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. 2018 Jun 21;115(1):168–178. doi: 10.1093/cvr/cvy157

Figure 5.

Figure 5

Isoflurane (ISO) induced increases in phosphorylated Akt (p-Akt) and endothelial nitric oxide synthase (eNOS) and nitric oxide (NO) production in endothelial cells. (A) Blockade of ISO-induced Akt phosphorylation by neutralizing anti-vascular endothelial growth factor (nVEGF) in endothelial cells. Top: western blot bands showing the expression of p-Akt, Akt, and β-actin as a loading control in endothelial cells; bottom: the ratio of p-Akt/Akt; (B) blockade of ISO-induced eNOS phosphorylation by nVEGF in endothelial cells. Top: representative western blot bands showing the expression of phosphorylated eNOS (p-eNOS) at the activation site Serine1177, eNOS, and β-actin; bottom: the ratio of p-eNOS/total eNOS. In A and B, endothelial cells were pre-treated with nVEGF or IgG prior to ISO and subsequently subjected to hypoxia/reoxygenation. *P < 0.05 vs. control; †P < 0.05 vs. ISO (n = 4). (C) Blockade of ISO-induced increases in NO production by wortmannin (WM) in endothelial cells. The values of the control groups were arbitrarily defined as one in each batch of experiments. Data are presented as mean ± SEM. Kruskal–Wallis test followed by Dunn’s test was used to analyse multiple group comparisons. *P < 0.05 vs. control; †P < 0.05 vs. WM, ‡P < 0.05 vs. ISO (n = 7).