Effects Of Resistin On NO And CAMP In Human Umbilical Vein Endothelial Cell

Background:Vascular endothelial cells dysfunction is a main trait of metabolic syndrome (MS), and resistin is a recently discovered adipokinine, which plays an important role in the pathophysiological development of MS. Resistin may cast adverse effects on endothelial cell dysfunction. Nitric oxide (NO) and cyclic adenosine monophosphate (cAMP) have been found to play important roles in maintenance of vascular endothelial function.Objective: In this study we evaluated the effects of resistin on NO and cAMP levels in cultured human umbilical vein endothelial cells (HUVECs) to explore the potential mechanism of resistin on vascular endothelial function mediation.Methods: (1) Cultured HUVECs within passage 4-6 were inoculated in 96-well plate to reach 80 percent of confluence to be divided into 3 treatment groups:Ⅰmedium only control group,Ⅱ50ng/ml resistin incubation group,Ⅲ20ng/ml tumor necrosis factor-α(TNF-α) incubation group for 12h, and the supernatant obtained from the cultured HUVECs were collected, centrifuged to remove cell debris, then measured with the method of Nitrate reductase.(2) Cultured HUVECs within passage 4-6 were inoculated in Cell Culture Flasks to reach 80 percent of confluence to be divided into 3 treatment groups:Ⅰmedium only control group,Ⅱ50ng/ml resistin incubation group,Ⅲ20ng/ml TNF-αincubation group for 6h. Extracted and then measured the cAMP levels with Enzyme Linked Immunosorbent Assay kits (ELISA).Result: (1) Compared with control group, neither 50ng/ml resistin nor 20ng/ml TNF-αdecreased NO levels significantly in cultured HUVECs (p>0.05).(2) Compared with that of the control group, cAMP levels were significantly lower in resistin or TNF-αtreatment cells (p<0.05).Conclusion: Resistin has no effect on the secretion of NO from HUVECs, but decreased the cAMP level significantly, suggesting that resistin may cause endothelial dysfunction, partly, by reducing cAMP concentration.