Objective To determine the protective effect of trimetazidine post-conditioning on cell apoptosis in rats induced by myocardial ischemia/reperfusion injury (MIRI). Methods Forty healthy adult Wistar rats were randomly assigned to sham-operation group, MIRI group, ischemic post-conditioning group and two trimetazidinee treatment groups (10 and 20mg/kg), with 8 rats in each group. MIRI model was established by ligation of coronary artery for 30min followed by 120min reperfusion. The rats in ischemic post-conditioning group were given another three times of ischemia/reperfusion for 30s at the interval of 30min ischemia and 120min reperfusion. Trimetazidinee or normal saline at same volume was given intragastrically to corresponding rats during the 30min ischemia. After MIRI, myocardial infarct area was measured, the expression of Bcl2 and bax was detected by immunohistochemical assays, and the myocardiocyte ultrastructure was observed with transmission electron microscopy. Results (1) Myocardial infarct area. No infarct was seen in the sham-operation group, but infarcts with different severities were found in the other groups, with those in the ischemic post-conditioning group and 20mg/kg trimetazidinee treatment group mildest (P＜0.01). (2) The expression of Bcl2/bax protein. The expression of Bax was very strong, while that of Bcl2 was very weak in the MIRI group, when compared with 20mg/kg trimetazidine group and ischemic post-conditioning group (both P＜0.01). (3) Morphology of cardiac muscle. Besides sham-operation group, ischemia/reperfusion injury and cardiocyte apoptosis were observed in other groups, with those in the ischemic post-conditioning group and 20mg/kg trimetazidinee treatment group most mildly. Conclusion Trimetazidine of 20mg/kg inhibits cardiocyte apoptosis in rats after MIRI.