FIGURE 6.

Aliskiren increases autophagy-induced cell viability by activation of the AMPK pathway in OGD-treated H9c2 cells. (A) Representative images of the effect of aliskiren on AMPK expression in cardiac tissues at 1 day after MI by immunohistochemistry. Bar: 100 μm. (B,C) H9c2 cells were treated with 20 μM aliskiren after OGD 15 min or 16 h, and then AMPK phophorylation and LC3BII expression were detected by Western blotting. (D) Cardiomyocytes co-treated with 20 μM aliskiren with or without bafilomycin A1 or chloroquine (autophagy inhibitors), or AICAR (an AMPK activator), or dorsomorphin (an AMPK inhibitor), were exposed to OGD for 16 h, and then cell viability was examined by the MTT assay. ^∗P < 0.05 compared with OGD. ^†P < 0.05 compared with OGD + ALI. (E) Cardiomyocytes treated with 20 μM aliskiren, AICAR or dorsomorphin were exposed to OGD for 16 h, and then p-AKT and total AKT were examined by Western blotting. p-AKT was normalized to total AKT. (F) Autophagosomes were examined by acridine orange staining. Bar: 100 μm. Each of the experiments was repeated three times. The data are means ± SEM. GAPDH was used as the internal control. ^∗P < 0.05 compared with the control. ^†P < 0.05 compared with OGD.