Apigenin suppresses the apoptosis of H9C2 rat cardiomyocytes subjected to myocardial ischemia‑reperfusion injury via upregulation of the PI3K/Akt pathway.

Apigenin, a flavonoid with multiple physiological and pharmacological activities, is associated with the prevention of cardiovascular diseases. The present study aimed to examine the roles and mechanisms of apigenin in the apoptosis of H9C2 rat cardiomyocytes, which were subjected to myocardial ischemia‑reperfusion (MI/R) injury. Cell viability, reactive oxygen species (ROS), mitochondrial membrane potential (MMP) and cellular apoptosis were evaluated using cell counting kit‑8 assays and flow cytometry. The content/activity of oxidative stress markers was determined using commercial kits. Western blot analysis and reverse transcription‑quantitative polymerase chain reaction assays were used to measure protein and mRNA expression, respectively. The results demonstrated that apigenin had limited cytotoxicity on the viability of H9C2 rat cardiomyocytes. Apigenin reduced the oxidative stress, ROS production and cellular apoptotic capacity of MI/R‑induced H9C2 cells. Apigenin additionally increased the MMP level of MI/R‑induced H9C2 cells. Furthermore, apigenin modulated apoptosis‑associated protein expression and phosphatidylinositol 3'-kinase (PI3K)/RAC‑α serine/threonine‑protein kinase (Akt) signaling in MI/R‑induced H9C2 cells. Treatment with LY294002 reversed the anti‑apoptotic effect of apigenin. In conclusion, apigenin suppressed the apoptosis of H9C2 cells that were subjected to MI/R injury by activating the PI3K/Akt pathway. It was suggested that apigenin may be effective as an MI/R therapy.