Upregulation of TRPC1 protects against high glucose-induced HUVECs dysfunction by inhibiting oxidative stress.

-To explore the effect of TRPC1 on endothelial cell function damage under a high glucose environment and its downstream molecular mechanism, and provide new theory and strategy for improving diabetic endothelial cell function and promoting vascular injury repair. In vitro, we use high glucose to treat human umbilical vein endothelial cells (HUVECs) and upregulated TRPC1 with adenovirus infection. HUVECs were split into 4 groups: (i) NG Group: Treated with normal glucose; (ii) HG Group: Treated with high glucose; (iii) HG + adGFP Group: High glucose + the control adenovirus (adGFP); (iv) HG + adTRPC1 Group: High glucose + recombinant adenovirus encoding TRPC1. We found that high glucose significantly decreased the expression level of TRPC1 protein, and impaired the proliferation and migration of HUVECs, which could be reversed by overexpression of TRPC1. In addition, high glucose induced an increase in ROS and MDA and a decrease in SOD activity, whereas TRPC1 overexpression could inhibit the growth of oxidative stress level. These findings suggest that overexpression of TRPC1 prevents HUVECs proliferation and migration dysfunction induced by high glucose via inhibiting oxidative stress injuries.