Ginsenoside Rg5 has been implicated in a variety of diseases. However, it is unknown whether Ginsenoside Rg5 can protect against hypoxia-induced neonatal rat cardiomyocytes (NRMs). The purpose of this study was to look into the effect of Ginsenoside Rg5 on hypoxia-induced NRMs apoptosis as well as the underlying molecular mechanism. In this study, following isolation and culture of ventricular myocardial cells from neonatal rats, the appropriate concentration of Rg5 was determined using the MTT assay, the effect of Rg5 on apoptosis was assessed employing TUNEL staining and flow cytometry assays. Levels of apoptosis-related proteins and phosphorylated level of Akt (ser 473 and ser 308) were analyzed using the western blot analysis. Finally, the experimental results shown that Ginsenoside Rg5 significantly inhibited hypoxia-induced NRMs apoptosis, decreased the expression pro-apoptotic protein Bax, increased the expression of anti-apoptotic protein Bcl-2 ratio and the level of cleaved caspase 3. Akt signaling activation was found to be the mechanism of Ginsenoside Rg5s protective effect on hypoxia-induced NRMs apoptosis, as an Akt inhibitor eliminated the anti-apoptotic effects of Ginsenoside Rg5. Various analyses were performed and verified, ginsenoside Rg5 suppressed hypoxia-induced apoptosis in NRMs via activation of the Akt signaling.
Keywords: Akt; apoptosis; ginsenoside Rg5; neonatal rat cardiomyocytes.
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