Ginsenoside Rg2 Attenuates Doxorubicin-induced Cardiomyocyte Apoptosis via PI3K/Akt Pathway

Abstract Doxorubicin (DOX) is an important drug for cancer therapy; however, its use is limited by its cardiotoxicity. Ginsenoside Rg2 is extracted from Panax ginseng, which is believed to have cardioprotective properties. However, to date, there have been no reports on whether ginsenoside Rg2 could protect cardiomyocytes against DOX. In this study, we investigated the action and underlying mechanisms of ginsenoside Rg2 upon DOX treatment. This study aimed to explore the cardioprotective effects of ginsenoside Rg2 against DOX treatment. Cell Counting kit-8 was used to determine cell viability and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling staining was used to detect apoptotic cells. Western blotting was used to investigate the relevant pathways. LY294002 (LY294), a PI3K inhibitor, was used in this study. We found that ginsenoside Rg2 significantly (P < 0.01) neutralized cardiomyocyte apoptosis induced by DOX in a dose-dependent manner, which was blocked by LY294. Moreover, ginsenoside Rg2 upregulated Akt phosphorylation through the PI3K/Akt pathway and inhibited p53 expression. Taken together, Ginsenoside Rg2 attenuates DOX-induced cardiomyocyte apoptosis via the PI3K/Akt pathway.