大鼠心肌细胞损伤,miR-221 z-bio 2021-09-24 636

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

　　Method: MTT method detects the damaging effect of different concentrations of H2O2 on H9c2 cells, and RT-PCR method detects the expression of miR-221. The miR-221 inhibitor and negative control were transferred into H9c2 cardiomyocytes through Lipofectamine 2000, and the experiment was divided 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 was used to detect cell apoptosis, Bax, Bcl-2, and Western blot were used to detect the expression of phosphatase deleted on chromosome 10, Tensin homologous gene protein (PTEN) and p protein kinase (AKT).

　　Results: 0, 25, 50, 100, 200, 400μmol/LH2O2 gradually increased the inhibitory effect on H9c2 cell viability, and 200μmol/LH2O2 moderately inhibited cell viability, which was used as a follow-up induction dose. Compared with the normal control group, the expression of miR-221 in the model group and the negative control group was significantly up-regulated (Pu003c0.01), H9c2 cell viability decreased (Pu003c0.01), and cell apoptosis decreased. The rate was significantly increased (Pu003c0.01), the expression of Bax and PTEN was up-regulated (Pu003c0.01), and the expression of Bcl-2 and p-AKT was down-regulated (Pu003c0.01). Compared with the model control group and the negative control group, the expression of miR-221 in the inhibition group was significantly down-regulated (Pu003c0.01), the viability of H9c2 cells was increased (Pu003c0.01), and the apoptosis rate was increased. Significantly decreased (Pu003c0.01) . The expression of Bax and PTEN was down-regulated (P\u003c0.01), and the expression of Bcl-2 and p-AKT was up-regulated (P\u003c0.01).

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