OBJECTIVE： To study the effects of simvastatin on oxidative stress and cell apoptosis in aged mice with myocardial ischemia-reperfusion （IR）. METHODS： Aged mice were randomly divided into sham operation group （phosphate buffer solution）， model group （phosphate buffer solution） and simvastatin low-dose， medium-dose and high-dose groups （2.5， 5 and 20 mg/kg） with 14 mice in each group. Those groups were given relevant medicine intraperitoneally before modeling for 7 d， once a day. IR model was induced in those groups except for sham operation group. The area ratio of myocardial infarction， myocardial cell apoptosis rate， activity of myocardial tissue apoptosis gene Caspase-3， the protein expression of Bax and Bcl-2， Akt phosphorylation， serum concent of MDA and activity of SOD were all detected. RESULTS： Compared with sham operation group， the area ratio of myocardial infarction， myocardial cell apoptosis rate， Caspase-3 activity， the protein expression of Bax and MDA content were all increased in model group， while the protein expression of Bcl-2， Akt phosphorylation and SOD activity were decreased （P＜0.01）. Compared with model group， the area ratio of myocardial infarction， myocardial apoptosis rate， Caspase-3 activity， the protein expression of Bax and MDA content were all decreased in simvastatin high-dose group， while the protein expression of Bcl-2， Akt phosphorylation and SOD activity were increased （P＜0.01）. There was no statistical significance in above indexes in simvastatin low-dose and medium-dose groups （P＞0.05）. CONCLUSIONS： Simvastatin can relieve myocardial IR injury in aged mice， and the mechanism of which may be associated with inhibiting myocardial cell apoptosis and the generation of oxidative stress.