Ginsenoside Rg3 attenuates myocardial ischemia/reperfusion injury via Akt/endothelial nitric oxide synthase signaling and the Bcell lymphoma/Bcell lymphomaassociated X protein pathway

Author：

Publisher： Spandidos Publications

E-ISSN： 1791-3004|11|6|4518-4524

ISSN： 1791-2997

Source： Molecular Medicine Reports, Vol.11, Iss.6, 2015-01, pp. : 4518-4524

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Abstract

Previous studies have suggested that ginsenoside Rg3 (GSRg3) extract from the medicinal plant Panax ginseng, may increase nitric oxide production via increases in the phosphorylation and expression of endothelial nitric oxide synthase (eNOS). The present study used an in vitro neonatal rat cardiomyocyte (NRC) model of anoxiareoxygenation injury and an in vivo rat model of myocardial ischemia/reperfusion (MI/R) injury. Hemodynamic, histopathological and biochemical assessment of the myocardial injury was performed and the expression levels of lactate dehydrogenase (LDH), superoxide dismutase and creatine kinase (CK) were measured in serum from the animal model, which may reflect myocardial injury. NRC injury was determined using a Cell Counting kit8. The GSRg3 antiapoptotic effects were assessed using flow cytometry to investigate the number of earlylate apoptotic cells and western blot analysis was performed to analyze the protein expression levels of caspase3, caspase9, Bcell lymphoma2 (Bcl2), phosphorylated (p)Akt and eNOS. The results suggested that pretreatment with GSRg3 (60 mg/kg) significantly improved rat cardiac function, as demonstrated by increased left ventricular systolic pressure, heart rate and first derivative of left ventricular pressure. GSRg3 also reduced the size of the myocardial infarct and LDH/CK levels in the blood following MI/R. In vitro investigations revealed that GSRg3 (10 mM) decreased NRC apoptosis through inhibiting the activation of caspase3 and caspase9, and increasing the expression levels of pAkt, eNOS and the ratio of Bcl2/Bcl2associated X protein (Bax). Overall, the present study revealed that GSRg3 mediated a cardioprotective effect against MI/Rinduced apoptosis via Akt/eNOS signaling and the Bcl2/Bax pathway.