Objective To investigate the impacts of aconitine on cardiac function and ventricular remodeling in heart failure model rats,and its regulatory effect on miR-150-5p during this process.Methods SPF grade SD male rats were randomly grouped into sham surgery group,model group,trimetazidine group,aconitine group,aconitine + antagonimir NC group,and aconitine + miR-150-5p antagonimir group,with 15 rats in each group.Except for the sham surgery group,all other groups established heart failure rat models by ligating the left anterior descending coronary artery.The left ventricular end diastolic diameter(LVEDD),left ventricular end systolic diameter(LVESD),and left ventricular ejection fraction(LVEF)were measured for cardiac function indicators of rats in each group.ELISA was applied to detect the levels of myocardial injury indicators cardiac troponin I(CTnI),brain natriuretic peptide(BNP),and N-terminal B-type brain natriuretic peptide precursor(NT-proBNP)of rats in each group.Heart and left ventricular mass index of rats in each group were measured.Masson staining was applied to observe the myocardial tissue morphology of rats in each group,TUNEL staining was applied to detect the apoptosis rate of myocardial cells of rats in each group.RT-qRCR was applied to detect the expression of miR-150-5p and cyclin D2(CCND2)in myocardial tissue of rats in each group.The double luciferase reporter gene experiment verified the targeting relationship between miR-150-5p and CCND2.Western blotting was used to detect the expression of CCND2 protein in myocardial cells.Results Compared with the model group,the cardiac function indicators LVEDD,LVESD,myocardial injury indicators CTnI,BNP,and NT proBNP levels,cardiac mass index,left ventricular mass index,myocardial fibrosis area,myocardial cell apoptosis rate and the level of CCND2 mRNA in the aconitine group decreased(P<0.05).The levels of LVEF and miR-150-5p increased(P<0.05).Supplementation experiments with miR-150-5p antagomir showed that the protective effects of aconitine on cardiac function and ventricular remodeling in rats with heart failure were reversed,and CCND2 mRNA levels were increased(P<0.05).Compared with miR-150-5p mimic-NC group,the expression of CCND2 protein in myocardial cells in miR-150-5p mimic group was significantly decreased(P<0.05),and the double luciferase reporter gene experiment verified that there was a targeted relationship between miR-150-5p and CCND2.Conclusion Aconitine plays a protective role in cardiac function and ventricular remodeling in rats with heart failure by up-regulating the expression of miR-150-5p.
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