Abstract：Objective To explore the influence of Exenatide on homocysteine (Hcy)-induced injury in human umbilical vein endothelial cells (HUVECs).Methods Hcy-induced HUVECs were used to establish an inflammatory injury model,which were divided into the normal group,the model group (200 μmol/L Hcy),the low dose of Exenatide treatment group (200 μmol/L Hcy,ExE-L 5 nmol/L),the medium dose of Exenatide treatment group (200 μmol/L Hcy,ExE-M 10 nmol/L),the high dose of Exenatide treatment group(200 μmol/L Hcy,ExE-H 20 nmol/L).The cell viability in each group was detected,and the content of nitric oxide(NO),the level of interleukin-6(IL-6),the level of intercellular adhesion factor-1(ICAM-1),the level of endothelin-1(ET-1),the expression of inhibitor protein kappa B-alpha(IκBα)and nuclear factor-κB (NF-κB)p65 protein were compared.Results The cell viability,the content of NO and protein expression of IκBα in the model group were significantly lower than that in the control group,the supernatant levels of IL-6,ICAM-1 and ET-1 and protein expression of NF-κB p65 in the model group were significantly higher than those in the control group,with significant difference (P＜0.05).The cell viability,the content of NO and protein expression of IκBα in the each Exenatide group were significantly lower than those in the model group,the supernatant levels of IL-6,ICAM-1,ET-1 and the protein expression of NF-κB p65 in the each Exenatide group were significantly lower than those in the model group,with significant difference(P＜0.05).Conclusion Exenatide can improve Hcy-induced HUVECs,injuried through inhibiting inflammatory response.
Wang R，Wang Y，Mu N，et al.Activation of NLRP3 inflammasomes contributes to hyperhomocysteinemia-aggravated inflammation and atherosclerosis in apoE-deficient mice[J].Lab Invest，2017，97（8）：922-934.
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