This inflammatory response which is triggered during ischemia, andgreatly amplified during reperfusion, is characterized by increased levels of inflammatoryand pro-inflammatory cytokines, including interleukin-1β (IL-1β), tumor necrosis factor-α(TNF-α), IL-6 and partially contributes to cardiac dysfunction and necrosis of cells (4-6).Increasing evidence suggests that inhibition of I/R-induced excessive inflammatory responsecan improve heart dysfunction caused by I/R injury (7, 8). This evidence concerns the gene TNF and ischemia.