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.
Keywords: Ginkgolide B; myocardial ischemia/reperfusion injury; oxidative stress; cell apoptosis; phosphatidyl inositol 3 kinase/protein kinase B/mammalian target of rapamycin.