Mechanism of miR-182-5p Promoting Myocardial Cell Apoptosis in Rats with Myocardial Infarction
Objective:To investigate the mechanism of miR-182-5p promoting myocardial cell apoptosis in rats with myocardial infarction.Methods:Myocardial infarction model of rats was constructed.Myocardial apoptosis was detected by terminal deoxyribonucleotidyl transferase(TdT)-mediated dUTP nick end labeling(TUNEL).The expression of miR-182-5p and apoptosis-related molecules were detected by real-time quantitative fluorescent reverse transcription polymerase chain reaction(qRT-PCR)and Western Blot.miR-182-5p mimics and inhibitor transfected rat cardiomyocytes H9c2 to construct hypoxia model.Cell count Kit 8(CCK-8)was used to detect cardiomyocyte cell viability.The expression levels of apoptosis-related factor were detected by Western Blot.Caspase-3/7 activity detection kit was used to detect the activity of Caspase-3/7.The overexpression virus of miR-182-5p was constructed using pAAV9-CMV adeno-associated virus and injected into the mouse model of myocardial infarction through the tail vein to detect the effect of AAV9-miR-182-5p on the level of myocardial apoptosis induced by myocardial infarction.Results:The expression level of miR-182-5p decreased and the apoptosis level increased in the rat model of myocardial infarction.In H9c2 myocardial hypoxia model,miR-182-5p could aggravate the inhibition of hypoxia on cardiomyocyte viability,reduce the anti-apoptotic molecule B-cell lymphoma 2(Bcl-2),and increase the expression of pro-apoptotic molecule Bcl-2 associated X protein(Bax).At the same time,the activity of Caspase-3/7 was significantly promoted.The injection of AAV9-miR-182-5p significantly increased the level of apoptosis of cardiomyocytes in mouse myocardial infarction models.Conclusion:miR-182-5p can aggravate myocardial damage after myocardial infarction by promoting apoptosis.
myocardial infarctionmiR-182-5pmyocardial hypoxiacell apoptosisexperimental study
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