The Effect Of MicroRNA-122 On H9C2 Cardiomyocyte Apoptosis Induced By Hypoxia

Objective: To investigate the effect of miR-122 on hypoxia-induced cardiomyocyte apoptosis and cell viability,explore the role of miR-122 in myocardial infarction,and provide a theoretical basis for clinical diagnosis and treatment of myocardial infarction.Methods:（1）Cell culture: rat H9C2 cardiomyocytel line was selected as the experimental object and cultured in complete serum medium.（2）The cells in logarithmic growth phase were selected and transfected into H9C2 cardiomyocytes by transient transfection.The transfection efficiency of miR-122-5p mimic and its control（mimic NC）,miR-122-5p inhibitor and its control（inhibitor NC）were detected by qRT-PCR 24-48 hours after transfection.（3）The transfected cardiomyocytes used anaerobic tank and anaerobic gas production bag to construct the cardiomyocyte hypoxia model.CCK-8experiment was used to detect the viability of cardiomyocytes in each group,annexin V-FITC / PI double staining flow cytometry was used to detect the apoptosis rate of cardiomyocytes in each group,Western blot was used to detect the expression of Caspase-8 and Bcl-2 proteins in each group,and image software was used to analyze whether there were differences in the expression levels of apoptosis-related proteins in each group.Results:（1）qRT-PCR showed that the expression level of miR-122 in cardiomyocytes transfected with miR-122-5p mimic was significantly increased compared with the control group（P < 0.0001）,and the expression level of miR-122 in cardiomyocytes transfected with miR-122-5p inhibitor was decreased compared with the control group（P < 0.001）;（2）Compared with the mimic NC group,the miR-122-5p mimic group exhibited decreased cardiomyocyte viability,higher apoptosis rate,increased Caspase-8 protein expression,and lower Bcl-2 protein expression;Compared with the inhibitor NC group,the miR-122-5p inhibitor group exhibited higher cardiomyocyte viability,lower apoptosis rate,lower Caspase-8 protein level,and higher Bcl-2protein expression level,all of which were statistically significant.Conclusions:（1）Transient transfection can regulate the expression level of miR-122 within cardiomyocytes;（2）Mi R-122 can reduce cardiomyocyte viability and aggravate cardiomyocyte apoptosis,affecting the expression levels of apoptosis-related proteins.