Abstract: Insulin-like Growth Factor-1 (IGF-1) and Apoptosis Repressor with Caspase recruitment domain (ARC) play an important role in regulating apoptosis. Although, the precise mechanisms of IGF-1 and ARC in this process have not been defined, they have similar anti-apoptotic effects in myocardial cells, suggesting that these effects are related. Researchers found that H2O2 can induce ARC reduction in H9C2 cells but IGF-1 can change this trend. To clarify this trend using immunofluorescence and immunoblot analysis, researchers found that LY294002 (PI3K inhibitor) blocked IGF-1 up-regulation of ARC protein and blocked the protective effect of IGF-1 on myocardial cell apoptosis induced by oxidative stress. These results indicate that IGF-1 up-regulates ARC protein expression via the PI3K pathway which protects against myocardial cell apoptosis induced by oxidative stress.