacterial effect and potential mechanisms of chlorogenic acid (CA) in Klebsiella pneumonia (KPN) induced infection in vitro and in vivo. 62 KPN strains were collected from the First People's Hospital of Yunnan Province. CA and CA combined Levofloxacin (LFX) were detected for KPN biofilm (BF) formation in vitro. The lung infection mice model were established by KPN. The effect of CA (500 mg/kg), LFX (50 mg/kg) and CA combined LFX (250 mg/kg + 25 mg/kg) were evaluated through the survival of mice, the changes of inflammation factors of tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1β and IL-6 in serum, the histopathological analysis of lung and the protein expression of NLRP3 signaling pathway in vivo. A total of 62 KPNs were isolated and identified, of which 13 (21%) strains were BF positive. 8 (13%) strains were extended spectrum β-lactamase strains (ESBLs), and 20 (32%) strains are ESBLs biofilm positive. In vitro study, CA and LFX showed a synergistic effect on KPN biofilm formation. In vivo mice experiment, CA, especially CA + LFX treated group significantly decreased the serum levels of TNF-α, IL-1β and IL-6, improved the survival ratio and lung pathology changes, and also reduced the protein expression of ASC, caspase 1 p20, IL-1β and phosphor NF-κB p65. CA could effectively alleviate lung infection of KPN infected mice, and the antibacterial effection is strengthened by combined with LFX. The study provide a theroy basis for making rational and scientific antibacterial therapy strategy in clinic.


greenmedinfo--2020-11-27--Chlorogenic acid promotes autophagy and alleviates Salmonella typhimurium infection.

Objective : This study aimed to investigate the mechanisms of CGA ininfection .
Methods : The intestinal pathological changes and @ @ @ @ @ were measured to verify the protection of CGA oninfection .
The antibacterial effects of CGAon @ @ @ @ @ cells and autophagy was evaluated .
The relationships among GAS5 , miR-23a , and PTEN @ @ @ @ @ inflammation- and autophagy-related proteins was detected .
Results : CGA treatment alleviated pathological damage , @ @ @ @ @ intestinal cytokines caused byinfection , and reduced the mortality of mice .
Intestinal GAS5 was @ @ @ @ @ LncRNA GAS5 competitively bound to miR-23a to upregulate PTEN and inhibit the p38 MAPK pathway @ @ @ @ @ MAPK pathway through lncRNA GAS5/miR-23a/PTEN axis to promote autophagy ininfection .
The functional rescue experiments @ @ @ @ @ identified these effects .
Conclusion : CGA promotes autophagy and inhibitsinfection through the GAS5/miR-23a/PTEN axis @ @ @ @ @ .

Background: ) causes several intestinal diseases. Polyphenols including chlorogenic acid (CGA) inhibit pathogenesis.
Objective: This study aimed to investigate the mechanisms of CGA ininfection.
Methods: The intestinal pathological changes and survival rate of ST-infected mice were measured to verify the protection of CGA oninfection. The antibacterial effects of CGAon the invasion to intestinal epithelial cells and autophagy was evaluated. The relationships among GAS5, miR-23a, and PTEN were verified. Expression of inflammation- and autophagy-related proteins was detected.
Results: CGA treatment alleviated pathological damage, improved the secretion disturbance of intestinal cytokines caused byinfection, and reduced the mortality of mice. Intestinal GAS5 was upregulated after CGA treatment. LncRNA GAS5 competitively bound to miR-23a to upregulate PTEN and inhibit the p38 MAPK pathway. CGA regulated the p38 MAPK pathway through lncRNA GAS5/miR-23a/PTEN axis to promote autophagy ininfection. The functional rescue experiments of miR-23a and PTEN further identified these effects.
Conclusion: CGA promotes autophagy and inhibitsinfection through the GAS5/miR-23a/PTEN axis and the p38 MAPK pathway.


greenmedinfo--2020-11-27--Chlorogenic acid abates male reproductive dysfunction in arsenic-exposure.

Arsenic , a major environmental pollutant of global concern , is well-known for its reproductive toxicity .
In this study , the protective potential of chlorogenic acid ( CGA ) , a caffeoylquinic acid isomer abundantly found in many plants , was investigated against sodium arsenite ( NaAsO ) -induced testicular dysfunctions .
Adult male Swiss mice were either administered NaAsOalone at 5 mg kgor co-treated with CGA at 100 mg kgor 200 mg kgbody weight for 4 weeks .
Results showed that NaAsO-treated mice exhibited marked declines in testes weight , sperm count , and viability accompanied by decreases @ @ @ @ @ @ @ NaAsOtoxicity evoked exhaustion of antioxidant markers ( SOD , CAT , GPx , GR , and GSH ) , down-regulation of Nrf2 ( nuclear factor erythroid 2-related factor 2 ) gene expression level , and elevations in malondialdehyde .
Further , elevations in inflammatory cytokines ( IL-1 , TNF-α , and IL-6 ) together with the up-regulation of pro-apoptotic biomarkers ( Bax and caspase- 3 ) and down-regulation of anti-apoptotic Bcl-2 were observed in NaAsOintoxication .
Immunohistochemical analysis of testis sections of NaAsO-treated mice showed high caspase-3 expression .
These findings were well @ @ @ @ @ @ @ , pretreatment of mice with CGA resulted in noteworthy improvements in testicular damage induced by arsenic in a dose-dependent manner possibly mediated by the Nrf2 signaling pathway .
Conclusively , CGA counteracted arsenic-induced testicular injury through its antioxidant , anti-inflammatory , and anti-apoptotic properties .
Therefore , CGA could serve as a favorable intervention in the alleviation of arsenic-induced reproductive toxicity .

Arsenic, a major environmental pollutant of global concern, is well-known for its reproductive toxicity. In this study, the protective potential of chlorogenic acid (CGA), a caffeoylquinic acid isomer abundantly found in many plants, was investigated against sodium arsenite (NaAsO)-induced testicular dysfunctions. Adult male Swiss mice were either administered NaAsOalone at 5 mg kgor co-treated with CGA at 100 mg kgor 200 mg kgbody weight for 4 weeks. Results showed that NaAsO-treated mice exhibited marked declines in testes weight, sperm count, and viability accompanied by decreases in sexual hormonal levels. Moreover, NaAsOtoxicity evoked exhaustion of antioxidant markers (SOD, CAT, GPx, GR, and GSH), down-regulation of Nrf2 (nuclear factor erythroid 2-related factor 2) gene expression level, and elevations in malondialdehyde. Further, elevations in inflammatory cytokines (IL-1, TNF-α, and IL-6) together with the up-regulation of pro-apoptotic biomarkers (Bax and caspase- 3) and down-regulation of anti-apoptotic Bcl-2 were observed in NaAsOintoxication. Immunohistochemical analysis of testis sections of NaAsO-treated mice showed high caspase-3 expression. These findings were well supported with testicular histopathological examination. However, pretreatment of mice with CGA resulted in noteworthy improvements in testicular damage induced by arsenic in a dose-dependent manner possibly mediated by the Nrf2 signaling pathway. Conclusively, CGA counteracted arsenic-induced testicular injury through its antioxidant, anti-inflammatory, and anti-apoptotic properties. Therefore, CGA could serve as a favorable intervention in the alleviation of arsenic-induced reproductive toxicity.


greenmedinfo--2020-11-27--Hypnosis Plus Meditation May Boost Relaxation Benefits

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greenmedinfo--2020-11-27--Inhibition of Staphylococcus aureus LC554891 by Moringa oleifera seed extract either singly or in co

Inhibition of Staphylococcus aureus LC554891 by Moringa oleifera seed extract either singly or in combination with antibiotics.

Bacterial outbreaks caused by ( ) are interesting due to the existence of multidrug resistant ( MDR ) isolates .
Therefore , there is a need to develop novel ways to control such MDR .
In this study , some natural agents such as honey bee ( HB ) , extracts of eitherseeds ( MSE ) , or leaves ( MLE ) and essential oils of garlic , clove , and moringa were studied for their inhibitory activity against thispathogen .
About 100 food samples including beef luncheon ( = 25 ) , potato chips ( = 50 ) , @ @ @ @ @ @ @ were investigated for possible pollution with thebacteria .
The isolated bacteria suspected to belongthat grew well onto Baird-Parker agar ( Oxoid ) and shiny halo zones and positive coagulase reaction were selected and identified by API-Kits ; all of them that were approved belong to ( 18 strains ) .
The sensitivity of the obtained 18bacterial strains to 12 antibiotics were evaluated ; all of them were resistant to ofloxacin ; however , other antibiotics tested showed variable results .
Interestingly , theNo .
B3 isolated from beef luncheon was resistant to10 antibiotics @ @ @ @ @ @ @ antibiotic resistance index ( MAR ) of thisstrain was about 83.3 % .
Therefore , its identification was confirmed by sequencing of a 16S rRNA gene which approved a successful biochemical identification carried out by API Kits and such strain was designatedLC 554891 .
The genome of such strain appeared to containgene encoding methicillin resistance ; it was found to containandthat encodeα-blood hemolysis , β-blood hemolysis , toxic shock syndrome gene , and fibrinogen-binding protein gene , respectively .
In addition , the virulence factors viz.encoding enterotoxins were detected in the DNA extracted @ @ @ @ @ @ @ MSE ) showed inhibitory activity againstLC 554891 better than that obtained by tetracycline , essential oils or HB .
Minimum inhibitory concentration ( MIC ) of MSE was 20µg/mL .
Instrumental analysis of MSE showed 14 bioactive chemical compounds .
Combinations of both MSE and tetracycline showed distinctive inhibitory activity againstLC 554891 than that obtained by either tetracycline or MSE singly .

Bacterial outbreaks caused by() are interesting due to the existence of multidrug resistant (MDR) isolates. Therefore, there is a need to develop novel ways to control such MDR. In this study, some natural agents such as honey bee (HB), extracts of eitherseeds (MSE), or leaves (MLE) and essential oils of garlic, clove, and moringa were studied for their inhibitory activity against thispathogen. About 100 food samples including beef luncheon (= 25), potato chips (= 50), and corn flakes (= 25) were investigated for possible pollution with thebacteria. The isolated bacteria suspected to belongthat grew well onto Baird-Parker agar (Oxoid) and shiny halo zones and positive coagulase reaction were selected and identified by API-Kits; all of them that were approved belong to(18 strains). The sensitivity of the obtained 18bacterial strains to 12 antibiotics were evaluated; all of them were resistant to ofloxacin; however, other antibiotics tested showed variable results. Interestingly, theNo. B3 isolated from beef luncheon was resistant to10 antibiotics out of 12 ones tested. Multiple antibiotic resistance index (MAR) of thisstrain was about 83.3%. Therefore, its identification was confirmed by sequencing of a 16S rRNA gene which approved a successful biochemical identification carried out by API Kits and such strain was designatedLC 554891. The genome of such strain appeared to containgene encoding methicillin resistance; it was found to containandthat encodeα-blood hemolysis, β-blood hemolysis, toxic shock syndrome gene, and fibrinogen-binding protein gene, respectively. In addition, the virulence factors viz.encoding enterotoxins were detected in the DNA extracted fromB3 strain. Aqueous extract ofseeds (MSE) showed inhibitory activity againstLC 554891 better than that obtained by tetracycline, essential oils or HB. Minimum inhibitory concentration (MIC) of MSE was 20µg/mL. Instrumental analysis of MSE showed 14 bioactive chemical compounds. Combinations of both MSE and tetracycline showed distinctive inhibitory activity againstLC 554891 than that obtained by either tetracycline or MSE singly.


greenmedinfo--2020-11-27--Astragalin alleviates cerebral ischemia-reperfusion injury by improving anti-oxidant and anti-inflam

Astragalin alleviates cerebral ischemia-reperfusion injury by improving anti-oxidant and anti-inflammatory activities.

BACKGROUND : Astragalin ( AG ) , a flavonoid from many traditional herbs and medicinal plants , has been described to exhibit in vitro anti-inflammatory activity .
The paper aimed to study the effects of astragalin on anti-inflammatory , anti-oxidative ability and apoptosis signaling pathway in brain tissue of rats with cerebral ischemia-reperfusion injury , and to explore its possible mechanism .
METHODS : The rat model of focal cerebral ischemia-reperfusion injury was established by suture method .
It was randomly divided into 5 groups , sham operation group , ischemia-reperfusion ( I/R ) treatment group , and astragalin treatment @ @ @ @ @ @ @ 25 , 50 mg / kg ) .
After 24 h of reperfusion , the neurological deficits of the rats were analyzed and HE staining was performed .
The volume of cerebral infarction was calculated by triphenyltetrazolium chloride ( TTC ) staining , and the apoptosis of nerve cells was detected by TUNEL staining .
In addition , the content of malondialdehyde ( MDA ) , nitric oxide ( NO ) , superoxide dismutase ( SOD ) , glutathione ( GSH ) assay and glutathione peroxidase ( GSH-Px ) were measured in rat @ @ @ @ @ @ @ used to determine the expression of related proteins .
RESULTS : Compared with I/R group , the neurological deficit score and infarct volume of I/R rats were reduced in the astragalin treatment group .
In the astragalin treatment group , MDA and NO levels in I/R rats were reduced , antioxidant enzymes and superoxide dismutase ( SOD ) activity were increased .
In the astragalin treatment group , NF-κB ( p65 ) and cyclooxygenase-2 ( COX-2 ) expression levels were down-regulated , NF-E2-related factor 2 ( Nrf2 ) nucleus and heme oxygenase-1 ( @ @ @ @ @ @ @ .
In addition , the astragalin treatment can inhibit apoptosis , down-regulate Bax and cleaved caspase-3 expression , up-regulate Bcl-Xl expression .
CONCLUSION : The antioxidant properties of astragalin may play an important role in improving cerebral ischemia-reperfusion injury .

BACKGROUND: Astragalin (AG), a flavonoid from many traditional herbs and medicinal plants, has been described to exhibit in vitro anti-inflammatory activity. The paper aimed to study the effects of astragalin on anti-inflammatory, anti-oxidative ability and apoptosis signaling pathway in brain tissue of rats with cerebral ischemia-reperfusion injury, and to explore its possible mechanism.
METHODS: The rat model of focal cerebral ischemia-reperfusion injury was established by suture method. It was randomly divided into 5 groups, sham operation group, ischemia-reperfusion (I/R) treatment group, and astragalin treatment I / R group (12.5, 25, 50 mg / kg). After 24 h of reperfusion, the neurological deficits of the rats were analyzed and HE staining was performed. The volume of cerebral infarction was calculated by triphenyltetrazolium chloride (TTC) staining, and the apoptosis of nerve cells was detected by TUNEL staining. In addition,the content of malondialdehyde (MDA), nitric oxide (NO), superoxide dismutase (SOD), glutathione (GSH) assay and glutathione peroxidase (GSH-Px) were measured in rat brain tissue. Western blot analysis was used to determine the expression of related proteins.
RESULTS: Compared with I/R group, the neurological deficit score and infarct volume of I/R rats were reduced in the astragalin treatment group. In the astragalin treatment group, MDA and NO levels in I/R rats were reduced, antioxidant enzymes and superoxide dismutase (SOD) activity were increased. In the astragalin treatment group, NF-κB (p65) and cyclooxygenase-2 (COX-2) expression levels were down-regulated, NF-E2-related factor 2 (Nrf2) nucleus and heme oxygenase-1 (HO-1) protein expression levels were up-regulated. In addition, the astragalin treatment can inhibit apoptosis, down-regulate Bax and cleaved caspase-3 expression, up-regulate Bcl-Xl expression.
CONCLUSION: The antioxidant properties of astragalin may play an important role in improving cerebral ischemia-reperfusion injury.


greenmedinfo--2020-11-27--Astragalin exerted antidepressant-like action through SIRT1 signalling modulated NLRP3 inflammasome

Astragalin exerted antidepressant-like action through SIRT1 signalling modulated NLRP3 inflammasome deactivation.

Inflammation plays a key role in the pathogenesis of depression and antidepressant therapies .
Astragalin ( AST ) is a bioactive flavonoid that possesses an anti-inflammatory property .
However , the antidepressant action of astragalin has not been addressed .
In this study , we explored the antidepressant effects of astragalin and its underlying mechanism .
Our results showed that AST significantly improved the behavioral defects in chronic unpredictable mild stress ( CUMS ) model , promoted SIRT1 expression , and decreased the protein levels of NF-κB p65 , NLRP3 , cleaved capase-1 , cleaved IL-1β and cleaved gasdermin D @ @ @ @ @ @ @ mitigated CUMS-induced microglia overactivation .
In vitro , AST profoundly increased the cell viability in lipopolysaccharides ( LPS ) and adenosine triphosphate ( ATP ) treatedBV2 cells , with upregulated SIRT1 expression and downregulated protein levels of nuclear NF-κB p65 , NLRP3 , cleaved capase-1 , and cleaved gasdermin D. Declined cleavage of gasdermin D was observed after AST administration in immunocytochemistry .
Nevertheless , the in vivo and in vitro effects of ASTwere compromised by SIRT1 inhibitor EX-527 .
These results indicated that AST possessed an antidepressant property , which was dependent @ @ @ @ @ @ @ .

Inflammation plays a key role in the pathogenesis of depression and antidepressant therapies. Astragalin (AST) is a bioactive flavonoid that possesses an anti-inflammatory property. However, the antidepressant action of astragalin has not been addressed. In this study, we explored the antidepressant effects of astragalin and its underlying mechanism. Our results showed that AST significantly improved the behavioral defects in chronic unpredictable mild stress (CUMS) model, promoted SIRT1 expression, and decreased the protein levels of NF-κB p65, NLRP3, cleaved capase-1, cleaved IL-1β and cleaved gasdermin D in the hippocampus. Immunohistochemistry revealed AST mitigated CUMS-induced microglia overactivation. In vitro, AST profoundly increased the cell viability in lipopolysaccharides (LPS) and adenosine triphosphate (ATP) treatedBV2 cells, with upregulated SIRT1 expression and downregulated protein levels of nuclear NF-κB p65, NLRP3, cleaved capase-1, and cleaved gasdermin D. Declined cleavage of gasdermin D was observed after AST administration in immunocytochemistry. Nevertheless, the in vivo and in vitro effects of ASTwere compromised by SIRT1 inhibitor EX-527. These results indicated that AST possessed an antidepressant property, which was dependent on SIRT1 signaling modulated NLRP3 inflammasome deactivation.


greenmedinfo--2020-11-27--Astragalin inhibits nuclear factor-κB signalling in human colonic epithelial cells and attenuates ex

Astragalin inhibits nuclear factor-κB signalling in human colonic epithelial cells and attenuates experimental colitis.

Background/Aims : Astragalin ( kaempferol-3-O-β-D-glucoside ) is a flavonoid isolated from the leaves of persimmon or .
Astragalin exhibits various anti-inflammatory properties ; however , little is known about its therapeutic potential for inflammatory bowel disease ( IBD ) .
This study aims to investigate the anti-inflammatory effect of astragalin via blockade of the nuclear factorκB ( NF-κB ) signaling pathway in human colonic epithelial cells and a murine colitis model .
Methods : HCT-116 and HT-29 human colonic epithelial cells were pretreated with astragalin and stimulated with tumor necrosis factor-α ( TNF-α ) .
Cell viability was assessed by @ @ @ @ @ @ @ polymerase chain reaction was used to analyze the messenger RNA expression of the inflammatory cytokines interleukin ( IL ) -6 and IL-8 .
The effect of astragalin on the NF-κB pathway was evaluated by Western blot analysis of inhibitor of NF-κB alpha ( IκBα ) phosphorylation/degradation and by electrophoretic mobility shift assay .
Dextran sulfate sodium ( DSS ) -induced acute murine colitis model was used forexperiments .
Results : Astragalin strongly suppressed the expression of proinflammatory cytokines in human colonic epithelial cells in a dose-dependent manner .
Western blot analysis showed that @ @ @ @ @ @ @ astragalin reduced the DNA binding activity of NF-κB .
Astragalin alleviated colon shortening and improved the pathologic scores in DSS-induced acute murine colitis model .
Furthermore , astragalin reduced the level of phosphorylated IκBα and decreased the production of the inflammatory cytokines IL-6 , IL-8 , and TNF-α in the DSS-treated colon mucosa .
Conclusions : Astragalin exerted an anti-inflammatory effect through NF-κB pathway inhibition and attenuated murine colitis .
Astragalin is thus a potential therapeutic agent for IBD .

Background/Aims: Astragalin (kaempferol-3-O-β-D-glucoside) is a flavonoid isolated from the leaves of persimmon or. Astragalin exhibits various anti-inflammatory properties; however, little is known about its therapeutic potential for inflammatory bowel disease (IBD). This study aims to investigate the anti-inflammatory effect of astragalin via blockade of the nuclear factorκB (NF-κB) signaling pathway in human colonic epithelial cells and a murine colitis model.
Methods: HCT-116 and HT-29 human colonic epithelial cells were pretreated with astragalin and stimulated with tumor necrosis factor-α (TNF-α). Cell viability was assessed by the MTS assay. Real-time reverse transcription polymerase chain reaction was used to analyze the messenger RNA expression of the inflammatory cytokines interleukin (IL)-6 and IL-8. The effect of astragalin on the NF-κB pathway was evaluated by Western blot analysis of inhibitor of NF-κB alpha (IκBα) phosphorylation/degradation and by electrophoretic mobility shift assay. Dextran sulfate sodium (DSS)-induced acute murine colitis model was used forexperiments.
Results: Astragalin strongly suppressed the expression of proinflammatory cytokines in human colonic epithelial cells in a dose-dependent manner. Western blot analysis showed that astragalin inhibited IκBα phosphorylation/degradation. Additionally, astragalin reduced the DNA binding activity of NF-κB. Astragalin alleviated colon shortening and improved the pathologic scores in DSS-induced acute murine colitis model. Furthermore, astragalin reduced the level of phosphorylated IκBα and decreased the production of the inflammatory cytokines IL-6, IL-8, and TNF-α in the DSS-treated colon mucosa.
Conclusions: Astragalin exerted an anti-inflammatory effect through NF-κB pathway inhibition and attenuated murine colitis. Astragalin is thus a potential therapeutic agent for IBD.


greenmedinfo--2020-11-27--Anti-inflammatory effect of astragalin and chlorogenic acid on Escherichia coli-induced inflammation

Anti-inflammatory effect of astragalin and chlorogenic acid on Escherichia coli-induced inflammation of sheep endometrial epithelium cells.

Endometritis is one of the main diseases which harm sheep husbandry .
Astragalin and chlorogenic acid ( CGA ) are common active ingredients of traditional Chinese medicine ( TCM ) with immunoprotective , antioxidant , and anti-inflammatory properties .
In the present study , sheep endometrial epithelium cells ( SEECs ) were successfully purified and identified , and theinflammation model of SEECs induced bywas successfully established .
To explore the effect of astragalin and CGA on the inflammation induced byand its potential mechanism , six groups were set up , namely , group C , M , astragalin , CGA @ @ @ @ @ @ @ in group C were incubated with DMEM/F12 for 6 h , while cells in group M , astragalin , CGA , BAY , and STR were incubated with DMEM/F12 , astragalin , CGA , BAY , and STR for 3 h , respectively , followed byinfection at a multiplicity of infection ( MOI ) of 1per cell for 3 h. Subsequently , the cells and the supernatant were collected to detect the expression of genes in the toll-like receptor 4 ( TLR4 ) /nuclear factor-kappa B ( NF-κB ) pathway by ELISA , @ @ @ @ @ @ @ results showed thatcould induce inflammation of SEECs , while astragalin and CGA could alleviate the inflammatory response induced byvia inhibiting the activation of the TLR4/NF-κB signaling pathway , which provides a theoretical and experimental foundation for preventing sheep endometritis clinically .

Endometritis is one of the main diseases which harm sheep husbandry. Astragalin and chlorogenic acid (CGA) are common active ingredients of traditional Chinese medicine (TCM) with immunoprotective, antioxidant, and anti-inflammatory properties. In the present study, sheep endometrial epithelium cells (SEECs) were successfully purified and identified, and theinflammation model of SEECs induced bywas successfully established. To explore the effect of astragalin and CGA on the inflammation induced byand its potential mechanism, six groups were set up, namely, group C, M, astragalin, CGA, BAY, and STR. Cells in group C were incubated with DMEM/F12 for 6 h, while cells in group M, astragalin, CGA, BAY, and STR were incubated with DMEM/F12, astragalin, CGA, BAY, and STR for 3 h, respectively, followed byinfection at a multiplicity of infection (MOI) of 1per cell for 3 h. Subsequently, the cells and the supernatant were collected to detect the expression of genes in the toll-like receptor 4 (TLR4)/nuclear factor-kappa B (NF-κB) pathway by ELISA, qPCR, and western blot. The results showed thatcould induce inflammation of SEECs, while astragalin and CGA could alleviate the inflammatory response induced byvia inhibiting the activation of the TLR4/NF-κB signaling pathway, which provides a theoretical and experimental foundation for preventing sheep endometritis clinically.


greenmedinfo--2020-11-27--Astragalin attenuates oxidative stress and acute inflammatory responses in carrageenan-induced paw e

Astragalin attenuates oxidative stress and acute inflammatory responses in carrageenan-induced paw edema.

Astragalin is a flavonoid existed in several edible and medicinal plants and was recorded to have multiple biological and pharmacological significances .
This work aimed to assess the possible protective effect of astragalin administration against oxidative tension , acute inflammation and histopathological deformations in a mouse paw edema model induced following intra sub-plantar injection of carrageenan .
Thirty-six male Swiss mice were divided into four groups : control , carrageenan , astragalin ( 75 mg/kg ) + carrageenan , and indomethacin ( 10 mg/kg ) + carrageenan .
Astragalin administration for five consecutive days to carrageenan injected mice showed a @ @ @ @ @ @ @ in a time dependent effect , inhibited lipoperoxidation by-product , malondialdehyde andincreased superoxide dismutase and catalase activities .
Astragalin was found also to suppress the inflammatory signaling in the inflamed tissue as exhibited by the decreased myeloperoxidase activity along with the decreased protein and transcriptional level of pro-inflammatory cytokines including tumor necrosis factor-alpha , interleukin-1 beta and interleukin-6 .
Moreover , inducible nitric oxide synthase and cyclooxygenase-2 expressions and their products ( nitric oxide and prostaglandin E2 ) were downregulated .
Additionally , astragalin decreased monocyte chemoattractant protein-1 and nuclear factor kappa B @ @ @ @ @ @ @ The recorded findings provide evidences for the potential application of astragalin as a plant-derived remedy for the treatment of acute inflammation due to its promising antioxidant and anti-inflammatory activities along with its ameliorative impact against the histopathological changes in the paw tissue .

Astragalin is a flavonoid existed in several edible and medicinal plants and was recorded to have multiple biological and pharmacological significances. This work aimed to assess the possible protective effect of astragalin administration against oxidative tension, acute inflammation and histopathological deformations in a mouse paw edema model induced following intra sub-plantar injection of carrageenan. Thirty-six male Swiss mice were divided into four groups: control, carrageenan, astragalin (75 mg/kg) + carrageenan, and indomethacin (10 mg/kg) + carrageenan. Astragalin administration for five consecutive days to carrageenan injected mice showed a significant reduction in the development of paw in a time dependent effect, inhibited lipoperoxidation by-product, malondialdehyde andincreased superoxide dismutase and catalase activities. Astragalin was found also to suppress the inflammatory signaling in the inflamed tissue as exhibited by the decreased myeloperoxidase activity along with the decreased protein and transcriptional level of pro-inflammatory cytokines including tumor necrosis factor-alpha, interleukin-1 beta and interleukin-6. Moreover, inducible nitric oxide synthase and cyclooxygenase-2 expressions and their products (nitric oxide and prostaglandin E2) were downregulated. Additionally, astragalin decreased monocyte chemoattractant protein-1 and nuclear factor kappa B expression in the inflamed paw tissue. The recorded findings provide evidences for the potential application of astragalin as a plant-derived remedy for the treatment of acute inflammation due to its promising antioxidant and anti-inflammatory activities along with its ameliorative impact against the histopathological changes in the paw tissue.


greenmedinfo--2020-11-27--Astragalin alleviates ischemia/reperfusion‑induced brain injury via suppression of endoplasmic retic

Astragalin alleviates ischemia/reperfusion‑induced brain injury via suppression of endoplasmic reticulum stress.

Excessive apoptosis and neuronal dysfunction are pathological features of ischemic stroke .
Previous studies have demonstrated that astragalin ( AST ) exerted both anti‑apoptotic and anti‑inflammatory effects in several types of disease , although its potential effect in ischemic stroke remains unclear .
The purpose of the present study was to investigate the effects of AST on cerebral ischemia/reperfusion ( I/R ) ‑induced brain injuryand the underlying mechanisms .
Brain injury was assessed in an experimental rat model using measurement of neurological scores and inflammatory factors .
To assess the role of AST in I/R‑induced brain injury and the potential @ @ @ @ @ @ @ with thapsigargin and AST .
Apoptotic rate and ER stress levels were measured by western blotting , reverse transcription‑quantitative PCR and immunofluorescence staining .
It was discovered that AST significantly improved long‑term neurological outcomes in rats following cerebral I/R injury , through the attenuation of the expression levels of apoptotic proteins ( Bax and cleaved‑caspase‑3 ) and the release of inflammatory cytokines , as well as upregulating the expression levels of the anti‑apoptotic protein Bcl‑2 .
Furthermore , AST attenuated the expression levels of the endoplasmic reticulum ( ER ) stress‑related protein , @ @ @ @ @ @ @ well as its downstream apoptotic mediators ( CHOP and caspase‑12 ) .
Thapsigargin‑induced ER stress activation and apoptosis were also attenuated by AST in an in vitro neuronal cell culture model .
In conclusion , these results suggested that AST mayprotect against I/R‑induced brain injury , thus , highlighting its therapeutic potential in patients with ischemic stroke .

Excessive apoptosis and neuronal dysfunction are pathological features of ischemic stroke. Previous studies have demonstrated that astragalin (AST) exerted both anti‑apoptotic and anti‑inflammatory effects in several types of disease, although its potential effect in ischemic stroke remains unclear. The purpose of the present study was to investigate the effects of AST on cerebral ischemia/reperfusion (I/R)‑induced brain injuryand the underlying mechanisms. Brain injury was assessed in an experimental rat model using measurement of neurological scores and inflammatory factors. To assess the role of AST in I/R‑induced brain injury and the potential mechanism of action, SH5Y were treated with thapsigargin and AST. Apoptotic rate and ER stress levels were measured by western blotting, reverse transcription‑quantitative PCR and immunofluorescence staining. It was discovered that AST significantly improved long‑term neurological outcomes in rats following cerebral I/R injury, through the attenuation of the expression levels of apoptotic proteins (Bax and cleaved‑caspase‑3) and the release of inflammatory cytokines, as well as upregulating the expression levels of the anti‑apoptotic protein Bcl‑2. Furthermore, AST attenuated the expression levels of the endoplasmic reticulum (ER) stress‑related protein, glucose‑regulated protein, 78 kDa, as well as its downstream apoptotic mediators (CHOP and caspase‑12). Thapsigargin‑induced ER stress activation and apoptosis were also attenuated by AST in an in vitro neuronal cell culture model. In conclusion, these results suggested that AST mayprotect against I/R‑induced brain injury, thus, highlighting its therapeutic potential in patients with ischemic stroke.