Abstract: Objective Investigate the relation between decrease of apoptosis caused by delayed preconditioning and expression of SMAC and XIAP. Methods Sprage－Dawleyt rats were divided into four groups: control, sham, I/R and IPC/SWOP. The rats in I/R group underwent ischemia for 1 hour by classic artery ligation and reperfusion for 1 hour. The rats in IPC/SWOP group underwent tree cycles of 5-minute ischemia and 5-minute reperfusion 24 hours prior to the index occlusion. Cell apoptosis was measured by flow cytometry, the activity of caspase-3 was also measured. The expression of SMAC and XIAP in cytosol of myocardial cell was analyzed by Western blot. Results Cell apoptosis rate, activity of caspase-3 and expression of SMAC increased significantly in I/R compared with control (p<0.01). The expression of XIAP decreased in I/R compared with control (p<0.01). In IPC/SWOP, cell apoptosis rate, activity of caspase-3 and expression of SMAC decreased significantly compared with I/R (p<0.01). The expression of XIAP increased in IPC/SWOP compared with I/R (p<0.01). Conclusion Myocardial ischemia delayed preconditioning can suppress apoptosis caused by MI/R, the mechanism is related to inhibition of SMAC release from Mitochondria, and in turn maintaining the inhibition of caspase family by XIAP.

Key words: ischemia-reperfusion injury, delayed preconditioning, Smac, XIAP