Mechanism of aerobic exercise ameliorating myocardial injury in rats with acute myocardial infarction by regulating autophagy through miR-34a/SIRT1 pathway
Objective To explore the regulatory mechanism of aerobic exercise ameliorating myocardial injury in acute myocardial infarction(AMI)rats.Methods A total of 24 male SD rats were randomly divided into sham-operated group,model group and aerobic exercise group,eight in each group.AMI model was constructed by ligating the left anterior descending branch of the coronary artery.Rats in the aerobic exercise group was subjected to 4 consecutive weeks of aerobic exercise.The histological morphology and degree of fibrosis of rat hearts in all groups were observed by HE staining and Masson staining.The plasma brain natriuretic peptide(BNP)level in rats was detected by enzyme-linked immunosorbent assay(ELISA).Fractional shortening(FS)and ejection fraction(EF)were assessed by transthoracic echocardiography(TTE).The expression of miR-34a was detected by RT-qPCR,and the autophagy related protein expression was analyzed by western blot(WB).The hypoxia cell model was constructed using H9C2 cells,and then transfected with miR-34a inhibitor or siSIRT1.The expression of miR-34a was detected by RT-qPCR.The lactate dehydrogenase(LDH)and superoxide dismutase(SOD)levels in cell supernatant were analyzed by ELISA.The expression of autophagy-related proteins was detected by WB.Results Compared with the model group,the aerobic exercise group showed significant improvement in cardiac tissue morphology,fibrosis,BNP expression,and autophagy level,the expression of miR-34a was down-regulated in the aerobic exercise group,and the differences were statistically significant(P<0.01).Compared with the hypoxia+miRNA NC group,the hypoxia+miR-34a inhibitor group showed down regulation in LDH and autophagy levels,but upregulation in SOD and SIRT1 expressions(all P<0.01).Compared with hypoxia+miR-34a inhibitor+siNC group,hypoxia+miR-34a inhibitor+siSIRT1 group had higher LDH and autophagy levels,and lower SOD and SIRT1 expressions(all P<0.01).Conclusion Aerobic exercise can inhibit cardiomyocyte autophagy levels via miR-34a/SIRT1 pathway,thereby ameliorates myocardial injury in AMI rats.This provides a new mechanism to study the improvement of myocardial injury in AMI by aerobic exercise and contributes to the prevention and treatment of AMI.
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