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provides coniferyl ferulate(CAS#:68406-26-8) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
Ginsenoside Rb3 is one of major ginsenosides in Panax ginseng with effect on cardio-vascular and central nervous system. The aim of this study is to develop a rapid resolution liquid chromatography coupled with quadrupole-time-of-flight mass spectrometry (RRLC-Q-TOF-MS) method for pharmacokinetic study of ginsenoside Rb3 and simultaneous determination of metabolites in rats. The results showed that the concentration-time profile of ginsenoside Rb3 conformed to a two-compartment pharmacokinetic model after intravenous administration at the dosage of 2.0 mg/kg for rats. The mean plasma elimination half-lives were 13.77 ± 1.23 min and 2045.70 ± 156.20 min for the distribution and exterminate phases t1/2α and t1/2β. In the metabolic study, prototype ginsenoside Rb3 and deglycosylation metabolites were characterized by comparison with the retention time of the standard compounds, accurate mass measurement and the characteristic fragment ions obtained from MS/MS. Two major metabolites Mb1 and M2′ were tentatively identified in rat urine samples after intravenous administration, and four possible metabolites Mb1, F2, M2′ and CK were detected in rat feces samples after oral administration. The deglycosylation was found to be the major metabolic pathways of ginsenoside Rb3 in rat. The in vivo metabolic pathway of ginsenoside Rb3 was summarized.
Pharmacokinetic and metabolic studies of ginsenoside Rb3 in rats using RRLC-Q-TOF-MS.
Zhao L1, Ma Y1, Chen C1, Liu S1,2, Wu W1.
2018 Jul 1
Heart failure (HF) leads to an increase in morbidity and mortality globally. Disorders of energy metabolism and apoptosis of cardiomyocytes are critically involved in the progression of HF. Ginsenoside Rb3 (G-Rb3) is a natural product derived from ginseng that has cardio-protective effect. The pharmacological mechanism of G-Rb3 in the treatment of HF remains to be clarified. In this study, we aimed to explore the regulative effects of G-Rb3 on fatty acids oxidation and apoptosis by in vivo and in vitro studies. Myocardial infarction (MI)-induced HF mice model and a cellular H9C2 injury model was induced by oxygen-glucose deprivation/reperfusion (OGD/R) stimulation. The results showed that G-Rb3 could protect heart functions in MI-induced HF model. G-Rb3 treatment up-regulated expressions of key enzymes involved in β-oxidation of fatty acids, including carnitine palmitoyltransterase-1α (CPT-1α), acyl-CoA dehydrogenase long chain (ACADL) and the major mitochondrial deacetylase enzyme sirtuin 3 (SIRT3). The upstream transcriptional regulator, peroxisome proliferator-activated receptor α (PPARα), was also up-regulated by G-Rb3 treatment. In vitro study demonstrated that G-Rb3 could protect mitochondrial membrane integrity and exert anti-apoptotic effects, in addition to regulating fatty acids oxidation. Impressively, after cells were co-treated with PPARα inhibitor, the regulative effects of G-Rb3 on energy metabolism and apoptosis were abrogated. Our study suggests that G-Rb3 is a promising agent and PPARα is potential target in the management of HF.
Copyright © 2019 The Authors. Published by Elsevier Masson SAS.. All rights reserved.
Apoptosis; Fatty acid; Ginsenoside Rb3; Heart failure; Oxidation; PPARα
Ginsenoside Rb3 regulates energy metabolism and apoptosis in cardiomyocytes via activating PPARα pathway.
Chen X1, Wang Q2, Shao M2, Ma L2, Guo D2, Wu Y3, Gao P2, Wang X2, Li W2, Li C4, Wang Y5.
Based on previous reports that ginsenosides have been shown to exert better preventive effects on cisplatin-induced kidney injury, the present work aims to evaluate the protective effects of ginsenoside Rb3 (G-Rb3) on cisplatin-induced renal damage and underlying mechanisms in vivo and in vitro.
MATERIALS AND METHODS:
The protective effect of G-Rb3 on cisplatin-induced acute renal failure in ICR mouse model and HEK293 cell model was investigated, and the underlying possible mechanisms were also explored. For animal experiment, renal function, kidney histology, inflammation, oxidative stress, relative protein molecules involved in apoptosis and autophagy signalling pathways were assessed. In addition, rapamycin (a specific inhibitor of mTOR), compound C (a specific inhibitor of AMPK) and acetylcysteine (NAC, a specific ROS scavenger) were employed to testify the effects of AMPK/mTOR signal pathway on the protective effects of G-Rb3 in HEK293 cells.
Pre-treatment with G-Rb3 at doses of 10 and 20 mg/kg for ten days significantly reversed the increases in serum creatinine (CRE), blood urea nitrogen (BUN) and malondialdehyde (MDA), and decrease in glutathione (GSH) content and superoxide dismutase (SOD) activity. Histopathological examination further revealed that G-Rb3 inhibited cisplatin-induced nephrotoxicity. G-Rb3 diminished cisplatin-induced increase in protein expression levels of p62, Atg3, Atg5 and Atg7, and decrease in protein expression level of p-mTOR and the ratio of LC3-I/LC3-II, indicating that G-Rb3 suppressed cisplatin-induced activation of autophagy. Inhibition of autophagy induced inactivation of apoptosis, which suggested that autophagy played an adverse effect on cisplatin-evoked renal damage. Further, we found that G-Rb3 might potentially modulate the expressions of AMPK-related signal pathways.
These findings clearly suggested that G-Rb3-mediated alleviation of cisplatin-induced nephrotoxicity was in part due to regulation of AMPK-/mTOR-mediated autophagy and inhibition of apoptosis in vitro and in vivo.
© 2019 The Authors. Cell Proliferation Published by John Wiley & Sons Ltd.
AMPK/mTOR; Ginsenoside Rb3; HEK293 cells; autophagy; cisplatin; nephrotoxicity
Ginsenoside Rb3 provides protective effects against cisplatin-induced nephrotoxicity via regulation of AMPK-/mTOR-mediated autophagy and inhibition of apoptosis in vitro and in vivo.
Xing JJ1,2, Hou JG1,3, Ma ZN1, Wang Z1,2, Ren S1,2, Wang YP1,2, Liu WC1,2, Chen C4, Li W1,2.