Expression and mechanism of miR-122 in rats with acute myocardial infarction

来源 :海南医科大学学报(英文版) | 被引量 : 0次 | 上传用户:jrff1
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Objective:To investigate the expression of miR-122 in acute myocardial infarction rats and its effect on cardiomyocyte apoptosis.Methods:80 male SD rats were randomly divided into Sham group, AMI group, empty virus group and virus group, and the rat model of acute myocardial infarction was constructed. The cardiac function index of rats was detected by echocardiography. The mRNA relative expression of miR-122 was analyzed by RT-PCR. The apoptosis of cardiomyocyte in rat was detected by TUNEL staining. The NC-shRNA and miR-122-shRNA stable cell lines were constructe, and the targeting relationship between miR-122 and XIAP was verified using luciferase reporter gene. West blot was used to analyze the effect of down-regulation of miR-122 on the expression of XIAP, Caspase-3 and Caspase-7.Results:Compared with Sham group, the miR-122 mRNA expression, LVEDD and LVESD in myocardial tissue of AMI group and empty virus group was significantly increased,while the LVFS and LVEF decreased significantly(P<0.05). Compared with the AMI group, the expression of miR-122 mRNA, LVEDD and LVESD decreased, and LVFS and LVEF increased in the myocardial tissue of the virus group (P<0.05). TUNEL staining showed that the apoptosis of cardiomyocytes in AMI group and empty virus group was significantly higher than that in Sham group (P<0.05), whereas the apoptotic index of cardiomyocytes in the virus group was significantly decreased compared with the AMI group (P<0.05).The luciferase reporter gene showed that miR-122 can down-regulate the expression of XIAP. West blot showed that compared with NC-shRNA cells, the expression of XIAP in miR-122-shRNA cells was significantly increased, while the expression of Caspase-3 and Caspase-7 was significantly decreased (P<0.05).Conclusion: The expression of miR-122 increased after acute myocardial infarction, and it may regulate the apoptosis of cardiomyocytes by targeting the expression of XIAP, Caspase-3 and Caspase-7.
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