Consistent with the previous reports3, 7, the present study also showed that the endogenous antioxidant proteins SOD-2 and thioredoxin, and the anti-apoptotic Bcl-2 were remarkably reduced in rat hearts subjected to ischemia/reperfusion injury, while pro-inflammatory factors Toll-like receptor 4 (TLR-4)43, IL-6 and TNFα, the pro-apoptotic molecules cleaved caspase-3 and Bax were significantly increased by ischemia/reperfusion injury. The gene discussed is BCL2; the disease is ischemia.