摘要
Abstract
Objective To investigate the molecular mechanism of tetramethylpyrazine(TMP)in the treatment of acute myocardial infarction(AMI).Methods SD rats were randomly divided into sham group(only threading without ligation),AMI(ligation of left anterior descending coronary artery),AMI+TMP(20 mg·kg-1 TMP),AMI+TMP+miR-155-5p(20 mg·kg-1 TMP+miR-155-5p 200 μL),AMI+TMP+miR-155-5p+ACTA1 group(20 mg·kg-1 TMP+miR-155-5p and ACTA1 200 μL).The cardiac function of rats was detected by ultrasound.The expression of cardiac troponin Ⅰ(cTn Ⅰ)was detected by immunohistochemistry.Creatine kinase MB(CK-MB)was detected by enzyme-linked immunosorbent assay(ELISA).Terminal deoxynucleotidyl transferase-mediated nick end labeling(Tunel)assay was used to detect the apoptosis rate of cardiomyocytes.The levels of miR-155-5p and ACTA1 mRNA were detected by real-time fluorescence quantitative polymerase chain reaction(RT-qPCR).Results The expression levels of cTn Ⅰ in sham group,AMI,AMI+TMP,AMI+TMP+miR-155-5p,AMI+TMP+miR-155-5p+ACTA1 group were 1.04±0.21,13.63±1.92,7.88±2.23,11.96±3.02,8.34±1.88;the expression levels of miR-155-5p were 1.03±0.21,3.67±0.56,1.85±0.43,3.12±0.66,1.92±0.64,respectively;CK-MB levels were(37.03±7.98),(163.39±20.04),(77.63±15.77),(147.98±11.30),(80.56±10.39)U·L-1,respectively;the above indexes were compared between AMI+TMP group and AMI group,AMI+TMP+miR-155-5p group and AMI+TMP group,AMI+TMP+miR-155-5p+ACTA1 group and AMI+TMP+miR-155-5p group,and the differences were statistically significant(all P＜0.05).Conclusion TMP may inhibit apoptosis,reduce inflammation and myocardial fibrosis through miR-155-5p/ACTA1 molecular axis,and improve myocardial injury in AMI.关键词
川芎嗪/急性心肌梗死/炎性反应/心肌纤维化/分子机制Key words
tetramethylpyrazine/acute myocardial infarction/inflammatory response/myocardial fibrosis/molecular mechanism分类
医药卫生
