Liraglutide ameliorates high glucose - induced endothelial cell injuryvia Nrf2.

Objective: This study aimed to investigate the effect and mechanism of Liraglutide on high glucose-induced vascular endothelial cell injury. Methods Human umbilical vein endothelial cells (HUVECs) were cultured and divided into 4 groups: control, high glucose stimulation (HG), Liraglutide, and Liraglutide + HG group. ELISA was used to detect the secretion of inflammatory cytokines in each group, kits the levels of intracellular reactive oxygen species (ROS), the activity of SOD2 and Gpx4,and the level of MDA, and Western blot and immun of luorescence method nuclear translocation of Nrf2. Results The HG groupexhibited a significantly higher levels of tumor necrosis factor (TNF-α), interleukin (IL-1), IL-6, as well as the levels of intracellular ROS and MDA, but less activity of SOD2 and Gpx4, less contents of NO, and less nuclear translocation of Nrf2, as compared with the control group. Compared with the HG group, the Liraglutide + HG grouppresented significantly higher levels of TNF-α, IL-1, and IL-6, but lower levels of intracellular ROS and MDA, less activities of SOD2 and Gpx4, less contents of NO and less nuclear translocation of Nrf2. Conclusion Liraglutide suppresses high glucose-induced endothelial cell injury by increasing the nuclear translocation of Nrf2. [ABSTRACT FROM AUTHOR]