Research Paper Volume 15, Issue 19 pp 10291—10306

Figure 3. DOP treatment ameliorated HG-induced oxidative stress, IR and DNA damage of MPC5 cells by activating the phosphorylation of IRS-1/AKT. (A, B) IRS-1/2 inhibitor NT157 treatment remarkably impeded DOP-induced protective effects on HG-treated MPC5 cells, exhibiting as markedly decreased glucose consumption and increased malondialdehyde (MDA) generations. (C, D) IRS-1/2 inhibitor NT157 treatment notably reversed HG-induced increased phosphorylation of IRS-1 (phospho Y632), AKT (phospho Ser473), AKT (phospho Thr308) and Nephrin. (E) IRS-1/2 inhibitor NT157 treatment distinctly augmented DNA damage, exhibiting as markedly increased the formation of γ-H2A.X foci compared with DOP treated group. The bar in the figure indicates 10 μm. (F) DOP treatment remarkably increased the nuclear translocation of AKT, while this effect was notably counteracted by IRS-1/2 inhibitor NT157 treatment. The bar in the figure indicates 10 μm (*p < 0.05; ** p < 0.01; *** p < 0.001, n=3).