Objective To observe the effect of ischemia postconditioning(IPostC)on myocardial ischemia-reperfusion(I/R)in-jury in atherosclerosis(Apoe-/-+AS)model mice,and to study the mechanism of the effect of AAV9-HIF-1α on IPostC.Methods Sixty Apoe-/-+AS model mice were randomly divided into 6groups:control group(AS-sham group),Apoe-/-+AS-myocardial ischemia-reperfusion group(AS-I/R group),Apoe-/-+AS-ischemia postconditioning group(AS-IPostC group),Apoe-/-+AS-AAV9-HIF-1 α+ischemia postconditioning group(AS-AAV9-HIF-1 α+IPostC group),Apoe-/-+AS-AAV9-NC+ischemia postconditioning group(AS-AAV9-NC+IPostC group),Apoe-/-+AS-AAV9-HIF-1α+HIF-1α in-hibitor+ischemia postconditioning group(AS-AAV9-HIF-1α+2ME2+IPostC group),6mice in each group.Establish myocardial I/R models and IPostC models;adeno-associated virus-9 with human cytomegalovirus promoter negative control(AAV9-NC)and ad-eno-associated virus-9 with human cytomegalovirus promoter expressing HIF-1α(AAV9-HIF-1α)was separately injected through the tail vein.The histopathological changes of myocardium was observed,reactive oxygen species(ROS),adenosine triphosphate(ATP),and the activities of mitochondrial respiratory enzyme were detected;hypoxia inducible factor-1 α(HIF-lα),ATP synthase subunit b(ATP5F1),adenylate transporter(ANT)were detected by Western blot assay.Results Compared with AS-sham group,myocardial tissue injury was serious,ROS content was increased,ATP content was significantly decreased in AS-I/R group;compared with the AS-I/R group,ROS content was decreased,ATP content was increased in the AS-IPostC group,but mitochondrial respiratory enzyme activity was still lower,while myocardial injury was significantly decreased in the AS-AAV9-HIF-1α+IPostC group,and mi-tochondrial respiratory function was significantly improved.Conclusion During myocardial I/R injury in atherosclerotic mice,oxygen free radical activated by oxidative stress was released,mitochondrial respiratory function was weakened,cell energy was decreased,and myocardial cell was damaged,while AAV9-HIF-1α+IPostC can enhance myocardial mitochondrial respiratory function to a certain ex-tent through the above mechanisms.