Verapamil modulates AMPK/GSK-3β/Nrf2 signaling pathway for myocardial protection in rats with acute myocardial infarction
Objective To investigate the myocardial protective effect of verapamil on acute myocardial infarction rats by regulating the AMPK/GSK-3β/Nrf2 pathway.Methods The rats were divided into sham operation group,model group,verapamil(0.165 and 0.660 mg/kg)group,verapamil+Compound C group,with 18 rats in each group.After successful modeling for 1 h,they were immediately administered once daily for 7 days.The changes in LVFS and LVEF in rats were detected,2,3,5-triphenyltetrazolium chloride staining was applied to detect the percentage of myocardial infarction area,HE staining was applied to detect pathological changes in myocardial tissue,the levels of MDA and cTnI and the activities of CK-MB and SOD in myocardial tissue were detected by the kit.TUNEL staining detect myocardial cell apoptosis,Western blotting detect p-AMPK,p-GSK-3β,and Nrf2 proteins in myocardial tissue.Results Compared with model group,the degree of myocardial cell disruption in the verapamil group was improved,the LVFS,LVEF,activities of SOD and the expression of p-AMPK,p-GSK-3β,and Nrf2 proteins in myocardial tissue increased,the percentage of myocardial infarction area,levels of MDA,cTnI,activities of CK-MB in myocardial tissue,and apoptosis rate of myocardial cells decreased(P<0.05).Compound C weakened the protective effect of verapamil on myocardial injury in acute myocardial infarction rats.Conclusion The mechanism of verapamil improving myocardial injury in acute myocardial infarction rats may be related to the activation of the AMPK/GSK-3β/Nrf2 pathway.
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