We found that IPC significantly reduced the I/R-induced complement system and JNK activation by up-regulating the expression of HSP90, leading to further reductions in the myocardial infarction area, cardiomyocyte apoptosis, the release of cTnT, CK-MB and LDH, and the release of inflammatory mediators such as TNF-α and IL-1β, whereas, treatment with GA reversed the protection of IPC. The gene discussed is TNF; the disease is myocardial infarction.