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. 2018 Nov 5;23(1):464–475. doi: 10.1111/jcmm.13949

Figure 5.

Figure 5

Effects of P‐II on oxidative stress in HUVECs induced by Hcy. HUVECs were stimulated with Hcy alone or in combination with different concentrations of P‐II, or siRNA LOX‐1, OR SIRT1 cDNA. (A). Hcy significantly increase ROS production after treatment for 24 hours, but pretreated with P‐II or siRNA LOX‐1 or SIRT1 cDNA for 24 hours, Hcy‐induced ROS production were decreased markedly; (B‐E). HUVECs that were treated with Hcy for 24 hours demonstrated a significant increase in MDA levels (B) and NADPH oxidase activity (C), and concomitant decrease in the activity of SOD (D) and CAT (E), P‐II or siRNA LOX‐1 or SIRT1 cDNA prevent Hcy‐induced lipid peroxidation, reduced NADPH oxidase activation and increased the activity of antioxidant enzymes in HUVECs (B‐E). Overexpressing of LOX‐1 (LOX‐1cDNA) partly abolished the P‐II‐induced protection against Hcy‐caused NADPH oxidase activation (Figure 6A‐E). (F) NF‐κBp65 was determined with nuclear protein from endothelial tissues. The data are shown as the mean ±SD of six separate experiments. *P < 0.05 as compared to control group cells, # P < 0.05 as compared to Hcy‐treated cells