Figure 6
From: Suppression of GRK2 expression reduces endothelial dysfunction by restoring glucose homeostasis

Normalization of glucose concentration improved impaired insulin-stimulated NO production in HUVECs induced GRK2 under high glucose (HG) and high insulin (HI). (A) Experimental protocol for HUVECs. L/L (Control) HUVECs were incubated in LG (5 × 10−3 mol/L) medium for 72 h, which was then replaced with the same medium. H/H (quasi-diabetic state) HUVECs were incubated in HG (22 × 10−3 mol/L)/HI (10−7 mol/L) medium for 72 h, which was then replaced with the same medium. H/L HUVECs were incubated in HG/HI medium for 72 h, which was then replaced with LG medium. (B) NO released from HUVECs was measured under insulin stimulation or non-stimulation. Data presented as insulin-stimulated NO production values after deduction of non-stimulated NO production values. HUVECs were treated with insulin (10−6 mol/L) for 20 min, 0, (2), 6 or 24 h after medium replacement. Values are mean ± SE; n = 6. * p < 0.05, ** p < 0.01, *** p < 0.001 vs. L/L (0 h); ††p < 0.01, †††p < 0.001 vs. H/L (0 h) by one-way analysis of variance.