心肌细胞损伤 z-bo 2020-11-17 355

　　Purpose: To investigate the role and mechanism of miR-221 in rat cardiomyocyte (H9c2) injury induced by hydrogen peroxide (H2O2).

　　Method: MTT method detects the damage effect of H2O2 at different concentrations on H9c2 cells, and RT-PCR method detects the expression of miR-221. Transfer miR-221 inhibitor and negative control into H9c2 cardiomyocytes through Lipofectamine 2000, and divide the experiment into 4 groups, normal control group, model control group (H2O2 group), negative control group (H2O2+ negative control group), and inhibition group ( H2O2+miR-221 inhibitor group). MTT method was used to detect cell viability, acridine orange staining to detect cell apoptosis, Western blot to detect Bax, Bcl-2, phosphatase of chromosome 10 deletion, tensin homologous gene protein (PTEN) and p-protein kinase (AKT) )expression.

　　Result: 0, 25, 50, 100, 200, 400μmol/L H2O2 gradually strengthened the inhibitory effect on H9c2 cell viability, and 200μmol/L H2O2 inhibited cell viability moderately, so it was used as the follow-up induction dose. Compared with the normal control group, the expression of miR-221 in the model control group and the negative control group was significantly up-regulated (P<0.01), the viability of H9c2 cells was reduced (P<0.01), and the apoptosis rate was significantly increased (P<0.01), Bax And the expression of PTEN was up-regulated (P<0.01), and the expression of Bcl-2 and p-AKT was down-regulated (P<0.01). Compared with the model control group and the negative control group, the expression of miR-221 in the inhibition group was significantly down-regulated (P<0.01), the viability of H9c2 cells was increased (P<0.01), and the apoptosis rate was significantly reduced (P<0.01). Bax and The expression of PTEN was down-regulated (P<0.01), and the expression of Bcl-2 and p-AKT was up-regulated (P<0.01).

　　Conclusion: The low expression of miR-221 can significantly inhibit H2O2 induced H9c2 cardiomyocyte oxidative stress damage, which is related to the regulation of PTEN/AKT signaling pathway.