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. 2023 Mar 4;62:102657. doi: 10.1016/j.redox.2023.102657

Fig. 6.

Fig. 6

Effect of AP123 on BAEC pre-treated with either PKA or PI3K inhibitor in HG conditions and on isolated vessels. (A) The concentration of total NOx levels in AP123-treated (10 nM, 2 h) BAEC pre-incubated with PKA inhibitor, KT5720 (1 μM, 30 min), or PI3K inhibitor, WM (100 nM, 30 min) and exposed to HG environment (3 h). *p < 0.05 vs. NG; #p < 0.05 vs. HG; §p < 0.05 vs. HG + AP123 + WM (B) Western blot analysis showing cropped images of the expression and/or phosphorylation of eNOS and CREB in AP123-stimulated BAEC pre-treated or not with KT5720 or WM exposed to HG environment. Densitometric analysis of (C) eNOS and (D) pCREB/CREB ratio. *p < 0.05 vs. NG; #p < 0.05 vs. HG; §p < 0.05 vs. HG + AP123 + WM. The graphs represent the mean ± SEM for each group (n = 3–5). (E) Ach-induced vasorelaxation in aorta rings stimulated with AP123 (10 nM) pre-treated with PI3K inhibitor, WM (100 nM, 30 min), and exposed to HG environment for 20 h (n = 5). The β-actin has been used as a housekeeping control protein. ###p < 0.001 vs. HG + AP123; §§§p < 0.001 vs. HG + AP123 + WM. Differences have been considered statistically significant when p was ≤0.05.