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. 2017 Apr 7;12:776–786. doi: 10.1016/j.redox.2017.04.008

Fig. 7.

Fig. 7.

Protective activation of PI3K/AKT/eNOS signaling pathway by high laminar flow is inhibited by CSEaq. (A–B) mRNA expression of eNOS (endothelial nitric oxide synthase) in HUVEC exposed to 50% CSEaq after subjected to high or low laminar flow conditions for 7 h, n≥6. (C) Phosphorylation status of AKT pathway in primary human endothelial cells after short-time stimulation with high laminar flow. Cells were resting in basal media without supplements for 60 min prior stimulation, n≥6. (D) Re-phosphorylation of AKT after resting in response to increasing dosages of CSEaq, n≥5. (E) eNOS phosphorylation status after 10 h of CSEaq treatment under static conditions and high laminar flow, n≥6. Data are shown as mean (x-fold basal controls) ±SD. Time-matched controls are normalized to basal controls as well. *p<0.05 vs. basal controls, #p<0.05.