Objective To explore the effects of ischemic postconditioning on myocardial apoplosis in the heart of diabetic rat and investigate (he signal transduction pathway changes induced by ischemia postconditioning. Methods Diabetic model was induced by streptozotozin (STZ)45 mg/kg. All rats were injected with STZ intravenously and randomly divided into 4 groups (n =8 /group):(1) Ischernia-reperrusion (IR) group:the rats were subjected to 30 minutes ischemia by left anterior descending coronary artery occlusion (LADO),and reperfusion without additional intervention; (2) IPost plus wortmannin group.after 30 minutes of LADO,rats were treated with wortmannin (15 μg/kg, iv) at 5 minutes before coronary reperfusion,and then followed by IPost treatment and 2 hours reperfusion; (3) IPost group:after 30 minutes of LADO,the coronary artery was occluded for 30 seconds and repeated 3 limes. The coronary artery was reperfused for 2 hours; (4)IR plus wortmannin group:at 5 minutes before coronary reperfusion, rats were treated with wortmannin (15 μg/kg,iv) and followed by 2 hours reperhision. Myocardial apoptosis was measured by TUNEL,and the myocardial Bcl-2,Bax, Phospho-Alct (ser473) and Akt expression were assessed by Western blot. Results Compared with other groups,myocardial apoptosis and Bax protein expression significantly reduced (P < 0.01),and the Bcl-2 protein expression,the ratio of Phospho-Akt (ser473) to Akt increased significantly (P< 0.01). Phosphatidylionsitol 3-kinase (PI3K) inhibitor wortmannin prevented the increase of Bcl-2 protein expression, the ratio of Phospho-Akt (ser473) to Akt. Conclu-sion Ischemic postconditioning can reduce the myocardial apoplosis in the heart of diabetic rat. The effects were partly mediated through PI3K/Akt signaling pathway.