This product is isolated and purified from the roots of Panax ginseng C. A. Mey.
β-D-Glucopyranoside, (3β,6α,12β)-3,12-dihydroxydammara-20,24-dien-6-yl/(3β,6α,12β)-3,12-Dihydroxydammara-20,24-dien-6-yl β-D-glucopyranoside
Biol Pharm Bull. 2011;34(6):898-900. Anti-complementary ginsenosides isolated from processed ginseng.[Pubmed: 21628891]METHODS AND RESULTS:As part of an ongoing search for immunomodulatory components aimed at the anti-complementary effect, ginsenosides isolated from processed ginseng were found to have inhibitory activity on complement activation through classical pathways. Activity-guided fractionation was used to isolate four ginsenosides, namely ginsenoside Rg₆, F₄, Rk₃, and Rh₄. Ginsenoside Rk₃ and Rh₄ had a 3 fold higher inhibition activity than rosmarinic acid which was used as a positive control while ginsenoside Rg₆ and F₄ showed only mild effects similar to that of the positive control. CONCLUSIONS:The results suggest that the activity of the corresponding ginsenosides may be increased by the glycosyl moiety at the C₆ position rather than the double bond conformation at C₂₀, and ginsenoside Rk₃ and Rh₄ could have a role in treating inflammatory diseases.
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provides coniferyl ferulate(CAS#:364779-15-7) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
Reperfusion therapy is widely utilized for acute myocardial infarction (AMI), but further injury induced by rapidly initiating reperfusion of the heart is often encountered in clinical practice. Ginsenoside RK3 (RK3) is reportedly present in the processed Radix notoginseng that is often used as a major ingredient of the compound preparation for ischemic heart diseases. This study aimed to investigate the possible protective effect of RK3 against hypoxia-reoxygenation (H/R) induced H9c2 cardiomyocytes damage and its underlying mechanisms. Our results showed that RK3 pretreatment caused increased cell viability and decreased levels of LDH leakage compared with the H/R group. Moreover, RK3 pretreatment inhibited cell apoptosis, as evidenced by decreased caspase-3 activity, TUNEL-positive cells, and Bax expression, as well as increased Bcl-2 level. Further mechanism investigation revealed that RK3 prevented H9c2 cardiomyocytes injury and apoptosis induced by H/R via AKT/Nrf-2/HO-1 and MAPK pathways. These observations indicate that RK3 has the potential to exert cardioprotective effects against H/R injury, which might be of great importance to clinical efficacy for AMI treatment.
Ginsenoside RK3 Prevents Hypoxia-Reoxygenation Induced Apoptosis in H9c2 Cardiomyocytes via AKT and MAPK Pathway
Jing Sun 1 , Guibo Sun, Xiangbao Meng, Hongwei Wang, Min Wang, Meng Qin, Bo Ma, Yun Luo, Yingli Yu, Rongchang Chen, Qidi Ai, Xiaobo Sun
Ginsenoside Rk3 (G-Rk3) is a main active ingredient of ginsenosides. Several recent studies demonstrated that ginsenosides have potential anti-type 2 diabetes mellitus (T2DM) properties. To evaluate the anti-T2DM effect of G-Rk3 and verify its potential mechanism, a high-fat-diet/streptozocin (HFD/STZ) induced model of T2DM in C57BL/6 mice and a high glucose induced insulin resistance model of HepG2 cells were applied in this research. Our analysis indicated that G-Rk3 reduced HFD/STZ induced hyperglycemia, and serum insulin and inflammation levels, and ameliorated glucose tolerance and insulin resistance, and prevented liver histological changes. Furthermore, it also significantly reduced lipid accumulation as shown by lower TG, LDL-C and TC serum concentrations and Oil Red O staining in liver tissues. The hypoglycemic effect of G-Rk3 seemed to be partially mediated via the inhibition of hepatic gluconeogenesis, which was supported by the activated p-Akt, p-FoxO1 and GLUT2 and inhibited FoxO1, PEPCK and G6pase protein expressions in the liver as well as increased glucose uptake in high glucose induced HepG2 cells. The gene expressions of hepatic gluconeogenesis were also down-regulated by G-Rk3 in HFD/STZ induced T2DM mice. In addition, G-Rk3 suppressed HFD/STZ induced lipid accumulation by regulating related gene and protein expressions such as p-ACC, FAS and SREBP-1, which are the downstream targets of AMPK. AMPK and Akt inhibitors significantly reversed G-Rk3 mediated hepatic gluconeogenesis and lipid accumulation. Thus, our study is the first to illustrate that G-Rk3 mediates hepatic gluconeogenesis and lipid accumulation via activating the AMPK/Akt signaling pathway in HFD/STZ induced T2DM mice.
Ginsenoside Rk3 Ameliorates High-Fat-Diet/Streptozocin Induced Type 2 Diabetes Mellitus in Mice via the AMPK/Akt Signaling Pathway
Yao Liu 1 , Jianjun Deng, Daidi Fan
2019 May 22
Alcoholic liver disease (ALD), as one of the most common diseases, has become a global threat to human health. The aim of this study was designed to investigate the hepatoprotective effects of ginsenoside Rk3 against ALD and to discover the potential mechanisms of these protective effects. Mice were intragastrically administered 50% alcohol and treated with ginsenoside Rk3 (25 and 50 mg/kg) once per day for 6 weeks. The results indicated that ginsenoside Rk3 promoted hepatic function through significant downgrading AST and ALT levels in the serum, attenuating oxidative stress, and restoring antioxidant balance in hepatic tissue. Additionally, ginsenoside Rk3 significantly reduced the expression of inflammatory cytokines, such as NF-κB, TNF-α, IL-6, and IL-1β in the mice. Furthermore, ginsenoside Rk3 supplementation significantly inhibited apoptotic protein expression in the liver. The present study clearly demonstrates that ginsenoside Rk3 exerts a protective effect against ALD-induced liver injury because of its antioxidant, anti-apoptotic, and anti-inflammatory activities. The findings from the present investigation show that ginsenoside Rk3 might be a promising candidate treatment agent against ALD.
Alcoholic liver disease; Apoptosis; Ginsenoside Rk3; Inflammation; Oxidation.
Protective Effects of Ginsenoside Rk3 Against Chronic Alcohol-Induced Liver Injury in Mice Through Inhibition of Inflammation, Oxidative Stress, and Apoptosis
Linlin Qu 1 , Yanyan Zhu 1 , Yannan Liu 1 , Haixia Yang 2 , Chenhui Zhu 1 , Pei Ma 1 , Jianjun Deng 3 , Daidi Fan 4