动物造模,心肌细胞损伤 z-bio 2023-03-01 393

　　Objective: To investigate the role and mechanism of miR-221 in hydrogen peroxide (H2O2)-induced myocardial cell injury in rats.

　　Methods: MTT method was used to detect the damage effect of different concentrations of H2O2 on H9c2 cells, and RT-PCR method was used to detect the expression of miR-221. miR-221 inhibitor and negative control were transferred into H9c2 cardiomyocytes by 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), inhibition group ( H2O2+miR-221 inhibitor group). MTT assay was used to detect cell viability, acridine orange staining was used to detect cell apoptosis, and Western blot was used to detect Bax, Bcl-2, chromosome 10 deletion phosphatase and tensin homologous gene protein (PTEN) and p-protein kinase (AKT) )Express.

　　Result: The inhibitory effect of 0, 25, 50, 100, 200, 400 μmol/L H2O2 on the viability of H9c2 cells was gradually strengthened, and 200 μmol/L H2O2 had a moderate degree of inhibition on cell viability, so it was used as the subsequent 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 increased (P<0.01), the viability of H9c2 cells was decreased (P<0.01), and the apoptosis rate was significantly increased (P<0.01). Bax The expressions of PTEN and PTEN were up-regulated (P<0.01), and the expressions of Bcl-2 and p-AKT were 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 decreased (P < 0.01). 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: Low expression of miR-221 can significantly inhibit H2O2-induced oxidative stress injury in H9c2 cardiomyocytes, which is related to the regulation of PTEN/AKT signaling pathway.