Objective:To investigate the effect of butorphanol regulating fatty acid synthetase(Fas)/fatty acid synthetase ligand(FasL) signaling pathway on myocardial cell apoptosis in rats with acute myocardial infarction(AMI).Methods:Rats were grouped into blank group,AMI group,low-dose butorphanol group(12.5μg/kg),high-dose butorphanol group(50μg/kg),urokinase group (50000 U/mL),rh-FasL group(0.017 mg/kg),and high-dose butorphanol+rh-FasL group(50μg/kg+0.017 mg/kg),with 18 rats in each group.Except for the blank group,all other groups were used to establish the AMI model by ligating the anterior descending branch of the left coronary artery.After 1 hour of successful modeling,medication was administered once a day for 7 days.The changes of left ventricular end-systolic diameter(LVESD),left ventricular end-diastolic diameter(LVEDD),left ventricular short-axis shortening rate(LVFS),and left ventricular ejection fraction(LVEF) were detected by color Doppler ultrasonography.Serum levels of interleukin-6(IL-6),tumor necrosis factor-α(TNF-α),creatine kinase isoenzyme(CK-MB),and cardiac troponin Ⅰ(cTnⅠ) were detected by enzyme-linked immunosorbent assay(ELISA).2,3,5-triphenyltetrazolium chloride(TTC) staining was used to detect the percentage of myocardial infarction in rats.Hematoxylin-eosin(HE) staining was used to detect pathological changes of myocardial tissue in rats.Apoptosis of rat cardiomyocytes was detected by terminal deoxyribonucleotidyl transferase(TdT)-mediated dUTP nick end labeling(TUNEL).The expressions of Bim,B lymphoblastoma-2 gene(Bcl-2),Fas and FasL protein in rat myocardium were detected by Western Blot.Results:Compared with the blank group,the myocardial tissue pathological damage in the AMI group rats was severe,the LVESD,LVEDD,the levels of IL-6,TNF-α,CK-MB,cTnⅠ,the percentage of myocardial infarction area,apoptosis rate of myocardial cells,and the expression of Bim,Fas,and FasL proteins increased,the LVFS,LVEF,and the expression of Bcl-2 protein decreased (P<0.05).Compared with the AMI group,the myocardial tissue pathological damage of rats in the low-dose group,high-dose group,and urokinase group reduced,the LVESD,LVEDD,the levels of IL-6,TNF-α,CK-MB,cTnⅠ,the percentage of myocardial infarction area,apoptosis rate of myocardial cells,and the expression of Bim,Fas,and FasL proteins decreased,the LVFS,LVEF,and the expression of Bcl-2 protein increased,and the corresponding indicators in the rh-FasL group showed opposite trends(P<0.05).Compared with the high-dose butorphanol group,the high-dose butorphanol+rh-FasL group of rats showed increased pathological damage in the myocardial tissue,the LVESD,LVEDD,the levels of IL-6,TNF-α,CK-MB,cTnⅠ,the percentage of myocardial infarction area,apoptosis rate of myocardial cells,and the expression of Bim,Fas and FasL proteins increased,the LVFS,LVEF,and the expression of Bcl-2 protein decreased (P<0.05).Conclusion:Butorphanol may inhibit inflammatory response and myocardial cell apoptosis in AMI rats by inhibiting the Fas/FasL pathway.
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