It is interesting to note that acacetin treatment remarkably prevented the ischemia/reperfusion–induced reduction of SOD-2 and Bcl-2, preserved their activities, and thereby inhibited inflammation mediators (TLR-4, IL-6, and TNFα) and cardiomyocyte apoptosis and decreased the myocardial infarct size (Fig. 8). This evidence concerns the gene BCL2 and myocardial infarction.