Objective To explore the role of NLRP3/Caspase-3 in myocardial apoptosis induced by ischemia/reperfusion(IR)injury and its effect on myocardiocyte autophagy in rats.Methods A total of 60 SPF-grade male rats were randomly divided into sham operation,model,and nimodip-ine treatment groups,with 20 rats in each group.Rat model of myocardial IR injury was estab-lished in the rats of the two latter groups.Cardiac function was assessed,and the levels of myocar-dial enzymes and cytokines were measured.Additionally,myocardial pathological changes were de-tected using HE staining.Furthermore,flow cytometry was utilized to determine the apoptotic rate of myocardiocytes,and the autophagosomes were counted under transmission electron micro-scope.Moreover,the expression of NLRP3 and Caspase-3 was measured using RT-PCR and West-ern blotting.Results Significant differences were observed in left ventricular end diastolic pres-sure,left ventricular systolic pressure,maximal rate of rise and fall in left ventricular pressure,ap-optotic rate of myocardial cells,and levels of TNF-α,IL-6,CK,AST and LDH in the three groups(P＜0.01).Notably,both the model group and nimodipine treatment group exhibited significantly higher autophagosome than the sham operation group(10.55±1.87 and 6.32±1.43 vs 3.45±0.67 units,P＜0.01),and the nimodipine group displayed a significantly lower autophagosome count than the model group(P＜0.01).The mRNA and protein levels of NLRP3 and Caspase-3 were notably higher in the model group and nimodipine group than the sham operation group(P＜0.01),and in the model group than the nimodipine group(P＜0.01).Conclusion Myocardial IR injury in rats can increase myocardiocyte apoptosis,reduce cardiac function,induce inflammatory response,and enhance autophagosome formation,which is related to the abnormal high expression of NLRP3/Caspase-3.