Figure 7
The Akt pro-survival pathway associated with GSK-3β signalling takes part in EGCg-mediated Cav-1 activation. (a) Western blotting with quantitative analyses of Akt phosphorylation at ser-473 and its downstream substrate GSK-3β phosphorylation at ser-9 in H9c2 cells. (b) Immunoblot analysis showing effects of EGCg and/or GSK-3β inhibition by GSK-3α/3β inhibitor, SB 216763, on the phosphorylation of pGSK-3β (S9) and pCav-1 (Y14) in H2O2-induced H9c2 cells. (c) MTT assay showing the improvement of H2O2,-suppressed cell viability by EGCg and/or GSK-3β inhibitor, SB 216763 pre-treatment in H2O2-induced H9c2 cells. In a and b, each value is the mean ± SEM (n = 6). *indicates significant difference compared to H9c2 cells in control condition, and # symbolizes a significant difference compared to cells treated with H2O2 (H). In a and c, each value is the mean ± SEM (n = 6). *indicates significant difference compared to H9c2 cells in control condition, # symbolizes a significant difference compared to cells treated with H2O2, and $ represents a significant difference compared to cells pretreated with EGCg in prior to H2O2 treatment.