Astragaloside IV Inhibits Oxidative Stress-Induced Mitochondrial Permeability Transition Pore Opening by Inactivating GSK-3𝛽 via Nitric Oxide in H9c2 Cardiac Cells

Figure 2

Western blotting analysis of GSK-3β at Ser⁹ and Akt at Ser⁴⁷³ phosphorylation and Tubulin protein in cardiac H9c2 cells. Astragaloside IV (50 μM) increased GSK-3β and Akt phosphorylation compared to control, the effect that was reversed by PI3 K inhibitor LY294002 (10 μM). Data are mean ± SD for 6 independent experiments performed in duplicate. *𝑃<0.05compared to control group; ^#𝑃<0.05 compared to astragaloside IV (ANOVA followed by Tukey’s test).