The Effect And Mechanism Of Hedysarum Polybotrys Saccharide On HUVECs Induced By AGEs

Objective:The present study was designed to investigate the effect of HPS on the human umbilical vein endothelial cells (HUVECs) in vitro by advanced glycation end products (AGEs) which induced oxidative stress formation and to explore the mechanism. Methods:HUVECs were isolated from freshly collected umbilical cords. HUVECs were treated with AGEs in the presence or absence of HPS. Generation of reactive oxygen species (ROS) were measured using flow cytometry. Lipid peroxidation was assayed by measuring malondialdehyde (MDA) content, and antioxidant capacity was quantified by superoxide dismutase (SOD). The activation of Phosphotylinosital 3 kinase (PI3K), Total serine/threonine kinase (T-Akt) and phosphorylated serine/threonine kinase (P-Akt) were assayed by enzyme-linked immunosorbent assay (ELISA) and Immunofluorescence staining analysis. Results: Cell viability was decreased by exposed to AGEs (P<0.05); AGEs could induce the oxidative stress; HPS exerted its prosurvival effect by inhibiting the AGEs-induced overproduction of intracellular ROS and elevation of MDA content, as well as by promoting the recovery of SOD activities. AGEs significantly inhibited the expression of PI3K while pretreatment with HPS increased the level of PI3K. HPS also increaed the fluorescence intensity of P-Akt compared to AGEs group. HPS-induced antioxidation correlated with P-Akt activity and was inhibited by the specific PI3K inhibitor. Conclusions:It was demonstrated that AGEs decreased the cell viability of HUVECs, and induce the oxidative stress. HPS has a certain protection effect on AGEs-induced oxidative stress via PI3K/Akt signaling in HUVECs.