Effect Of High Glucose On MiR-26 Expression In H9C2 Cardiomyocytes And Its Mechanism

Objective: Diabetic cardiomyopathy(DCM)is one of the complications of diabetes mellitus,and the changes of mi RNAs is closely related to the development of DCM.By observing the proliferative activity,apoptosis and changes of mi R-26a/b expression in H9C2 cardiomyocytes treated with high glucose,and exploring the proliferative activity and apoptosis of H9C2 cardiomyocytes treated with high glucose after over-expressing/inhibiting mi R-26 a,then we revealed the relationship between mi R-26 and the development of DCM.Methods: The proliferative activity of H9C2 cardiomyocytes treated with different concentrations of glucose(5.5 mmol/l,15 mmol/l,25 mmol/l,35 mmol/l)at different times was detected by CCK-8.The apoptosis rate of H9C2 cardiomyocytes with different concentrations of glucose intervention was detected by flow cytometry.The expression levels of mi R-26a/b in H9C2 cardiomyocytes treated with different concentrations of glucose was detected by RT-PCR.The expression levels of mi R-26a/b in H9C2 cardiomyocytes treated with high glucose(25 mmol/l)in different time was detected by RT-PCR.And we measured the levels of mi R-26 b in the heart,adipose tissue,liver and other tissues of C57BL/6J and ob/ob mice by RT-PCR.After over-expressing and inhibiting mi R-26 a,we detected the proliferative activity of H9C2 cardiomyocytes treated with high glucose(25 mmol/l)by CCK-8 and the apoptosis rate of H9C2 cardiomyocytes treated with high glucose(25 mmol/l)by flow cytometry.Results: 1.Compared with 5.5 mmol/l glucose group,the proliferative activity of H9C2 cardiomyocytes was significantly increased in 15 mmol/l,25 mmol/l and 35 mmol/l glucose group(p<0.05);2.Compared with 5.5 mmol/l glucose group,the apoptosis rate of H9C2 cardiomyocytes was significantly decreased in 15 mmol/l,25 mmol/l and 35 mmol/l glucose group(p<0.05);3.High glucose can decrease the expression of mi R-26a/b in H9C2 cardiomyocytes,while the reduction is more significant with the prolongation of intervention time(p<0.05);4.The expression of mi R-26 b was the highest in the heart of the C57BL/6J mice,significantly higher than in the cardiac and white adipose tissues of the ob/ob mice(p<0.05);5.Mi R-26 a over-expression can inhibit the proliferative activity of H9C2 cardiomyocytes treated with high glucose,and mi R-26 a inhibition can enhance the proliferative activity of H9C2 cardiomyocytes(p<0.05),but mi R-26 a over-expression and inhibition can not effect the apoptosis rate of H9C2 cardiomyocytes(p>0.05).Conclusion: 1.High glucose can promote the proliferation,reduce apoptosis and decrease mi R-26a/b expression of H9C2 cardiomyocytes;2.Over-expressing/inhibiting mi R-26 a affects the proliferation of cardiomyocytes,but does not affect apoptosis;3.MiR-26 may participate in the pathogenesis of DCM by regulating the proliferation of cardiomyocytes.