动物造模,急性心肌梗死 z-bio 2022-02-25 505

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

　　Methods: The AMI model was established by ligating 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. miR-126 mimics NC and miR-126 mimics were transfected by lentivirus injection, and the left anterior descending coronary artery was threaded without ligation in the sham operation group. The cardiac function of rats was recorded, the myocardial apoptosis index and infarct size were detected by TCC method and in situ terminal apoptosis method (TUNEL), the activities of aspartate proteolytic enzyme (Caspase 3) and Caspase 8 were detected by colorimetric method, Western-blot The expressions of Bax and Bcl-2 were detected by RT-PCR, and the mRNA expressions of Fas and Fas-L were detected by RT-PCR.

　　Results: Compared with the sham operation group, the left ventricular ejection fraction (LVEF) and left ventricular long-axis fractional shortening (FS) in the AMI group and the NC group were increased, and the left ventricular end-diastolic diameter (LVDd) and left ventricular end-systolic diameter (LVDs) were increased. ) decreased, myocardial apoptosis 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 could reverse this change, and the difference was statistically significant (P<0.01).

　　Conclusion: miR-126 can significantly inhibit the apoptosis of cardiomyocytes in AMI rats, which is related to the regulation of apoptosis-related protein expression.