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. 2012 Jun 5;7(6):e38787. doi: 10.1371/journal.pone.0038787

Figure 7. Activation of eNOS signaling pathway mediated protective effects of G1.

Figure 7

The endothelial cells were treated with high glucose (HG) for 72 h, and then treated with L-NAME (100 µM) for 40 min and G15 (1 µM) or without them in presence of G1 (10 nM) for 10 min. (A) G1 treatment (10 nM, 10 min) reversed the down-regulation of phosphorylation level of eNOS by high concentration of glucose. This effect was blocked by G15. (B) G1 reversed the NO reduction in endothelial cells exposure to HG. This effect of G1 was blocked by L-NAME and G15. High concentration of mannitol (33 mM) did not alter the phosphorylation level of eNOS. ** p<0.01 compared with the glucose treated before; # p<0.05, ## p<0.01 compared with the HG treated; $ p<0.05, $$ p<0.01 compared with the HG+G1 treated. Results are given as the mean ± SEM of three independent experiments.