miR-126,急性心肌梗死大鼠 z-bo 2020-11-12 394

　　Objective: To investigate the effect of miR-126 on myocardial cell apoptosis in rats with acute myocardial infarction (AMI).

　　Methods: The AMI model was established through ligation of the left anterior descending coronary artery in rats, and they were randomly divided into AMI group, miR-126 mimics negative control (NC) group and miR-126 group. The NC group and miR-126 group used local myocardial tissues. The miR-126 mimics NC and miR-126 mimics were transfected with lentivirus, and the left anterior descending coronary artery was threaded and not ligated in the sham operation group. Record rat heart function, TCC method and in situ terminal apoptosis method (TUNEL) to detect myocardial apoptotic index and infarct size, colorimetric method to detect aspartate proteolytic enzyme (Caspase 3) and Caspase 8 activity, Western-blot Method to detect the expression of Bax and Bcl-2, while RT-PCR method to detect the expression of Fas and Fas-L mRNA.

　　Results: Compared with the sham operation group, left ventricular ejection fraction (LVEF) and left ventricular long axis shortening fraction (FS) increased, left ventricular end diastolic diameter (LVDd) and left ventricular end systolic diameter (LVDs) were increased in AMI group and NC group ) Decreased, myocardial apoptotic index increased, myocardial infarction area increased, Caspase 3 and Caspase 8 activities increased, Bax protein expression increased, Bcl-2 protein expression decreased, Fas and Fas-L mRNA levels increased, the difference was statistically significant Significance (P<0.01). Compared with the AMI group and the NC group, the miR-126 group can reverse this change, and the difference is statistically significant (P<0.01).

　　Conclusion: miR-126 can significantly inhibit cardiomyocyte apoptosis in AMI rats, which is related to regulating the expression of apoptosis-related proteins.