greenmedinfo--2020-09-04--Biochemical evaluation of the antioxidant effects of hydroxytyrosol on pancreatitis-associated gut i

Biochemical evaluation of the antioxidant effects of hydroxytyrosol on pancreatitis-associated gut injury.

Acute pancreatitis is a severe abdominal pathology often associated with several complications including gut dysfunction .
Oxidative stress is one of the most important pathways involved in this pathology .
Hydroxytyrosol ( HT ) , a phenolic compound obtained from olive oil , has shown anti-inflammatory and antioxidant properties .
We evaluated the effects of HT administration on pancreatic and intestinal injury induced by caerulein administration .
CD1 female mice were administered caerulein ( 50μg/kg ) for 10 h. HT treatment ( 5 mg/kg ) was performed 30 min after the first caerulein injection and for two consecutive hours afterwards @ @ @ @ @ @ @ injection , mice were sacrificed and serum , colon and pancreatic tissue samples were collected .
HT was able to reduce the serumhallmarks of pancreatitis ( amylase and lipase ) , histological damage score in both pancreas and colon tissue , inflammatory cells recruitment ( mast cells ) in both injured tissues , intrapancreatic trypsin activity and overexpression of the adhesion molecules ( Intercellular Adhesion Molecule-1 ( ICAM-1 ) and P-selectin ) in colon .
Additionally , HT reduced cytokine ( interleukin 1 beta ( IL- 1β ) , interleukin 6 ( IL-6 @ @ @ @ @ @ @ TNF-α ) ) levels in serum , pancreas and colon tissue and chemokine release ( monocyte chemotactic protein-1 ( MCP1/CCL2 ) ) in pancreas and colon tissue .
HT decreased lipid peroxidation and oxidative stress ( superoxide dismutase ( SOD ) , glutathione peroxidase ( GPx ) , glutathione reductase ( GR ) and glutathione S-transferase ( GST ) activity ) by enhancing the nuclear factor erythroid 2-related factor 2 ( Nrf2 ) and heme oxygenase 1 ( HO-1 ) in both injured tissues.Moreover , HT preserved intestinal barrier integrity , as shown @ @ @ @ @ @ @ serum levels and tight junction ( zonula occludens ( ZO ) and occludin ) expression in pancreas and colon .
Our findings demonstrated that HT would be an important therapeutic tool against pancreatitis-induced injuries in the pancreas and gut .

Acute pancreatitis is a severe abdominal pathology often associated with several complications including gut dysfunction. Oxidative stress is one of the most important pathways involved in this pathology. Hydroxytyrosol (HT), a phenolic compound obtained from olive oil, has shown anti-inflammatory and antioxidant properties. We evaluated the effects of HT administration on pancreatic and intestinal injury induced by caerulein administration. CD1 female mice were administered caerulein (50μg/kg) for 10 h. HT treatment (5 mg/kg) was performed 30 min after the first caerulein injection and for two consecutive hours afterwards. One hour after the last caerulein injection, mice were sacrificed and serum, colon and pancreatic tissue samples were collected. HT was able to reduce the serumhallmarks of pancreatitis (amylase and lipase), histological damage score in both pancreas and colon tissue, inflammatory cells recruitment (mast cells) in both injured tissues, intrapancreatic trypsin activity and overexpression of the adhesion molecules (Intercellular Adhesion Molecule-1 (ICAM-1)and P-selectin) in colon. Additionally, HT reduced cytokine (interleukin 1 beta (IL- 1β), interleukin 6 (IL-6) and tumor necrosis factor alpha (TNF-α)) levels in serum, pancreas and colon tissue and chemokine release (monocyte chemotactic protein-1 (MCP1/CCL2)) in pancreas and colon tissue. HT decreased lipid peroxidation and oxidative stress (superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GR) and glutathione S-transferase (GST) activity) by enhancing the nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase 1 (HO-1) in both injured tissues.Moreover, HT preserved intestinal barrier integrity, as shown by the diamine oxidase (DAO) serum levels and tight junction (zonula occludens (ZO) and occludin) expression in pancreas and colon. Our findings demonstrated that HT would be an important therapeutic tool against pancreatitis-induced injuries in the pancreas and gut.


greenmedinfo--2020-09-04--Hydroxytyrosol ameliorates oxidative challenge and inflammatory response associated with lipopolysac

Hydroxytyrosol ameliorates oxidative challenge and inflammatory response associated with lipopolysaccharide-mediated sepsis.

Hydroxytyrosol ( HT ) is among the main bioactive ingredients isolated from olive tree with a variety of biological and pharmacological activities .
In the current study , the antioxidative and anti-inflammatory activities of HT were distinguished in the splenic tissue following lipopolysaccharide ( LPS ) -mediated septic response .
Thirty-five Swiss mice were divided into five groups ( n = 7 ) : control , HT ( 40 mg/kg ) , LPS ( 10 mg/kg ) , HT 20 mg+LPS and HT 40 mg+LPS .
HT was administered for 10 days , while a single LPS dose was applied @ @ @ @ @ @ @ administration enhanced the survival rate and decreased lactate dehydrogenase level in LPS-challenged mice .
Treatment with HT inhibited the incidence of oxidative damage in splenic tissue through decreasing lipoperoxidation and increasing antioxidant molecules , namely glutathione , superoxide dismutase and catalase .
HT also decreased total leukocytes count , C-reactive protein , monocyte chemoattractant protein-1 , and myeloperoxidase levels .
Additionally , HT suppressed the production levels of tumor necrosis factor-α , interleukin-1β , and interleukin-6 .
Moreover , mRNA expression of inducible nitric oxide synthase and nitric oxide production were increased after @ @ @ @ @ @ @ resulted in a downregulation of p38 mitogen-activated protein kinase , inhibited the activation of the nuclear factor kappa-B from the nucleus to the cytoplasm , and attenuated infiltration of activated immune cells and tissue injury following LPS injection .
Collectively , these findings demonstrate the antioxidative and anti-inflammatory properties of HT against LPS-mediated inflammation and sepsis .
Therefore , HT could be applied as an alternative anti-inflammatory agent to minimize or prevent the development of systemic inflammatory response associated with septic shock .

Hydroxytyrosol (HT) is among the main bioactive ingredients isolated from olive tree with a variety of biological and pharmacological activities. In the current study, the antioxidative and anti-inflammatory activities of HT were distinguished in the splenic tissue following lipopolysaccharide (LPS)-mediated septic response. Thirty-five Swiss mice were divided into five groups (n = 7): control, HT (40 mg/kg), LPS (10 mg/kg), HT 20 mg+LPS and HT 40 mg+LPS. HT was administered for 10 days, while a single LPS dose was applied. The obtained findings demonstrate that HT administration enhanced the survival rate and decreased lactate dehydrogenase level in LPS-challenged mice. Treatment with HT inhibited the incidence of oxidative damage in splenic tissue through decreasing lipoperoxidation and increasing antioxidant molecules, namely glutathione, superoxide dismutase and catalase. HT also decreased total leukocytes count, C-reactive protein, monocyte chemoattractant protein-1, and myeloperoxidase levels. Additionally, HT suppressed the production levels of tumor necrosis factor-α, interleukin-1β, and interleukin-6. Moreover, mRNA expression of inducible nitric oxide synthase and nitric oxide production were increased after HT administration. Furthermore, HT supplementation resulted in a downregulation of p38 mitogen-activated protein kinase, inhibited the activation of the nuclear factor kappa-B from the nucleus to the cytoplasm, and attenuated infiltration of activated immune cells and tissue injury following LPS injection. Collectively, these findings demonstrate the antioxidative and anti-inflammatory properties of HT against LPS-mediated inflammation and sepsis. Therefore, HT could be applied as an alternative anti-inflammatory agent to minimize or prevent the development of systemic inflammatory response associated with septic shock.


greenmedinfo--2020-09-04--The role of glutathione in protecting against the severe inflammatory response triggered by COVID-19

The role of glutathione in protecting against the severe inflammatory response triggered by COVID-19.

The novel COVID-19 pandemic is affecting the world 's population differently : mostly in the presence of conditions such as aging , diabetes and hypertension the virus triggers a lethal cytokine storm and patients die from acute respiratory distress syndrome , whereas in many cases the disease has a mild or even asymptomatic progression .
A common denominator in all conditions associated with COVID-19 appears to be the impaired redox homeostasis responsible for reactive oxygen species ( ROS ) accumulation ; therefore , levels of glutathione ( GSH ) , the key anti-oxidant guardian in all tissues , could be @ @ @ @ @ @ @ triggers organ failure in COVID-19 .
The present review provides a biochemical investigation of the mechanisms leading to deadly inflammation in severe COVID-19 , counterbalanced by GSH .
The pathways competing for GSH are described to illustrate the events concurring to cause a depletion of endogenous GSH stocks .
Drawing on evidence from literature that demonstrates the reduced levels of GSH in the main conditions clinically associated with severe disease , we highlight the relevance of restoring GSH levels in the attempt to protect the most vulnerable subjects from severe symptoms of COVID-19 @ @ @ @ @ @ @ data about the feasibility of increasing GSH levels , which could be used to prevent and subdue the disease .

The novel COVID-19 pandemic is affecting the world's population differently: mostly in the presence of conditions such as aging, diabetes and hypertension the virus triggers a lethal cytokine storm and patients die from acute respiratory distress syndrome, whereas in many cases the disease has a mild or even asymptomatic progression. A common denominator in all conditions associated with COVID-19 appears to be the impaired redox homeostasis responsible for reactive oxygen species (ROS) accumulation; therefore, levels of glutathione (GSH), the key anti-oxidant guardian in all tissues, could be critical in extinguishing the exacerbated inflammation that triggers organ failure in COVID-19. The present review provides a biochemical investigation of the mechanisms leading to deadly inflammation in severe COVID-19, counterbalanced by GSH. The pathways competing for GSH are described to illustrate the events concurring to cause a depletion of endogenous GSH stocks. Drawing on evidence from literature that demonstrates the reduced levels of GSH in the main conditions clinically associated with severe disease, we highlight the relevance of restoring GSH levels in the attempt to protect the most vulnerable subjects from severe symptoms of COVID-19. Finally, we discuss the current data about the feasibility of increasing GSH levels, which could be used to prevent and subdue the disease.


greenmedinfo--2020-09-04--N-acetylcysteine provides cytoprotection in murine oligodendrocytes through heme oxygenase-1 activit

N-acetylcysteine provides cytoprotection in murine oligodendrocytes through heme oxygenase-1 activity.

Oligodendrocytic injury by oxidative stress can lead to demyelination , contributing to neurodegeneration .
We investigated the mechanisms by which an antioxidant , N-acetylcysteine ( NAC ) , reduces oxidative stress in murine oligodendrocytes .
We used normal 158N and mutant 158JP cells with endogenously high reactive oxygen species ( ROS ) levels .
Oxidative stress was induced in 158N cells using hydrogen peroxide ( HO , 500μM ) , and both cells were treated with NAC ( 50 µM to 500 µM ) .
ROS production , total glutathione ( GSH ) and cell survival were measured 24 h @ @ @ @ @ @ @ HOtreatment resulted in a ~5.5-fold increase in ROS and ~50 % cell death .
These deleterious effects of oxidative stress were attenuated by NAC , resulting in improved cell survival .
Similarly , NAC treatment resulted in decreased ROS levels in 158JP cells .
Characterization of mechanisms underlying cytoprotection in both cell lines revealed an increase in GSH levels by NAC , which was partially blocked by an inhibitor of GSH synthesis .
Interestingly , we observed heme oxygenase-1 ( HO-1 ) , a cytoprotective enzyme , play a critical role in cytoprotection @ @ @ @ @ @ @ cytoprotective effect of NAC with a corresponding decrease in total antioxidant capacity .
Our results indicate that NAC promotes oligodendrocyte survival in oxidative stress-related conditions through multiple pathways .

Oligodendrocytic injury by oxidative stress can lead to demyelination, contributing to neurodegeneration. We investigated the mechanisms by which an antioxidant, N-acetylcysteine (NAC), reduces oxidative stress in murine oligodendrocytes. We used normal 158N and mutant 158JP cells with endogenously high reactive oxygen species (ROS) levels. Oxidative stress was induced in 158N cells using hydrogen peroxide (HO, 500μM), and both cells were treated with NAC (50 µM to 500 µM). ROS production, total glutathione (GSH) and cell survival were measured 24 h after treatment. In normal cells, HOtreatment resulted in a ~5.5-fold increase in ROS and ~50% cell death. These deleterious effects of oxidative stress were attenuated by NAC, resulting in improved cell survival. Similarly, NAC treatment resulted in decreased ROS levels in 158JP cells. Characterization of mechanisms underlying cytoprotection in both cell lines revealed an increase in GSH levels by NAC, which was partially blocked by an inhibitor of GSH synthesis. Interestingly, we observed heme oxygenase-1 (HO-1), a cytoprotective enzyme, play a critical role in cytoprotection. Inhibition of HO-1 activity abolished the cytoprotective effect of NAC with a corresponding decrease in total antioxidant capacity. Our results indicate that NAC promotes oligodendrocyte survival in oxidative stress-related conditions through multiple pathways.


greenmedinfo--2020-09-04--N-acetylcysteine as an adjunctive treatment for smoking cessation.

OBJECTIVE : This randomized controlled trial examined the efficacy and safety of N-acetylcysteine as an adjunctive treatment for smoking cessation .
METHODS : Heavy smokers were recruited from smoking cessation treatment for this 12- week randomized controlled trial .
Eligible tobacco use disorder outpatients ( n=34 ) were randomized to N-acetylcysteine or placebo plus first-line treatment .
Abstinence was verified by exhaled carbon monoxide ( COexh ) .
The assessment scales included the Fagerström Test for Nicotine Dependence , the Hamilton Depression Rating Scale , the Hamilton Anxiety Rating Scale , the Minnesota Nicotine Withdrawal Scale , and the Medication @ @ @ @ @ @ @ anthropometrics , blood pressure , lipid profile , and soluble tumor necrosis factor receptor ( sTNF-R ) levels 1 and 2 .
RESULTS : First-line treatment for smoking cessation plus adjunctive N-acetylcysteine or placebo significantly reduced COexh ( p < 0.01 ) .
In the N-acetylcysteine group , no significant changes were found in nicotine withdrawal symptoms , depressive and anxiety symptoms , anthropometric measures , blood pressure , or glucose compared to placebo .
However , there was a significant reduction in sTNF-R2 levels between baseline and week 12 in the N-acetylcysteine @ @ @ @ @ @ @ the need to associate N-acetylcysteine with first-line treatment for smoking cessation , since combined treatment may affect inflammation and metabolism components .

OBJECTIVE: This randomized controlled trial examined the efficacy and safety of N-acetylcysteine as an adjunctive treatment for smoking cessation.
METHODS: Heavy smokers were recruited from smoking cessation treatment for this 12- week randomized controlled trial. Eligible tobacco use disorder outpatients (n=34) were randomized to N-acetylcysteine or placebo plus first-line treatment. Abstinence was verified by exhaled carbon monoxide (COexh). The assessment scales included the Fagerström Test for Nicotine Dependence, the Hamilton Depression Rating Scale, the Hamilton Anxiety Rating Scale, the Minnesota Nicotine Withdrawal Scale, and the Medication Adherence Rating Scale. We also assessed anthropometrics, blood pressure, lipid profile, and soluble tumor necrosis factor receptor (sTNF-R) levels 1 and 2.
RESULTS: First-line treatment for smoking cessation plus adjunctive N-acetylcysteine or placebo significantly reduced COexh (p<0.01). In the N-acetylcysteine group, no significant changes were found in nicotine withdrawal symptoms, depressive and anxiety symptoms, anthropometric measures, blood pressure, or glucose compared to placebo. However, there was a significant reduction in sTNF-R2 levels between baseline and week 12 in the N-acetylcysteine group.
CONCLUSIONS: These findings highlight the need to associate N-acetylcysteine with first-line treatment for smoking cessation, since combined treatment may affect inflammation and metabolism components.
CLINICAL TRIAL REGISTRATION: NCT02420418.


greenmedinfo--2020-09-05--Anti-inflammatory effect of a flavonoid-rich extract of orange juice in adult zebrafish subjected to

Anti-inflammatory effect of a flavonoid-rich extract of orange juice in adult zebrafish subjected to Vibrio anguillarum-induced enteritis.

Inflammation-related pathologies remain a serious health problem with high costs for the community.flavonoids are known to possess important pharmacological properties @ @ @ @ @ In this study we evaluated the effects of a flavonoid-rich extract of orange juice ( @ @ @ @ @ model of enteritis induced byin adult zebrafish ( ) .
Administration ofthrough live feed ( @ @ @ @ @ days caused evident signs of enteritis in zebrafish .
Three days of treatment with OJe @ @ @ @ @ in a remarkable reduction of tissue inflammatory events as well as a molecular down-regulation of @ @ @ @ @ IL-1β , IL-6 and TNFα .
Our data suggest that OJe counteracts the inflammation of @ @ @ @ @ that the pool of flavonoids present in orange juice could be useful for the prevention @ @ @

Inflammation-related pathologies remain a serious health problem with high costs for the community.flavonoids are known to possess important pharmacological properties, including anti-inflammatory activity. In this study we evaluated the effects of a flavonoid-rich extract of orange juice (OJe) in an experimental model of enteritis induced byin adult zebrafish (). Administration ofthrough live feed (nauplii) for three consecutive days caused evident signs of enteritis in zebrafish. Three days of treatment with OJe before the pathogenic insult resulted in a remarkable reduction of tissue inflammatory events as well as a molecular down-regulation of the inflammatory genes such as IL-1β, IL-6 and TNFα. Our data suggest that OJe counteracts the inflammation of zebrafish intestinal mucosa, indicating that the pool of flavonoids present in orange juice could be useful for the prevention of enteritis.


greenmedinfo--2020-09-05--Effects of grape juice, red wine and resveratrol on liver parameters of rat submitted high-fat diet.

This work evaluated the effect of grape juice , red wine and resveratrol in liver parameters of rats submitted to high-fat diet .
Experimental model was conducted with groups of adult females Rattus norvegicus : control ( CG ) ; high-fat ( HG ) ; grape juice ( JG ) ; red wine ( RW ) and resveratrol solution ( RG ) .
The high-fat diet significantly altered hepatocytes and Kupffer cells in all treated groups .
HG group presented severe steatosis followed hepatocyte ballooning and tissue damages .
JG group minimized hepatic histological lesion caused by high-fat diet and @ @ @ @ @ @ @ in hepatocytes , similar to HG .
Still , resveratrol protected the tissue against fatty liver disease by reducing fat infiltration and inflammation , indicating possible therapeutic effects on the liver .
Cell cycle analysis showed that HG promoted damage to the tissue , reducing the viable cell content and increasing apoptosis , even when associated with wine consumption or isolated resveratrol .
However , JG protected the liver against cell damage generated by the diet .
Consumption of grape juice , even associated with a high-fat diet , represents a promising protection @ @ @ @ @ @ @ but red wine further affects the tissue , and resveratrol alone was able to reduce damage but did not minimize cellular damage to the liver .

This work evaluated the effect of grape juice, red wine and resveratrol in liver parameters of rats submitted to high-fat diet. Experimental model was conducted with groups of adult females Rattus norvegicus: control (CG); high-fat (HG); grape juice (JG); red wine (RW) and resveratrol solution (RG). The high-fat diet significantly altered hepatocytes and Kupffer cells in all treated groups. HG group presented severe steatosis followed hepatocyte ballooning and tissue damages. JG group minimized hepatic histological lesion caused by high-fat diet and WG group also induced steatosis and inflammation in hepatocytes, similar to HG. Still, resveratrol protected the tissue against fatty liver disease by reducing fat infiltration and inflammation, indicating possible therapeutic effects on the liver. Cell cycle analysis showed that HG promoted damage to the tissue, reducing the viable cell content and increasing apoptosis, even when associated with wine consumption or isolated resveratrol. However, JG protected the liver against cell damage generated by the diet. Consumption of grape juice, even associated with a high-fat diet, represents a promising protection of the liver against cellular damage, but red wine further affects the tissue, and resveratrol alone was able to reduce damage but did not minimize cellular damage to the liver.


greenmedinfo--2020-09-05--Ginsenoside Rb1 improves cognitive impairment induced by insulin resistance.

The relationship between diabetes mellitus ( DM ) and Alzheimer 's disease ( AD ) has attracted wide attention .
@ @ @ @ @ Rb1 can improve human cognitive ability and glucose tolerance during the development of diabetes .
@ @ @ @ @ in cognitive ability and glucose tolerance still remains unclear .
In this study , streptozotocin- @ @ @ @ @ were used as models to explore the mechanisms behind the cognitive improvement of ginsenoside Rb1 @ @ @ @ @ of behavioral tests , ginsenoside Rb1 improved memory and cognitive ability of STZ-lesioned mice .
@ @ @ @ @ ginsenoside Rb1 also relieved glucose intolerance induced by STZ injection by enhancing insulin sensitivity .
@ @ @ @ @ Rb1 is most likely mediated by upregulating the expression of NMDAR1 and IDE in the @ @ @ @ @ of Cdk5/p35 .
This work will be of great importance in illustrating the mechanisms of @ @ @ @ @ ability , as well as revealing the relationship between diabetes and AD .

The relationship between diabetes mellitus (DM) and Alzheimer's disease (AD) has attracted wide attention. Studies have reported that ginsenoside Rb1 can improve human cognitive ability and glucose tolerance during the development of diabetes. The mechanism behind the improvement in cognitive ability and glucose tolerance still remains unclear. In this study, streptozotocin- (STZ-) injected mice were used as models to explore the mechanisms behind the cognitive improvement of ginsenoside Rb1. According to the results of behavioral tests, ginsenoside Rb1 improved memory and cognitive ability of STZ-lesioned mice. In addition to that, ginsenoside Rb1 also relieved glucose intolerance induced by STZ injection by enhancing insulin sensitivity. These beneficial effects of ginsenoside Rb1 is most likely mediated by upregulating the expression of NMDAR1 and IDE in the hippocampus through inhibiting the activity of Cdk5/p35. This work will be of great importance in illustrating the mechanisms of ginsenoside Rb1 for improving cognitive ability, as well as revealing the relationship between diabetes and AD.


greenmedinfo--2020-09-05--The Advances on the protective effects of ginsenosides on myocardial ischemia and ischemia-reperfusi

The Advances on the protective effects of ginsenosides on myocardial ischemia and ischemia-reperfusion injury.

Ginseng is a traditional medicine with a complex chemical composition , wide bioactivity and unique pharmacological action .
Many studies @ @ @ @ @ the active ingredients of ginseng , and ginsenosides have always been the focus of different @ @ @ @ @ of modern separation and analysis technology , more than 150 kinds of ginsenosides have been @ @ @ @ @ , Rb2 , Rc , Rg1 and Re account for more than 80 % of @ @ @ @ @ saponins , such as Rd , Rg3 and Rh2 , which are minor constituents , @ @ @ @ @ portion of the total amount .
In recent years , ginsenosides have been found to @ @ @ @ @ such as antioxidation , clearing of oxygen free radicals , reducing calcium overload and anti-apoptosis @ @ @ @ @ role in ischemia-reperfusion injury .
This paper reviews the protective effects of ginsenosides on myocardial @ @ @ @ @

Ginseng is a traditional medicine with a complex chemical composition, wide bioactivity and unique pharmacological action. Many studies have confirmed that ginsenosides are the active ingredients of ginseng, and ginsenosides have always been the focus of different researchers. With the development of modern separation and analysis technology, more than 150 kinds of ginsenosides have been isolated. The ginsenosides Rb1, Rb2, Rc, Rg1 and Re account for more than 80% of total ginsenosides, and other saponins, such as Rd, Rg3 and Rh2, which are minor constituents, account for only a small portion of the total amount. In recent years, ginsenosides have been found to possess strong pharmacological activities, such as antioxidation, clearing of oxygen free radicals, reducing calcium overload and anti-apoptosis. Ginsenosides play a protective role in ischemia-reperfusion injury. This paper reviews the protective effects of ginsenosides on myocardial ischemia and ischemia-reperfusion injury.


greenmedinfo--2020-09-05--These results suggest that ginsenosides Rb1 and Rg1 could improve the cognitive impairment.

This present study was designed to investigate the different effects of ginsenosides Rb1 and Rg1 on improving cognitive deficits in 4-month-old SAMP8 mice .
Mice were divided into six groups , including the SAMP8 group , the SAMP8 + Donepezil ( 1.6 mg/kg ) group , the SAMP8 + Rb1 ( 30 and 60µmol/kg ) , and SAMP8 + Rg1 ( 30 and 60 µmol/kg ) groups .
SAMR1 mice of the same age were used as the control group .
Ginsenosides and donepezil were administrated orally to animals for 8 weeks , then the learning and memory ability of @ @ @ @ @ @ @ maze ( MWM ) test , object recognition test and passive avoidance experiments .
The possible mechanisms were studied including the anti-glial inflammation of Rb1 and Rg1 using HE staining , immunohistochemistry and western blot experiments .
Results revealed that Rb1 and Rg1 treatment significantly improved the discrimination indexof SAMP8 mice in the object recognition test .
Rb1 ( 60 µmol/kg ) and Rg1 ( 30 , 60 µmol/kg ) could significantly shorten the escape latency in the acquisition test of the MWM test in SAMP8 mice .
Furthermore , Rb1 and Rg1 @ @ @ @ @ @ @ in the passive avoidance taskin SAMP8 mice .
Western blot experiments revealed that Rb1 showed higher effect than Rg1 in decreasing protein expression levels of ASC , caspase-1 and Aβ in the hippocampus of SAMP8 mice , while Rg1 was more effective than Rb1 in decreasing the protein levels of iNOS .
In addition , although Rb1 and Rg1 treatments showed significant protective effects in repairing neuronal cells loss and inhibiting the activation of astrocyte and microglia in hippocampus of SAMP8 mice , Rb1 was more effective than Rg1 .
These results suggest @ @ @ @ @ @ @ cognitive impairment in SAMP8 mice , andthey have different mechanisms for the treatment of Alzheimer 's disease .

This present study was designed to investigate the different effects of ginsenosides Rb1 and Rg1 on improving cognitive deficits in 4-month-old SAMP8 mice. Mice were divided into six groups, including the SAMP8 group, the SAMP8 + Donepezil (1.6 mg/kg) group, the SAMP8 + Rb1 (30 and 60µmol/kg), and SAMP8 + Rg1 (30 and 60 µmol/kg) groups. SAMR1 mice of the same age were used as the control group. Ginsenosides and donepezil were administrated orally to animals for 8 weeks, then the learning and memory ability of mice were measured by using Morris water maze (MWM) test, object recognition test and passive avoidance experiments. The possible mechanisms were studied including the anti-glial inflammation of Rb1 and Rg1 using HE staining, immunohistochemistry and western blot experiments. Results revealed that Rb1 and Rg1 treatment significantly improved the discrimination indexof SAMP8 mice in the object recognition test. Rb1 (60 µmol/kg) and Rg1 (30, 60 µmol/kg) could significantly shorten the escape latency in the acquisition test of the MWM test in SAMP8 mice. Furthermore, Rb1 and Rg1 treatments effectively reduced the number of errors in the passive avoidance taskin SAMP8 mice. Western blot experiments revealed that Rb1 showed higher effect than Rg1 in decreasing protein expression levels of ASC, caspase-1 and Aβ in the hippocampus of SAMP8 mice, while Rg1 was more effective than Rb1 in decreasing the protein levels of iNOS. In addition, although Rb1 and Rg1 treatments showed significant protective effects in repairing neuronal cells loss and inhibiting the activation of astrocyte and microglia in hippocampus of SAMP8 mice, Rb1 was more effective than Rg1. These results suggest that Rb1 and Rg1 could improve the cognitive impairment in SAMP8 mice, andthey have different mechanisms for the treatment of Alzheimer's disease.


greenmedinfo--2020-09-05--Ginsenoside Rb2 improves insulin resistance by inhibiting adipocyte pyroptosis.

Pyroptosis plays a critical role in the development of obesity-associated inflammation and insulin resistantance ( IR ) .
Ginsenoside Rb2 @ @ @ @ @ main component of ginsenosides has drawn appreciable interest in the context of glucose metabolism .
@ @ @ @ @ we investigated Rb2-mediated protection against obesity-induced IR and the related mechanisms .
Rb2 could significantly @ @ @ @ @ ) -induced body weight changes , fat accumulation and IR .
In addition , Rb2 @ @ @ @ @ proteins , such as caspase-1 , ASC , NLRP3 , IL-1β and GSDMD in HFD-fed @ @ @ @ @ were recapitulated in 3T3-L1 adipocytes and demonstrated that Rb2 improved TNF-α induced IR and pyroptosis @ @ @ @ @ , Rb2 reduced the phosphorylation levels of p65 and IκBα both in vitro and in @ @ @ @ @ showedthat Rb2 , which could serve as a promising agent for the treatment of IR @ @ @ @ @ by inhibiting pyroptosis in adipocytes in vivo and in vitro through the NF-κB pathway .

Pyroptosis plays a critical role in the development of obesity-associated inflammation and insulin resistantance (IR). Ginsenoside Rb2 (Rb2), the main component of ginsenosides has drawn appreciable interest in the context of glucose metabolism. In the present study, we investigated Rb2-mediated protection against obesity-induced IR and the related mechanisms. Rb2 could significantly reduce high-fat diet (HFD)-induced body weight changes, fat accumulation and IR. In addition, Rb2 treatment inhibited pyroptosis-related genes and proteins, such as caspase-1, ASC, NLRP3, IL-1β and GSDMD in HFD-fed mice. The above results were recapitulated in 3T3-L1 adipocytes and demonstrated that Rb2 improved TNF-α induced IR and pyroptosis in 3T3-L1 adipocytes. Furthermore, Rb2 reduced the phosphorylation levels of p65 and IκBα both in vitro and in vivo. The present study showedthat Rb2, which could serve as a promising agent for the treatment of IR and obesity, ameliorated IR by inhibiting pyroptosis in adipocytes in vivo and in vitro through the NF-κB pathway.


greenmedinfo--2020-09-05--Green Coffee Extract Benefits Weight Control

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greenmedinfo--2020-09-05--The protective effect of ginsenoside Rg1 on depression may benefit from the gap junction function in

The protective effect of ginsenoside Rg1 on depression may benefit from the gap junction function in hippocampal astrocytes.

Studies have shown that the ginsenoside Rg1 can improve depressive symptoms in vitro and in vivo .
However , the efficacy of Rg1on the hippocampal astrocyte gap junctions in depression are unclear .
We mainly aimed to explore the relationship between Rg1 , hippocampal astrocyte gap junctions and depression .
Using primary cultured astrocytes , corticosterone ( CORT ) was used to induce stress .
CORT ( 100 μM ) significantly reduced the survival rate in astrocytes , and this effect was prevented by additional Rg1 administration .
Interestingly , the gap junction blocker carbenoxolone ( CBX ) was able @ @ @ @ @ @ @ in vivo models , one group was exposed to chronic unpredictable stress ( CUS ) for 47 days , while another group was bilaterally injected with CBX ( 100 μM ) into the hippocampal CA1 region .
Rats treated with Rg1 ( 20 mg/kg ) showed an improvement in the sucrose preference and the forced swimming test in both models , indicating an antidepressive activity of Rg1 .
The levels of astrocyte gap junction connexin 43 ( Cx43 ) were detected by immunofluorescence ( IF ) and western blotting .
The levels of @ @ @ @ @ @ @ were detected by IF .
The gap junctions in the hippocampal CA1 area were evaluated using dye transfer and electron microscopy .
The reduction inCx43 expression , the decrease in the Cx43 to GFAP ratio , the shorter dye diffusion distance , and the abnormal ultrastructure of gap junctions in rats exposed to CUS were markedly alleviated by concomitant Rg1 treatment .
Taken together , the ginsenoside Rg1 could improve depression-like behavior in rats induced by astrocyte gap junction dysfunction in the hippocampus .

Studies have shown that the ginsenoside Rg1 can improve depressive symptoms in vitro and in vivo. However, the efficacy of Rg1on the hippocampal astrocyte gap junctions in depression are unclear. We mainly aimed to explore the relationship between Rg1, hippocampal astrocyte gap junctions and depression. Using primary cultured astrocytes, corticosterone (CORT) was used to induce stress. CORT (100 μM) significantly reduced the survival rate in astrocytes, and this effect was prevented by additional Rg1 administration. Interestingly, the gap junction blocker carbenoxolone (CBX) was able to revert this Rg1 effect. In in vivo models, one group was exposed to chronic unpredictable stress (CUS)for 47 days, while another group was bilaterally injected with CBX (100 μM) into the hippocampal CA1 region. Rats treated with Rg1 (20 mg/kg) showed an improvement in the sucrose preference and the forced swimming test in both models, indicating an antidepressive activity of Rg1. The levels of astrocyte gap junction connexin 43 (Cx43) were detected by immunofluorescence (IF) and western blotting. The levels of glial fibrillary acidic protein (GFAP) were detected by IF. The gap junctions in the hippocampal CA1 area were evaluated using dye transfer and electron microscopy. The reduction inCx43 expression, the decrease in the Cx43 to GFAP ratio, the shorter dye diffusion distance, and the abnormal ultrastructure of gap junctions in rats exposed to CUS were markedly alleviated by concomitant Rg1 treatment. Taken together, the ginsenoside Rg1 could improve depression-like behavior in rats induced by astrocyte gap junction dysfunction in the hippocampus.


greenmedinfo--2020-09-05--The effect of Ginsenoside Rg1 in hepatic ischemia reperfusion (I/R) injury ameliorates ischemia-repe

The effect of Ginsenoside Rg1 in hepatic ischemia reperfusion (I/R) injury ameliorates ischemia-reperfusion-induced liver injury by inhibiting apoptosis.

Hepatic ischemia reperfusion ( I/R ) injury ( HIRI ) HIRI is a complex , multifactorial pathophysiological process and in liver surgery has been known to significantly affect disease prognosis , surgical success rates , and patient survival .
Ginsenoside Rgl ( Rgl ) monomer is one of the main active ingredients of ginseng .
Previous studies have demonstrated that Rgl exerts various pharmacological effects through several mechanisms including suppression of apoptosis-related proteins levels , downregulation of inflammatory mediators and as well as antioxidant , which effectively exerts an organ protective effect I/R-induced damage .
However , the exact mechanisms @ @ @ @ @ @ @ elucidated .
In the present study , we investigated the protective effect of Rg1 on hepatic ischemia-reperfusion ( I/R ) injury ( HIRI ) and explored its underlying molecular mechanism .
A rat warm I/R injury model in vivo and an oxygen-glucose deprivation/reperfusion ( OGD/R ) -treated BRL-3A cell model in vitro were established after pretreating with Rg1 ( 20 mg/kg ) .
The results showed that Rg1 reduced the levels of alanine aminotransferase ( ALT ) and aspartate aminotransferase ( AST ) .
TUNEL staining showed that pretreated with Rg1 inhibited the @ @ @ @ @ @ @ .
Moreover , pretreated with Rg1 significantly reduced the expression of Cyt-C , Caspase-9 and Caspase-3 to inhibit the cell apoptosis .
Flow cytometry analysis showed the MMP in the I/R group was significantly increased , whereas pretreated with Rg1 effectively stabilized the MMP compared with the I/R group .
in vitro , the proliferation of BRL-3A cells was significantly decreased by the OGD/R treatment , while Rg1 effectively reversed this phenomenon .
In addition , western blotting showed that the increase of Cyt-C , Caspase-9 and Caspase-3 was inhibited by HO .
@ @ @ @ @ @ @ protective effect by inhibiting the CypD protein-mediated mitochondrial apoptotic pathway .

Hepatic ischemia reperfusion (I/R) injury (HIRI) HIRI is a complex, multifactorial pathophysiological process and in liver surgery has been known to significantly affect disease prognosis, surgical success rates, and patient survival. Ginsenoside Rgl (Rgl) monomer is one of the main active ingredients of ginseng. Previous studies have demonstrated that Rgl exerts various pharmacological effects through several mechanisms including suppression of apoptosis-related proteins levels, downregulation of inflammatory mediators and as well as antioxidant, which effectively exerts an organ protective effect I/R-induced damage. However, the exact mechanisms of Rg1 on HIRI remain to be elucidated. In the present study, we investigated the protective effect of Rg1 on hepatic ischemia-reperfusion (I/R) injury (HIRI) and explored its underlying molecular mechanism. A rat warm I/R injury model in vivo and an oxygen-glucose deprivation/reperfusion (OGD/R)-treated BRL-3A cell model in vitro were established after pretreating with Rg1(20 mg/kg). The results showed that Rg1 reduced the levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST). TUNEL staining showed that pretreated with Rg1 inhibited the apoptosis rate compared with the I/R group. Moreover, pretreated with Rg1 significantly reduced the expression of Cyt-C, Caspase-9 and Caspase-3 to inhibit the cell apoptosis. Flow cytometry analysis showed the MMP in the I/R group was significantly increased, whereas pretreated with Rg1 effectively stabilized the MMP compared with the I/R group. in vitro, the proliferation of BRL-3A cells was significantly decreased by the OGD/R treatment, while Rg1 effectively reversed this phenomenon. In addition, western blotting showed that the increase of Cyt-C, Caspase-9 and Caspase-3 was inhibited by HO. These observations suggest that Rg1 exerts the protective effect by inhibiting the CypD protein-mediated mitochondrial apoptotic pathway.


greenmedinfo--2020-09-05--Antidepressant effects of ginsenoside Rf on behavioral change in the glial degeneration model of dep

Antidepressant effects of ginsenoside Rf on behavioral change in the glial degeneration model of depression by reversing glial loss.

Background : Depression is a common neuropsychiatric disease that shows astrocyte pathology .
Ginsenoside Rf ( G-Rf ) is a saponin found inwhich has been used to treat neuropsychiatric diseases .
We aimed to investigate antidepressant properties of G-Rf when introduced into the L-alpha-aminoadipic acid ( L-AAA ) -infused mice model which is representative of a major depressive disorder that features diminished astrocytes in the brain .
Methods : L-AAA was infused into the prefrontal cortex ( PFC ) of mice to induce decrease of astrocytes .
Mice were orally administered G-Rf ( 20 mg/kg ) as well as vehicle @ @ @ @ @ @ @ as controls .
Depression-like behavior of mice was evaluated using forced swimming test ( FST ) and tail suspension test ( TST ) .
We observed recovery of astroglial impairment and increased proliferative cells in the PFC and its accompanied change in the hippocampus by Western blot and immunohistochemistry to assess the effect of G-Rf .
Results : After injection of L-AAA into the PFC , mice showed increased immobility time in FST and TST and loss of astrocytes without significant neuronal change in the PFC .
G-Rf-treated mice displayed significantly more decreased @ @ @ @ @ @ @ did vehicle-treated mice , and their immobility time almost recovered to those of the sham mice and imipramine-treated mice .
G-Rf upregulated glial fibrillary acidic protein ( GFAP ) expression and Ki-67 expression in the PFC reduced by L-AAA and also alleviated astroglial change in the hippocampus .
Conclusion : G-Rf markedly reversed depression-like behavioral changes and exhibited protective effect against the astrocyte ablation in the PFC induced by L-AAA .
These protective properties suggest that G-Rf might be a therapeutic agent for major depressive disorders .

Background: Depression is a common neuropsychiatric disease that shows astrocyte pathology. Ginsenoside Rf (G-Rf) is a saponin found inwhich has been used to treat neuropsychiatric diseases. We aimed to investigate antidepressant properties of G-Rf when introduced into the L-alpha-aminoadipic acid (L-AAA)-infused mice model which is representative of a major depressive disorder that features diminished astrocytes in the brain.
Methods: L-AAA was infused into the prefrontal cortex (PFC) of mice to induce decrease of astrocytes. Mice were orally administered G-Rf (20 mg/kg) as well as vehicle only or imipramine (20 mg/kg) as controls. Depression-like behavior of mice was evaluated using forced swimming test (FST) and tail suspension test (TST). We observed recovery of astroglial impairment and increased proliferative cells in the PFC and its accompanied change in the hippocampus by Western blot and immunohistochemistry to assess the effect of G-Rf.
Results: After injection of L-AAA into the PFC, mice showed increased immobility time in FST and TST and loss of astrocytes without significant neuronal change in the PFC. G-Rf-treated mice displayed significantly more decreased immobility time in FST and TST than did vehicle-treated mice, and their immobility time almost recovered to those of the sham mice and imipramine-treated mice. G-Rf upregulated glial fibrillary acidic protein (GFAP) expression and Ki-67 expression in the PFC reduced by L-AAA and also alleviated astroglial change in the hippocampus.
Conclusion: G-Rf markedly reversed depression-like behavioral changes and exhibited protective effect against the astrocyte ablation in the PFC induced by L-AAA. These protective properties suggest that G-Rf might be a therapeutic agent for major depressive disorders.


greenmedinfo--2020-09-05--Biological effects of Korean red ginseng polysaccharides in aged rat using global proteomic approach

Biological effects of Korean red ginseng polysaccharides in aged rat using global proteomic approach.

Much has been written on the physiological benefits of Korean Red Ginseng ( KRG ) .
Among its various components , ginsenosides have been widely investigated for their various pharmacological effects .
However , polysaccharides are a major KRG component that has not received scrutiny similar to that of ginsenosides .
The present study aims to fill that gap in the existing literature and to investigate the possible functions of polysaccharide in KRG .
The researchers evaluated proteomic changes in non-saponin fractions with rich polysaccharides ( NFP ) in KRG .
Based on the serum analysis , proteomics analysis of @ @ @ @ @ @ @ conducted to identify related functions .
We validated the suggested functions of NFP with the galactosamine-induced liver injury model and the cyclophosphamide-induced immunosuppression model .
Then , we evaluated the antimetastatic potential of NFP in the lungs .
Further proteomics analysis of the spleen and liver after ingestion confirmed functions related to immunity , cancer , hepatoprotection , and others .
Then , we validated the suggested corresponding functions of the NFP in vivo model .
NFP showed immune-enhancing effects , inhibited melanoma cell metastasis in the lung , and decreased liver damage @ @ @ @ @ @ @ proteomic approach uncovers the potential effects of polysaccharides in KRG , which include enhancing the immune system and protecting the liver .

Much has been written on the physiological benefits of Korean Red Ginseng (KRG). Among its various components, ginsenosides have been widely investigated for their various pharmacological effects. However, polysaccharides are a major KRG component that has not received scrutiny similar to that of ginsenosides. The present study aims to fill that gap in the existing literature and to investigate the possible functions of polysaccharide in KRG. The researchers evaluated proteomic changes in non-saponin fractions with rich polysaccharides (NFP) in KRG. Based on the serum analysis, proteomics analysis of the liver and the spleen was additionally conducted to identify related functions. We validated the suggested functions of NFP with the galactosamine-induced liver injury model and the cyclophosphamide-induced immunosuppression model. Then, we evaluated the antimetastatic potential of NFP in the lungs. Further proteomics analysis of the spleen and liver after ingestion confirmed functions related to immunity, cancer, hepatoprotection, and others. Then, we validated the suggested corresponding functions of the NFP in vivo model. NFP showed immune-enhancing effects, inhibited melanoma cell metastasis in the lung, and decreased liver damage. The results show that using the proteomic approach uncovers the potential effects of polysaccharides in KRG, which include enhancing the immune system and protecting the liver.


greenmedinfo--2020-09-05--Ginsenoside compound-Mc1 attenuates oxidative stress and apoptosis in cardiomyocytes.

Background : Ginsenoside compound-Mc1 ( Mc1 ) is a member of the deglycosylated ginsenosides obtained from ginseng extract .
Although several ginsenosides have a cardioprotective effect , this has not been demonstrated in ginsenoside Mc1 .
Methods : We treated H9c2 cells with hydrogen peroxide ( HO ) and ginsenoside Mc1 to evaluate the antioxidant effects of Mc1 .
The levels of antioxidant molecules , catalase , and superoxide dismutase 2 ( SOD2 ) were measured , and cell viability was determined using the Bcl2-associated X protein ( Bax ) : B-cell lymphoma-extra large ratio , a cytotoxicity assay , @ @ @ @ @ @ @ with high-fat diet ( HFD ) -induced obesity using ginsenoside Mc1 and assessed their heart tissues to evaluate theantioxidant effect and the fibrosis-reducing capability of ginsenoside Mc1 .
Results : Ginsenoside Mc1 significantly increased the level of phosphorylated AMP-activated protein kinase ( AMPK ) in the H9c2 cells .
The expression levels of catalase and SOD2 increased significantly after treatment with ginsenoside Mc1 , resulting in a decrease in the production of HO-mediated reactive oxygen species .
Treatment with ginsenoside Mc1 also significantly reduced the HO-mediated elevation of the Bax : Bcl2 ratio @ @ @ @ @ @ @ which was significantly attenuated by treatment with an AMPK inhibitor .
Consistent with thedata , ginsenoside Mc1 upregulated the levels of catalase and SOD2 and decreased the Bax : B-cell lymphoma-extra large ratio and caspase-3 activity in the heart tissues of HFD-induced obese mice , resulting in reduced collagen deposition .
Conclusion : Ginsenoside Mc1 decreases oxidative stress and increases cell viability in H9c2 cells and the heart tissue isolated from HFD-fed mice via an AMPK-dependent mechanism , suggesting its potential as a novel therapeutic agent for oxidative stress-related cardiac diseases .

Background: Ginsenoside compound-Mc1 (Mc1) is a member of the deglycosylated ginsenosides obtained from ginseng extract. Although several ginsenosides have a cardioprotective effect, this has not been demonstrated in ginsenoside Mc1.
Methods: We treated H9c2 cells with hydrogen peroxide (HO) and ginsenoside Mc1 to evaluate the antioxidant effects of Mc1. The levels of antioxidant molecules, catalase, and superoxide dismutase 2 (SOD2) were measured, and cell viability was determined using the Bcl2-associated X protein (Bax):B-cell lymphoma-extra large ratio, a cytotoxicity assay, and flow cytometry. We generated mice with high-fat diet (HFD)-induced obesity using ginsenoside Mc1 and assessed their heart tissues to evaluate theantioxidant effect and the fibrosis-reducing capability of ginsenoside Mc1.
Results: Ginsenoside Mc1 significantly increased the level of phosphorylated AMP-activated protein kinase (AMPK) in the H9c2 cells. The expression levels of catalase and SOD2 increased significantly after treatment with ginsenoside Mc1, resulting in a decrease in the production of HO-mediated reactive oxygen species. Treatment with ginsenoside Mc1 also significantly reduced the HO-mediated elevation of the Bax:Bcl2 ratio and the number of DNA-damaged cells, which was significantly attenuated by treatment with an AMPK inhibitor. Consistent with thedata, ginsenoside Mc1 upregulated the levels of catalase and SOD2 and decreased the Bax:B-cell lymphoma-extra large ratio and caspase-3 activity in the heart tissues of HFD-induced obese mice, resulting in reduced collagen deposition.
Conclusion: Ginsenoside Mc1 decreases oxidative stress and increases cell viability in H9c2 cells and the heart tissue isolated from HFD-fed mice via an AMPK-dependent mechanism, suggesting its potential as a novel therapeutic agent for oxidative stress-related cardiac diseases.


greenmedinfo--2020-09-05--Rare ginsenoside 20(R)-Rg3 inhibits D-galactose-induced liver and kidney injury by regulating oxidat

Rare ginsenoside 20(R)-Rg3 inhibits D-galactose-induced liver and kidney injury by regulating oxidative stress-induced apoptosis.

Oxidative stress is considered as a major factor in aging and exacerbates aging process through a variety of molecular mechanisms .
D-galactose , a normal reducing sugar with high dose can cause the accumulation of reactive oxygen species ( ROS ) or stimulate free radical production indirectly by the formation of advanced glycation end products in tissues , finally resulting in oxidative stress .
20 ( R ) -ginsenoside Rg3 ( 20 ( R ) -Rg3 ) , a major and representative component isolated from red ginseng ( C.A Meyer ) , has been shown to observably have an anti-oxidative @ @ @ @ @ @ @ effects of 20 ( R ) -Rg3 on D-galactose-induced oxidative stress injury and its underlying mechanisms .
Our results showed that continuous injection of D-galactose with 800 [ Formula : see text ] mg/kg/day for 8 weeks increased the levels of alanine aminotransferase ( ALT ) and blood urea nitrogen ( BUN ) .
However , such increases were attenuated by the treatment of 20 ( R ) -Rg3 for 4 weeks .
Meanwhile , 20 ( R ) -Rg3 markedly inhibited D-galactose-caused oxidative stress in liver and kidney .
The anti-oxidants , @ @ @ @ @ @ @ dismutase ( SOD ) , were elevated in the mice from 20 ( R ) -Rg3-treated group compared with that from D-galactose group .
In contrast , a significant decrease in levels of cytochrome P450 E1 ( CYP2E1 ) and the lipid peroxidation product malondialdehyde ( MDA ) and 4-hydroxynonenal ( 4-HNE ) were observed in the 20 ( R ) -Rg3-treated group .
These effects were associated with a significant increase of AGEs .
More importantly , 20 ( R ) -Rg3 effectively attenuated D-galactose induced apoptosis in liver and kidney via @ @ @ @ @ @ @ Taken together , our study suggests that 20 ( R ) -Rg3 may be a novel and promising anti-oxidative therapeutic agent to prevent aging-related injuries in liver and kidney .

Oxidative stress is considered as a major factor in aging and exacerbates aging process through a variety of molecular mechanisms. D-galactose, a normal reducing sugar with high dose can cause the accumulation of reactive oxygen species (ROS) or stimulate free radical production indirectly by the formation of advanced glycation end products in tissues, finally resulting in oxidative stress. 20(R)-ginsenoside Rg3 (20(R)-Rg3), a major and representative component isolated from red ginseng (C.A Meyer), has been shown to observably have an anti-oxidative effect. We thereby investigated the beneficial effects of 20(R)-Rg3 on D-galactose-induced oxidative stress injury and its underlying mechanisms. Our results showed that continuous injection of D-galactose with 800[Formula: see text]mg/kg/day for 8 weeks increased the levels of alanine aminotransferase (ALT) and blood urea nitrogen (BUN). However, such increases were attenuated by the treatment of 20(R)-Rg3 for 4 weeks. Meanwhile, 20(R)-Rg3 markedly inhibited D-galactose-caused oxidative stress in liver and kidney. The anti-oxidants, including catalase (CAT) and superoxide dismutase (SOD), were elevated in the mice from 20(R)-Rg3-treated group compared with that from D-galactose group. In contrast, a significant decrease in levels of cytochrome P450 E1 (CYP2E1) and the lipid peroxidation product malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE) were observed in the 20(R)-Rg3-treated group. These effects were associated with a significant increase of AGEs. More importantly, 20(R)-Rg3 effectively attenuated D-galactose induced apoptosis in liver and kidney via restoring the upstream PI3K/AKT signaling pathway. Taken together, our study suggests that 20(R)-Rg3 may be a novel and promising anti-oxidative therapeutic agent to prevent aging-related injuries in liver and kidney.


greenmedinfo--2020-09-05--New insight into 20(S)-ginsenoside Rh2 against T-cell acute lymphoblastic leukemia associated with t

New insight into 20(S)-ginsenoside Rh2 against T-cell acute lymphoblastic leukemia associated with the gut microbiota and the immune system.

T-cell acute lymphoblastic leukemia ( T-ALL ) is a hematopoietic malignancy associated with unfavorable factors including male gender and over nine years of age .
Chemotherapy toxicity continues to present a major challenge .
There is a need to develop novel natural agents to improve survival and quality of life in patients with T-ALL .
20 ( S ) -ginsenoside Rh2 ( GRh2 ) exhibits immune regulation and anti-tumor effects in both cellular and murine xenograft models .
In the present study , the anti-cancer mechanisms of 20 ( S ) -GRh2 involved in the immune system and intestinal microbiota @ @ @ @ @ @ @ revealed that 20 ( S ) -Rh2 suppressed T-ALL by blocking the PI3K/Akt/mTOR signaling pathway , and enhanced immunity in the spleen by regulating immune factors .
In addition , 20 ( S ) -GRh2 altered the composition of the gut microbiota , and promoted intestinal homeostasis by elevating the levels of tight junction proteins , antimicrobial peptides and IgA .
20 ( S ) -GRh2 ameliorated the LPS-induced inflammatory response in the intestine of T-ALL mice .
Furthermore , Bacteroidetes , Verrucomicrobia , Akkermansia , Lactobacillus , and Lachnospiraceae_NK4A136_group were positively correlated @ @ @ @ @ @ @ factors , and the anti-inflammatory response .
Conversely , Firmicutes , Proteobacteria , Parabacteroides and Alistipes had the opposite correlation .
Collectively , these results suggest that 20 ( S ) -GRh2 is a safe and effective natural product , that shows promise for the prevention and treatment of T-ALL .

T-cell acute lymphoblastic leukemia (T-ALL) is a hematopoietic malignancy associated with unfavorable factors including male gender and over nine years of age. Chemotherapy toxicity continues to present a major challenge. There is a need to develop novel natural agents to improve survival and quality of life in patients with T-ALL. 20(S)-ginsenoside Rh2 (GRh2) exhibits immune regulation and anti-tumor effects in both cellular and murine xenograft models. In the present study, the anti-cancer mechanisms of 20(S)-GRh2 involved in the immune system and intestinal microbiota were investigated in T-ALL mice. We revealed that 20(S)-Rh2 suppressed T-ALL by blocking the PI3K/Akt/mTOR signaling pathway, and enhanced immunity in the spleen by regulating immune factors. In addition, 20(S)-GRh2 altered the composition of the gut microbiota, and promoted intestinal homeostasis by elevating the levels of tight junction proteins, antimicrobial peptides and IgA. 20(S)-GRh2 ameliorated the LPS-induced inflammatory response in the intestine of T-ALL mice. Furthermore, Bacteroidetes, Verrucomicrobia, Akkermansia, Lactobacillus, and Lachnospiraceae_NK4A136_group were positively correlated with anti-tumor immune factors, intestinal barrier-related factors, and the anti-inflammatory response. Conversely, Firmicutes, Proteobacteria, Parabacteroides and Alistipes had the opposite correlation. Collectively, these results suggest that 20(S)-GRh2 is a safe and effective natural product, that shows promise for the prevention and treatment of T-ALL.


greenmedinfo--2020-09-05--Ginsenoside Rd reverses cognitive deficits by modulating BDNF-dependent CREB pathway in chronic rest

Ginsenoside Rd reverses cognitive deficits by modulating BDNF-dependent CREB pathway in chronic restraint stress.

Cognitive impairment has been widely recognized as a common symptom of chronic stress .
Ginsenoside Rd ( GRd ) , the major active compound in Panax ginseng , was previously reported in various neurological researches .
However , little research is available regarding on the effect of GRd on cognitive improvement in mice subjected to chronic stress .
In the present study , we investigated the neuroprotective effects of GRd in chronic restraint stress ( CRS ) -induced cognitive deficits and explored the potential mechanism in male C57BL/6J mice .
Our results demonstrated that oral administration of GRd for 28 @ @ @ @ @ @ @ Y-maze and the relative discrimination index in novel object or location recognition tests following CRS .
Additionally , GRd treatment considerably increased the antioxidant enzymes activities in the hippocampus .
The expression levels of hippocampus and serum inflammation factors in the CRS groups were also counter-regulated by GRd treatment .
Meanwhile , GRd treatment could reverse CRS-induced the decrease in phosphorylated phosphoinositide 3-kinase ( PI3K ) , camp-reflecting element binding protein ( CREB ) , brain-derived neurotrophic factor ( BDNF ) and tyrosine kinase B ( TrkB ) expression in the hippocampus .
@ @ @ @ @ @ @ cognitive impairment in CRS mice by mitigating oxidative stress and inflammation , while upregulating the hippocampal BDNF-mediated CREB signaling pathway .

Cognitive impairment has been widely recognized as a common symptom of chronic stress. Ginsenoside Rd (GRd), the major active compound in Panax ginseng, was previously reported in various neurological researches. However, little research is available regarding on the effect of GRd on cognitive improvement in mice subjected to chronic stress. In the present study, we investigated the neuroprotective effects of GRd in chronic restraint stress (CRS)-induced cognitive deficits and explored the potential mechanism in male C57BL/6J mice. Our results demonstrated that oral administration of GRd for 28 days markedly increased the spontaneous alternation in Y-maze and the relative discrimination index in novel object or location recognition tests following CRS. Additionally, GRd treatment considerably increased the antioxidant enzymes activities in the hippocampus. The expression levels of hippocampus and serum inflammation factors in the CRS groups were also counter-regulated by GRd treatment. Meanwhile, GRd treatment could reverse CRS-induced the decrease in phosphorylated phosphoinositide 3-kinase (PI3K), camp-reflecting element binding protein (CREB), brain-derived neurotrophic factor (BDNF) and tyrosine kinase B (TrkB) expression in the hippocampus. These findings provided evidences that GRd improves cognitive impairment in CRS mice by mitigating oxidative stress and inflammation, while upregulating the hippocampal BDNF-mediated CREB signaling pathway.


greenmedinfo--2020-09-05--Ginsenoside Rh1 alleviated HK-2 apoptosis in a cisplatin-induced injury model.

Background : Cisplatin is widely used in the treatment of malignant patients ; however , its adverse nephrotoxic effects limit its clinical use .
Ginsenoside Rh1 is a main component of ginseng and has many pharmaceutical effects , including immunomodulatory effects .
Objective : The objective of this research is to assess the effects of ginsenoside Rh1 on a cisplatin-induced HK-2 injury model and to study its potential effect mechanisms .
Methods : HK-2 cell vitality was assessed via Cell Counting Kit-8 ( CCK-8 ) assay .
Carboxyfluorescein succinimidyl ester/propidium iodide ( CFSF/PI ) staining was used to detect the @ @ @ @ @ @ @ was detected by DCFDA .
The expressions of JNK , p53 , caspase-3 , Bax , and NGAL were detected by western blot .
Results : Ginsenoside Rh1 was found to increase the vitality of HK-2 cells and inhibit ROS production and the apoptosis of HK-2 cells in a cisplatin-induced injury model .
Ginsenoside Rh1 was found to inhibit the expression of JNK , p53 , caspase-3 , Bax , and NGAL in a cisplatin-induced injury model .
Conclusion : Ginsenoside Rh1 alleviated HK-2 apoptosis in a cisplatin-induced injury model by inhibiting ROS @ @ @ @ @ @ @ Rh1 may be a promising drug for the alleviation of cisplatin-induced nephrotoxicity in malignant patients .

Background: Cisplatin is widely used in the treatment of malignant patients; however, its adverse nephrotoxic effects limit its clinical use. Ginsenoside Rh1 is a main component of ginseng and has many pharmaceutical effects, including immunomodulatory effects.
Objective: The objective of this research is to assess the effects of ginsenoside Rh1 on a cisplatin-induced HK-2 injury model and to study its potential effect mechanisms.
Methods: HK-2 cell vitality was assessed via Cell Counting Kit-8 (CCK-8) assay. Carboxyfluorescein succinimidyl ester/propidium iodide (CFSF/PI) staining was used to detect the apoptosis of HK-2 cells. ROS expression was detected by DCFDA. The expressions of JNK, p53, caspase-3, Bax, and NGAL were detected by western blot.
Results: Ginsenoside Rh1 was found to increase the vitality of HK-2 cells and inhibit ROS production and the apoptosis of HK-2 cells in a cisplatin-induced injury model. Ginsenoside Rh1 was found to inhibit the expression of JNK, p53, caspase-3, Bax, and NGAL in a cisplatin-induced injury model.
Conclusion: Ginsenoside Rh1 alleviated HK-2 apoptosis in a cisplatin-induced injury model by inhibiting ROS production and the JNK/p53 pathway. Ginsenoside Rh1 may be a promising drug for the alleviation of cisplatin-induced nephrotoxicity in malignant patients.


greenmedinfo--2020-09-05--Anticancer property of ginsenoside Rh2 from ginseng

Ginseng has been used as a well-known traditional Chinese medicine since ancient times .
Ginsenosides as its main active constituents possess a broad scope of pharmacological properties including stimulating immune function , enhancing cardiovascular health , increasing resistance to stress , improving memory and learning , developing social functioning and mental health in normal persons , and chemotherapy .
Ginsenoside Rh2 ( Rh2 ) is one of the major bioactive ginsenosides from Panax ginseng .
When applied to cancer treatment , Rh2 not only exhibits the anti-proliferation , anti-invasion , anti-metastasis , induction of cell cycle arrest , promotion of @ @ @ @ @ @ @ activities against multiple tumor cells , but also alleviates the side effects after chemotherapy or radiotherapy .
In the past decades , nearly 200 studies on Rh2 in the treatment of cancer have been published , however no specific reviews have been conducted by now .
So the purpose of this review is to provide a systematic summary and analysis of the anticancer effects and the potential mechanisms of Rh2 extracted from Ginseng then give a future prospects about it .
In the end of this paper the metabolism and derivatives of Rh2 @ @ @ @ @

Ginseng has been used as a well-known traditional Chinese medicine since ancient times. Ginsenosides as its main active constituents possess a broad scope of pharmacological properties including stimulating immune function, enhancing cardiovascular health, increasing resistance to stress, improving memory and learning, developing social functioning and mental health in normal persons, and chemotherapy. Ginsenoside Rh2 (Rh2) is one of the major bioactive ginsenosides from Panax ginseng. When applied to cancer treatment, Rh2 not only exhibits the anti-proliferation, anti-invasion, anti-metastasis, induction of cell cycle arrest, promotion of differentiation, and reversal of multi-drug resistance activities against multiple tumor cells, but also alleviates the side effects after chemotherapy or radiotherapy. In the past decades, nearly 200 studies on Rh2 in the treatment of cancer have been published, however no specific reviews have been conducted by now. So the purpose of this review is to provide a systematic summary and analysis of the anticancer effects and the potential mechanisms of Rh2 extracted from Ginseng then give a future prospects about it. In the end of this paper the metabolism and derivatives of Rh2 also have been documented.


greenmedinfo--2020-09-05--Ginsenoside Rg2 attenuates myocardial fibrosis and improves cardiac function after myocardial infarc

Ginsenoside Rg2 attenuates myocardial fibrosis and improves cardiac function after myocardial infarction.

: With the popularization of percutaneous coronary intervention technology in clinical applications , the mortality rate of acute myocardial infarction @ @ @ @ @ However , ventricular remodeling following myocardial infarction ( MI ) has attracted extensive attention for @ @ @ @ @ arrhythmia , heart failure , and even death .
We aimed to investigate the effects @ @ @ @ @ function and myocardial fibrosis after MI and its potential mechanism .
The results demonstrated that @ @ @ @ @ and inhibited collagen deposition in mice after MI .
In addition , ginsenoside Rg2 reduced @ @ @ @ @ Collagen I ( Col 1 ) , Collagen III ( Col 3 ) , and @ @ @ @ @ ) by activating phosphorylated AKT in angiotensin II-induced cardiac fibroblasts .
Taken together , ginsenoside @ @ @ @ @ attenuates cardiac fibrosis via the AKT pathway , suggesting that ginsenoside Rg2 may be a @ @ @ @ @ of ventricular remodelingafter MI .

: With the popularization of percutaneous coronary intervention technology in clinical applications, the mortality rate of acute myocardial infarction has been significantly reduced. However, ventricular remodeling following myocardial infarction (MI) has attracted extensive attention for that it can cause malignant arrhythmia, heart failure, and even death. We aimed to investigate the effects of ginsenoside Rg2 on cardiac function and myocardial fibrosis after MI and its potential mechanism. The results demonstrated that ginsenoside Rg2 improved cardiac function and inhibited collagen deposition in mice after MI. In addition, ginsenoside Rg2 reduced the levels of fibrosis-associated genes Collagen I (Col 1), Collagen III (Col 3), and alpha-smooth muscle actin (α-SMA) by activating phosphorylated AKT in angiotensin II-induced cardiac fibroblasts. Taken together, ginsenoside Rg2 improves cardiac function and attenuates cardiac fibrosis via the AKT pathway, suggesting that ginsenoside Rg2 may be a promising drug for the prevention of ventricular remodelingafter MI.
ABBREVIATIONS: MI: myocardial infarction; AMI: acute myocardial infarction; LAD: left anterior descending; ECM: extracellular matrix; Col 1: collagen I; Col 3: collagen III;α-SMA: alpha-smooth muscle actin; ROS: reactive oxygen species; SOD: superoxide dismutase; GSH: glutathione; HO-1: heme oxygenase-1; WST8: water-soluble tetrazolium salt 8.


greenmedinfo--2020-09-05--Ginsenoside Rg1 prevent and treat inflammatory diseases.

Ginseng has been used as reinforcing drugs or for traditional Chinese medicine in aging , inflammation , stress , diabetes mellitus , hepatic diseases and cancer .
The aim of this current review is to provide an integrative overview of the uses , relative human diseases and related mechanisms of ginseng .
Nowadays , numerous animal experiments and clinical studies conducted to investigate the efficacy and safety of ginseng components .
Inflammation is an immune response that protects human from pathogens , toxins and other dangers , which is initiated by recognizing pathogen- or danger- associated molecular patterns .
Inflammasomes @ @ @ @ @ @ @ response to challenges , which also controls the activity of caspase-1 , important for maturation and release of cytokines .
Ice protease-activating factor , oligomerization domain-like receptor family pyrin domain-containing 1 and absent in melanoma 2 inflammasome recognize peculiar substances , while NLRP3 inflammasome responds towards structurally and chemically diverse triggers .
The functional relationship between ginsenosides and inflammasome provides new insight into the understanding of molecular mechanisms of ginsenoside-mediated anti-inflammatory actions .
It also has applications regarding the development of anti-inflammatory remedies by ginsenoside-mediated targeting inflammasomes , which could prevent and treat @ @ @

Ginseng has been used as reinforcing drugs or for traditional Chinese medicine in aging, inflammation, stress, diabetes mellitus, hepatic diseases and cancer. The aim of this current review is to provide an integrative overview of the uses, relative human diseases and related mechanisms of ginseng. Nowadays, numerous animal experiments and clinical studies conducted to investigate the efficacy and safety of ginseng components. Inflammation is an immune response that protects human from pathogens, toxins and other dangers, which is initiated by recognizing pathogen- or danger- associated molecular patterns. Inflammasomes are cytosolic protein complexes which form in response to challenges, which also controls the activity of caspase-1, important for maturation and release of cytokines. Ice protease-activating factor, oligomerization domain-like receptor family pyrin domain-containing 1 and absent in melanoma 2 inflammasome recognize peculiar substances, while NLRP3 inflammasome responds towards structurally and chemically diverse triggers. The functional relationship between ginsenosides and inflammasome provides new insight into the understanding of molecular mechanisms of ginsenoside-mediated anti-inflammatory actions. It also has applications regarding the development of anti-inflammatory remedies by ginsenoside-mediated targeting inflammasomes, which could prevent and treat inflammatory diseases.


greenmedinfo--2020-09-05--Ginsenoside Rg3 inhibits the growth of osteosarcoma and attenuates metastasis.

Osteosarcoma ( OS ) is the most common primary malignant bone cancer .
An increasing number of studies have demonstrated that ginsenoside Rg3 ( Rg3 ) , which is extracted from the roots of the traditional Chinese herb Panax ginseng , plays a tumor suppression role in various malignant tumors .
In the present study , we aimed at investigating the role of Rg3 in the proliferation , migration , and invasion of OS and at exploring the underlying mechanisms .
Cell viability and proliferation were observed by MTT assay and crystal violet staining .
The migration and invasion of @ @ @ @ @ @ @ Transwell method .
Signaling pathway screening was investigated using luciferase reporter gene assay .
qRT-PCR and western blot were performed to measure the expression of molecules involved in cell epithelial-mesenchymal transition ( EMT ) , and Wnt/-catenin pathway .
Results suggested that Rg3 could not only inhibit proliferation but also hamper the migration and invasion of OS .
qRT-PCR and western blot demonstrated that a reduced level of MMP2/MMP7/MMP9 was induced after Rg3 treatment .
In addition , the expression levels of proteins related to EMT and the Wnt/-catenin pathway were downregulated .
@ @ @ @ @ @ @ Rg3 could inhibit the proliferation , migration , and invasion of OS cells .
This effect of Rg3 might be mediated by downregulating MMP2 , MMP7 , and MMP9 expression and suppressing EMT as well as the Wnt/-catenin pathway .
Thus , Rg3 might be a potential agent for the treatment of OS .

Osteosarcoma (OS) is the most common primary malignant bone cancer. An increasing number of studies have demonstrated that ginsenoside Rg3 (Rg3), which is extracted from the roots of the traditional Chinese herb Panax ginseng, plays a tumor suppression role in various malignant tumors. In the present study, we aimed at investigating the role of Rg3 in the proliferation, migration, and invasion of OS and at exploring the underlying mechanisms. Cell viability and proliferation were observed by MTT assay and crystal violet staining. The migration and invasion of cells were measured by wound-healing assay and Transwell method. Signaling pathway screening was investigated using luciferase reporter gene assay. qRT-PCR and western blot were performed to measure the expression of molecules involved in cell epithelial-mesenchymal transition (EMT), and Wnt/-catenin pathway. Results suggested that Rg3 could not only inhibit proliferation but also hamper the migration and invasion of OS. qRT-PCR and western blot demonstrated that a reduced level of MMP2/MMP7/MMP9 was induced after Rg3 treatment. In addition, the expression levels of proteins related to EMT and the Wnt/-catenin pathway were downregulated. In summary, our data revealed that Rg3 could inhibit the proliferation, migration, and invasion of OS cells. This effect of Rg3 might be mediated by downregulating MMP2, MMP7, and MMP9 expression and suppressing EMT as well as the Wnt/-catenin pathway. Thus, Rg3 might be a potential agent for the treatment of OS.


greenmedinfo--2020-09-05--Ginsenoside Rb1 alleviated high fat diet-induced apoptosis of hepatocytes of mice via PPAR-γ.

Objective : High-fat-diet- ( HFD- ) induced hepatic cell apoptosis is common in mice with nonalcoholic fatty liver disease ( @ @ @ @ @ to investigate the effect of Ginsenoside Rb1 ( GRb1 ) on hepatocyte apoptosis .
Methods @ @ @ @ @ were used to induce a liver-injured model with cell apoptosis .
In addition , GRb1 @ @ @ @ @ apoptosis in a liver with or without inhibitor of peroxisome proliferator-activated receptor ( PPAR- ) @ @ @ @ @ C57BL/6J mice with common chow , there are downregulated PPAR-but upregulated cell apoptosis in the @ @ @ @ @ .
Furthermore , GRb1 elevated the hepatic PPAR-level and suppressed hepatocytic apoptosis .
However , @ @ @ @ @ GRb1 on apoptosis in the liver .
Conclusions : GRb1 alleviated HFD-induced apoptosis of hepatocytes @ @ @ @ @

Objective: High-fat-diet- (HFD-) induced hepatic cell apoptosis is common in mice with nonalcoholic fatty liver disease (NAFLD). We aim to investigate the effect of Ginsenoside Rb1 (GRb1) on hepatocyte apoptosis.
Methods: C57BL/6J mice with HFD were used to induce a liver-injured model with cell apoptosis. In addition, GRb1 was used to treat HFD-induced apoptosis in a liver with or without inhibitor of peroxisome proliferator-activated receptor(PPAR-).
Results: Compared with C57BL/6J mice with common chow, there are downregulated PPAR-but upregulated cell apoptosis in the liver of mice with HFD. Furthermore, GRb1 elevated the hepatic PPAR-level and suppressed hepatocytic apoptosis. However, GW9662 abolished the effects of GRb1 on apoptosis in the liver.
Conclusions: GRb1 alleviated HFD-induced apoptosis of hepatocytes of mice via PPAR-.


greenmedinfo--2020-09-05--Ginsenoside Rh2 might serve as a promising candidate compound for Alzheimer's disease.

Rh2 is a rare ginsenoside and there are few reports of its effect on cognition compared with other similar molecules .
This study aimed to establish the impact of Rh2 treatment on improving scopolamine ( Scop ) -induced memory deficits in mice and illuminate the underlying mechanisms .
First , memory-related behavior was evaluated using two approaches : object location recognition ( OLR ) , based on spontaneous activity , and a Morris water maze ( MWM ) task , based on an aversive stimulus .
Our results suggested that Rh2 treatment effectively increased the discrimination index of the mice @ @ @ @ @ @ @ , Rh2 elevated the crossing numbers and decreased the escape latency during the MWM task .
Moreover , Rh2 markedly upregulated the phosphorylation of the extracellular signal-regulated kinase ( ERK ) -cAMP response element binding ( CREB ) -brain derived neurotrophic factor ( BDNF ) pathway in the hippocampus .
Meanwhile , the administration of Rh2 significantly promoted the cholinergic system and dramatically suppressed oxidative stress in the hippocampus .
Taken together , Rh2 exhibited neuroprotective effects against Scop-induced memory dysfunction in mice .
Rh2 activity might be ascribed to several underlying mechanisms @ @ @ @ @ @ @ cholinergic transmission , inhibiting oxidative stress and activating the ERK-CREB-BDNF signaling pathway .
Consequently , the ginsenoside Rh2 might serve as a promising candidate compound for Alzheimer 's disease .

Rh2 is a rare ginsenoside and there are few reports of its effect on cognition compared with other similar molecules. This study aimed to establish the impact of Rh2 treatment on improving scopolamine (Scop)-induced memory deficits in mice and illuminate the underlying mechanisms. First, memory-related behavior was evaluated using two approaches: object location recognition (OLR), based on spontaneous activity, and a Morris water maze (MWM) task, based on an aversive stimulus. Our results suggested that Rh2 treatment effectively increased the discrimination index of the mice in the OLR test. In addition, Rh2 elevated the crossing numbers and decreased the escape latency during the MWM task. Moreover, Rh2 markedly upregulated the phosphorylation of the extracellular signal-regulated kinase (ERK)-cAMP response element binding (CREB)-brain derived neurotrophic factor (BDNF) pathway in the hippocampus. Meanwhile, the administration of Rh2 significantly promoted the cholinergic system and dramatically suppressed oxidative stress in the hippocampus. Taken together, Rh2 exhibited neuroprotective effects against Scop-induced memory dysfunction in mice. Rh2 activity might be ascribed to several underlying mechanisms, including its effects on modulating the cholinergic transmission, inhibiting oxidative stress and activating the ERK-CREB-BDNF signaling pathway. Consequently, the ginsenoside Rh2 might serve as a promising candidate compound for Alzheimer's disease.


greenmedinfo--2020-09-05--Ginsenoside Rb1 attenuates microglia activation to improve spinal cord injury.

Ginsenoside Rb1 ( GRb1 ) , a major ingredient of ginseng , has been found to be a potential protective @ @ @ @ @ ( SCI ) and in activated microglia-induced neuronal injury .
This study discovered that GRb1 @ @ @ @ @ SCI rats and Toll-like receptor 4 ( TLR4 ; a crucial player in inflammation ) @ @ @ @ @ miR-130b-5p .
Hence , we further investigated whether GRb1 could relieve SCI by reducing microglia-mediated @ @ @ @ @ via miR-130b-5p/TLR4 pathways .
The results showed that GRb1 alleviated SCI through inhibiting neuronal apoptosis @ @ @ @ @ increasing miR-130b-5p.GRb1 weakened the damage of activated microglia to neurons through upregulating miR-130b-5p .
miR-130b-5p @ @ @ @ @ via targeting TLR4 .
GRb1 inactivated TLR4/nuclear factor-κB ( NF-κB ) activation and inhibited proinflammatory @ @ @ @ @ in activated microglia .
As a conclusion , GRb1 alleviated SCI through reducing activated microglia-induced @ @ @ @ @ , providing a deep insight into the molecular basis of GRb1 in the treatment of @ @

Ginsenoside Rb1 (GRb1), a major ingredient of ginseng, has been found to be a potential protective agent in spinal cord injury (SCI) and in activated microglia-induced neuronal injury. This study discovered that GRb1 could facilitate miR-130b-5p expression in SCI rats and Toll-like receptor 4 (TLR4; a crucial player in inflammation) was a potential target of miR-130b-5p. Hence, we further investigated whether GRb1 could relieve SCI by reducing microglia-mediated inflammatory responses and neuronal injury via miR-130b-5p/TLR4 pathways. The results showed that GRb1 alleviated SCI through inhibiting neuronal apoptosis and proinflammatory factor expression via increasing miR-130b-5p.GRb1 weakened the damage of activated microglia to neurons through upregulating miR-130b-5p. miR-130b-5p attenuated activated microglia-induced neuron injury via targeting TLR4. GRb1 inactivated TLR4/nuclear factor-κB (NF-κB) activation and inhibited proinflammatory cytokine secretion by increasing miR-130b-5p in activated microglia. As a conclusion, GRb1 alleviated SCI through reducing activated microglia-induced neuronal injury via miR-130b-5p/TLR4/NF-κB axis, providing a deep insight into the molecular basis of GRb1 in the treatment of SCI.


greenmedinfo--2020-09-05--Ginsenoside Rh2 impedes proliferation and migration and induces apoptosis in osteosarcoma cells.

Ginsenoside Rh2 is a primary bioactive compound obtained from ginseng that indicated anticancer activities against several malignant tumors .
However , previous studies have reported little about the inhibitory effect of Rh2 on osteosarcoma ( OS ) .
This study aims to explore whether Rh2 could exert anticancer effects in OS cells and further investigate the proliferation , migration , and apoptosis mechanisms induced by Rh2 in human OS U20S cell line .
The viability of U20S cells was obtained by the 3- ( 4,5-dimethyl-2-thiazolyl ) -2,5-diphenyl-2-H-tetrazolium bromide assay .
Cell migration property was analyzed by wound-healing assay .
Apoptosis @ @ @ @ @ @ @ nick-end labeling ( TUNEL ) , 4',6-diamidino-2-phenylindole ( DAPI ) , and annexin V/propidium iodide ( PI ) staining .
Relative protein expressed was confirmed through Western blot analysis .
Mitochondrial membrane potential was evaluated by JC-1 staining .
In this study , we used broad-spectrum anticancer drug cisplatin ( CP ) as a positive control .
The results indicated that Rh2 remarkably inhibited cell viability of U20S cells in a dose- and time-dependent manner , and suppressed migration .
TUNEL , DAPI , annexin V/PI , and JC-1 assay suggested that Rh2 @ @ @ @ @ @ @ reduce the levels of Bcl-2 , caspase 3 , and caspase 9 , and promote the expression level of Bax in U20S cells .
Moreover , Rh2 could induce apoptosis by promoting mitogen-activated protein kinase ( MAPK ) signaling pathway and inhibit PI3K/Akt/mTOR and nuclear factor-κB ( NF-κB ) signaling pathway in U20S cells .
These findings indicated that Rh2 has an anticancer effect on U20S cells by regulating MAPK , PI3K/Akt/mTOR , and NF-κB signaling pathway .

Ginsenoside Rh2 is a primary bioactive compound obtained from ginseng that indicated anticancer activities against several malignant tumors. However, previous studies have reported little about the inhibitory effect of Rh2 on osteosarcoma (OS). This study aims to explore whether Rh2 could exert anticancer effects in OS cells and further investigate the proliferation, migration, and apoptosis mechanisms induced by Rh2 in human OS U20S cell line. The viability of U20S cells was obtained by the 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide assay. Cell migration property was analyzed by wound-healing assay. Apoptosis was visualized using terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL), 4',6-diamidino-2-phenylindole (DAPI), and annexin V/propidium iodide (PI) staining. Relative protein expressed was confirmed through Western blot analysis. Mitochondrial membrane potential was evaluated by JC-1 staining. In this study, we used broad-spectrum anticancer drug cisplatin (CP) as a positive control. The results indicated that Rh2 remarkably inhibited cell viability of U20S cells in a dose- and time-dependent manner, and suppressed migration. TUNEL, DAPI, annexin V/PI, and JC-1 assay suggested that Rh2 could induce cellular apoptosis. Rh2 could reduce the levels of Bcl-2, caspase 3, and caspase 9, and promote the expression level of Bax in U20S cells. Moreover, Rh2 could induce apoptosis by promoting mitogen-activated protein kinase (MAPK) signaling pathway and inhibit PI3K/Akt/mTOR and nuclear factor-κB (NF-κB) signaling pathway in U20S cells. These findings indicated that Rh2 has an anticancer effect on U20S cells by regulating MAPK, PI3K/Akt/mTOR, and NF-κB signaling pathway.


greenmedinfo--2020-09-05--Ginsenoside Rg1 exerts anti-aging effects via the regulation of SIRT1-FOXO3 and SIRT3-SOD2 signallin

Ginsenoside Rg1 exerts anti-aging effects via the regulation of SIRT1-FOXO3 and SIRT3-SOD2 signalling pathways.

Aging is characterized by a progressive deterioration in metabolic functions .
The present study aimed to investigate the antagonistic effects of ginsenoside Rg1 ( Rg1 ) on theγ-ray irradiation-induced aging of mixed hematopoietic stem cells ( HSCs ) and hematopoietic progenitor cells ( HPCs ) .
C57BL/6 mice were divided into a control group , a γ-ray irradiation group that served as an aging mouse model , and an Rg1 group .
The Rg1 group was treated with Rg1 at dosage of 20 mg/kg/day for 7 days prior to γ-ray irradiation .
The aging mouse model was established by exposing @ @ @ @ @ @ @ .
Stem cell antigen 1 positive ( Sca-1 ) HSC/HPCs isolated from the mice were examined using a senescence-associatedβ-galactosidase ( SA-β-Gal ) staining assay .
The cell cycle of the HSC/HPCs was examined using flow cytometry .
A mixed hematopoietic progenitor cell colony-forming unit ( CFU-mix ) assay was also conducted .
The mRNA and protein expression levels of sirtuin 1 ( SIRT1 ) , SIRT3 , forkhead box O3 ( FOXO3 ) andsuperoxide dismutase ( SOD2 ) were evaluated using western blot and reverse transcription-quantitative PCR assays .
The results indicated that @ @ @ @ @ @ @ , red blood cell and platelet counts in peripheral blood compared with those in the γ-ray irradiation group ( P < 0.05 ) .
However , Rg1 significantly attenuated the senescence of Sca-1HSC/HPCs in theγ-ray irradiation aging mice model .
The proportion of SA-β-Gal stained HSC/HPCs was significantly decreased and CFU-Mix counts were significantly increased in the Rg1 group compared with the γ-ray irradiation group ( P < 0.05 ) .
Rg1 significantly increased the mRNA and protein levels of SIRT1 , SIRT3 , FOXO3 and SOD2 in the Sca-1HSC/HPCs compared with those @ @ @ @ @ @ @ 0.05 ) .
The percentage of Sca-1HSC/HPCs arrested at the G1 phase in the Rg1 group was significantly decreased compared with that in theγ-ray irradiation group ( P < 0.05 ) .
In conclusion , the present study indicates that Rg1 exerts anti-aging effects via the regulation of SIRT1-FOXO3 and SIRT3-SOD2 signaling pathways , and triggering the progression of Sca-1HSC/HPCs from the G1 phase to the S phase inγ-ray irradiation-induced aging mice .

Aging is characterized by a progressive deterioration in metabolic functions. The present study aimed to investigate the antagonistic effects of ginsenoside Rg1 (Rg1) on theγ-ray irradiation-induced aging of mixed hematopoietic stem cells (HSCs) and hematopoietic progenitor cells (HPCs). C57BL/6 mice were divided into a control group, a γ-ray irradiation group that served as an aging mouse model, and an Rg1 group. The Rg1 group was treated with Rg1 at dosage of 20 mg/kg/day for 7 days prior to γ-ray irradiation. The aging mouse model was established by exposing the mice to 6.5-Gy γ-ray total-body irradiation. Stem cell antigen 1 positive (Sca-1) HSC/HPCs isolated from the mice were examined using a senescence-associatedβ-galactosidase (SA-β-Gal) staining assay. The cell cycle of the HSC/HPCs was examined using flow cytometry. A mixed hematopoietic progenitor cell colony-forming unit (CFU-mix) assay was also conducted. The mRNA and protein expression levels of sirtuin 1 (SIRT1), SIRT3, forkhead box O3 (FOXO3) andsuperoxide dismutase (SOD2) were evaluated using western blot and reverse transcription-quantitative PCR assays. The results indicated that Rg1 treatment significantly increased white blood cell, red blood cell and platelet counts in peripheral blood compared with those in the γ-ray irradiation group (P<0.05). However, Rg1 significantly attenuated the senescence of Sca-1HSC/HPCs in theγ-ray irradiation aging mice model. The proportion of SA-β-Gal stained HSC/HPCs was significantly decreased and CFU-Mix counts were significantly increased in the Rg1 group compared with the γ-ray irradiation group (P<0.05). Rg1 significantly increased the mRNA and protein levels of SIRT1, SIRT3, FOXO3 and SOD2 in the Sca-1HSC/HPCs compared with those in theγ-ray irradiation group (P<0.05). The percentage of Sca-1HSC/HPCs arrested at the G1 phase in the Rg1 group was significantly decreased compared with that in theγ-ray irradiation group (P<0.05). In conclusion, the present study indicates that Rg1 exerts anti-aging effects via the regulation of SIRT1-FOXO3 and SIRT3-SOD2 signaling pathways, and triggering the progression of Sca-1HSC/HPCs from the G1 phase to the S phase inγ-ray irradiation-induced aging mice.


greenmedinfo--2020-09-05--Ginsenoside Rk1 alleviates LPS-induced depression-like behavior in mice by promoting BDNF and suppre

Ginsenoside Rk1 alleviates LPS-induced depression-like behavior in mice by promoting BDNF and suppressing the neuroinflammatory response.

Ginsenoside Rk1 , a saponin component produced by heat-processed ginseng , possesses anti-inflammatory and antitumor activities .
The aim of our study was to explore the effects of Rk1 on Lipopolysaccharide ( LPS ) -induced depression-like behavior in mice and to observe its effects on oxidative stress , the inflammatory response and brain-derived neurotrophic factor ( BDNF ) - tropomyosin-related kinase B ( TrkB ) signaling .
After mice were pretreated with Rk1 ( 5 , 10 , and 20 mg/kg ) , the immobility time in both the forced swimming test ( FST ) and the tail suspension test @ @ @ @ @ @ @ that Rk1 effectively improved depression-like symptoms .
Rk1 ( 10 and 20 mg/kg ) and Fluoxetine ( Flu , 20 mg/kg ) increased the activity of the antioxidant enzyme SOD in the brain and protected against lipid peroxidation .
Different concentrations of Rk1 ( 10 and 20 mg/kg ) and Flu significantly decreased the levels of tumor necrosis factor ( TNF ) -α and interleukin ( IL ) -1 in serum , while Rk1 ( 5 , 10 , and 20 mg/kg ) and Flu reduced the concentrations of IL-6 in a dose-dependent @ @ @ @ @ @ @ the administration of Rk1 ( 20 mg/kg ) and Flu significantly downregulated the level of Sirt1 and that Rk1 ( 5 , 10 , and 20 mg/kg ) and Flu inhibited the p-NF-κb/NF-κb and p-IκB-α/IκB-α ratios , which indicated that the neuroprotective effect of Rk1 may be related to the suppression of inflammation .
In addition 5 , 10 and 20 mg/kg Rk1 significantly attenuated the LPS-induced decreases in BDNF and TrkB .
These results indicated that Rk1 acts as an antidepressant through its antioxidant activity , the inhibition of neuroinflammation , and @ @ @ @ @ @ @ This study may help develop active ginsenoside-based compounds for neurodegenerative diseases .

Ginsenoside Rk1, a saponin component produced by heat-processed ginseng, possesses anti-inflammatory and antitumor activities. The aim of our study was to explore the effects of Rk1 on Lipopolysaccharide (LPS)-induced depression-like behavior in mice and to observe its effects on oxidative stress, the inflammatory response and brain-derived neurotrophic factor (BDNF) - tropomyosin-related kinase B (TrkB) signaling. After mice were pretreated with Rk1 (5, 10, and 20 mg/kg), the immobility time in both the forced swimming test (FST) and the tail suspension test (TST) was reduced, suggesting that Rk1 effectively improved depression-like symptoms. Rk1 (10 and 20 mg/kg) and Fluoxetine (Flu, 20 mg/kg) increased the activity of the antioxidant enzyme SOD in the brain and protected against lipid peroxidation. Different concentrations of Rk1 (10 and 20 mg/kg) and Flu significantly decreased the levels of tumor necrosis factor (TNF)-α and interleukin (IL)-1 in serum, while Rk1 (5, 10, and 20 mg/kg) and Flu reduced the concentrations of IL-6 in a dose-dependent manner. Western blot analysis showed that the administration of Rk1 (20 mg/kg) and Flu significantly downregulated the level of Sirt1 and that Rk1 (5, 10, and 20 mg/kg) and Flu inhibited the p-NF-κb/NF-κb and p-IκB-α/IκB-α ratios, which indicated that the neuroprotective effect of Rk1 may be related to the suppression of inflammation. In addition 5, 10 and 20 mg/kg Rk1 significantly attenuated the LPS-induced decreases in BDNF and TrkB. These results indicated that Rk1 acts as an antidepressant through its antioxidant activity, the inhibition of neuroinflammation, and the positiveregulation of the BDNF-TrkB pathway. This study may help develop active ginsenoside-based compounds for neurodegenerative diseases.


greenmedinfo--2020-09-05--Ginsenoside Rg1 drives stimulations of timosaponin AIII-induced anticancer effects in human osteosar

Ginsenoside Rg1 drives stimulations of timosaponin AIII-induced anticancer effects in human osteosarcoma cells.

A ginsenoside Rg1 is an active compound extracted from the stem and/or root of ginseng .
Rg1 has been known to affect various human organ systems including the immune , cardiovascular , and nervous systems with its pharmacological effects .
Timosaponin AIII ( TA3 ) is a type of spirostanol saponins that are the major compounds of .
TA3 exerts anticancer effects in various human cancers , and the effects include attenuations of cancer cell migration and induction of apoptosis .
In this study , I report that Rg1 drives the stimulation of TA3-induced cytotoxic effects in MG63 human osteosarcoma @ @ @ @ @ @ @ MG63 cells via selective intensification of caspase-3 activation .
Rg1 and TA3 synergistically induced antimetastatic effects such as attenuation of MG63 cell migration and inhibitions of matrix metalloproteinases ( MMP-2 and MMP-9 ) .
Rg1 and TA3 synergistically suppressed JNK , p38 , ERK , -catenin , and CREB signaling , which are key regulators of cancer metastasis .
Finally , the synergistic anticancer effects of Rg1 and TA3 were also observed in U2OS human osteosarcoma cells , and this may indicate that the synergy is not limited specifically to MG63 cells .
@ @ @ @ @ @ @ combinatorial use of Rg1 and TA3 may be a promising way to develop an effective antiosteosarcoma agent .

A ginsenoside Rg1 is an active compound extracted from the stem and/or root of ginseng. Rg1 has been known to affect various human organ systems including the immune, cardiovascular, and nervous systems with its pharmacological effects. Timosaponin AIII (TA3) is a type of spirostanol saponins that are the major compounds of. TA3 exerts anticancer effects in various human cancers, and the effects include attenuations of cancer cell migration and induction of apoptosis. In this study, I report that Rg1 drives the stimulation of TA3-induced cytotoxic effects in MG63 human osteosarcoma cells. Rg1 stimulates TA3-induced apoptosis in MG63 cells via selective intensification of caspase-3 activation. Rg1 and TA3 synergistically induced antimetastatic effects such as attenuation of MG63 cell migration and inhibitions of matrix metalloproteinases (MMP-2 and MMP-9). Rg1 and TA3 synergistically suppressed JNK, p38, ERK,-catenin, and CREB signaling, which are key regulators of cancer metastasis. Finally, the synergistic anticancer effects of Rg1 and TA3 were also observed in U2OS human osteosarcoma cells, and this may indicate that the synergy is not limited specifically to MG63 cells. The results presented here suggest that the combinatorial use of Rg1 and TA3 may be a promising way to develop an effective antiosteosarcoma agent.