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Involvement of p38 MAPK pathway in GLP-1-induced inhibition of apoptosis in human umbilical vein endothelial cells
Authors:Xu Hua  Li Hai-Long  Niu Zi-Yong  Li Gui-Zhong  Cao Jun  Jiang Yi-Deng
Affiliation:Department of Pathophysiology, Ningxia Medical University, Yinchuan 750004; Department of Internal Medicine, Ningxia Third Hospital, Yinchuan 750021. E-mail: JIANG Yi-Deng: jwcjyd@163.com; CAO Jun: caojun@nxmu.edu.cn.
Abstract:The aim of the present study was to investigate the effect of glucagon-like peptide-1 (GLP-1) on palmitate-induced apoptosis of human umbilical vein endothelial cells (HUVECs) and the underlying mechanism. HUVECs were cultured in vitro, and then treated by palmitate to induce apoptosis. Meanwhile, GLP-1 was added to explore its effect. After 24 h of the treatments, Caspase-3 activity and DNA fragmentation were measured using ELISA kits. Phospho-p38 mitogen-activated protein kinase (p-p38 MAPK) expression was detected by Western blot. The results showed that incubating HUVECs with 0.125 mmol/L GLP-1 increased Caspase-3 activity and DNA fragmentation. GLP-1 significantly inhibited palmitate-induced increases of Caspase-3 activity and DNA fragmentation in a concentration-dependent manner. Moreover, GLP-1 inhibited the up-regulation of p-p38 MAPK expression induced by palmitate in HUVECs. These results suggest GLP-1 protects HUVECs against lipo-apoptosis, and this effect may be mediated through inhibiting p38 MAPK pathway.
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