Cardioprotective effect of salvianolic acid B against arsenic trioxide-induced injury in cardiac H9c2 cells via the PI3K/Akt signal pathway.

The clinical use of arsenic trioxide (ATO), a potent anti-neoplastic agent, is often limited because of its severe cardiotoxicity. Salviae miltiorrhiza is widely used for the treatment of cardiovascular diseases. One of the most abundant ingredients of S. miltiorrhiza is salvianolic acid B (Sal B). The present study was designed to evaluate whether Sal B protects against ATO-induced cardiac cell injury in vitro. With MTT cell viability assay, LDH release, ROS generation, caspase-3 activity assay and Hoechst 33342/PI staining, we found that Sal B pretreatment provided significantly protection against ATO-induced cell death. The effect was correlated with the activation of the PI3K/Akt signal pathway. Conversely, blocking Akt activation with the PI3K inhibitor LY294002 effectively suppressed the protective effect of Sal B against ATO-induced cell apoptosis. In addition, the PI3K inhibitor partially blocked the effects of Sal B on the upregulation of Bcl-2 and Bcl-xl protein expression, and downregulation of Bax protein expression. Collectively, the results showed that Sal B decreased the apoptosis and necrosis of H9c2 cardiomyocytes caused by ATO treatment, and PI3K played a crucial role in enhancing cell survival during this process. These observations indicate that Sal B has the potential to exert cardioprotective effects against ATO toxicity.