Abstract: Objective To observe the changes of miR-138 on Sirt1 expression in ethanol induced Rat H9C2 myocardial cell lines and its downstream oxidative stress and mitochondrial apoptosis-related protein expression. Methods Cells were divided into control group, ethanol group (E group) and miR-138 inhibitor group (I group), every groups were cultured with different concentrations of alcohol culture media for 24h, cell viability was detected by MTT assay and 200mmol/L alcohol culture media was selected as the optimal concentration for following experiment. Group I was cultured with miR-138 inhibitor transfection media. After 12-hour-incubation, total superoxide dismutase (T-SOD) activity was analysed by hydroxylamine method and the content of malondialdehyde (MDA) was detected by thiobarbituric acid method. The expression of mRNA of miR-138 and Sirt1 were detected by RT-qPCR. The expression of Sirt1, Bax, Bcl-2 and caspase-3 protein was detected by Western blot. Results 1.Cell viability could be suppressed by alcohol. 2.Compared with control group, the content of MDA, the expression of miR-138 and both the protein expressions of Bax and caspase-3 were increased significantly (P<0.05) in ethanol group, the T-SOD activity, the mRNA expression of Sirt1, protein expressions of Sirt1 and Bcl-2 decreased significantly (P<0.05) in ethanol group. Compared with ethanol group, the content of MDA, the expression of miR-138 and both the protein expressions of Bax and caspase-3 decreased significantly (P<0.05) in miR-138 inhibitor group, the T-SOD activity, the mRNA expression of Sirt1, protein expressions of Sirt1 and Bcl-2 increased significantly (P<0.05) in miR-138 inhibitor group. Conclusions miR-138 increases oxidative stress of rat H9C2 cardiomyocytes induced by ethanol, Sirt1 may be the target of miR-138.

Key words: alcoholic cardiomyopathy, miR-138, silent information regulator 1, oxidative stress, apoptosis