Ginkgolide B inhibits hydrogen peroxide‑induced apoptosis and attenuates cytotoxicity via activating the PI3K/Akt/mTOR signaling pathway in H9c2 cells.

Abstract

Ginkgolide B (GB) is a diterpene lactone found in the leaves of the traditional Chinese medicinal plant Ginkgo that has been shown to have various pharmacological effects. However, the anti-apoptotic properties of GB in cardiovascular disease remain poorly understood. The present study aimed to investigate the effect of GB on hydrogen peroxide-induced cell injury in cardiac H9c2 cells, and to further clarify its protective mechanism of action. An in vitro hydrogen peroxide-treated H9c2 cell model was used in order to mimic myocardial ischemia-reperfusion (I/R) injury. Cell viability was assessed by the Cell Counting Kit-8 assay. The induction of apoptosis was determined by flow cytometry and staining was performed using Hoechst 33342. In addition, the effect of GB on the expression levels of apoptosis-associated proteins was evaluated by western blot analysis. The present study demonstrated that GB protected against hydrogen peroxide-induced cytotoxicity and cell apoptosis in H9c2 cardiac cells. GB upregulated the expression level of the anti-apoptotic protein Bcl-2 and downregulated the expression levels of the pro-apoptotic proteins cleaved caspase-3 and Bax in hydrogen peroxide-treated H9c2 cells. The molecular mechanism underlying the anti-apoptotic effects of GB was subsequently detected. GB pretreatment activated the PI3K/Akt/mTOR signaling pathway and caused an increase in the phosphorylation levels of Akt and mTOR in hydrogen peroxide-treated H9c2 cells. These results revealed that GB inhibited hydrogen peroxide-induced apoptosis in H9c2 cells via activation of the PI3K/Akt/mTOR signaling pathway. These findings indicate the potential therapeutic benefits of GB in the treatment of myocardial I/R injury.