Involvement of p38 MAPK pathway in GLP-1-induced inhibition of apoptosis in human umbilical vein endothelial cells.
- Author:
Hua XU
1
;
Hai-Long LI
;
Zi-Yong NIU
;
Gui-Zhong LI
;
Jun CAO
;
Yi-Deng JIANG
Author Information
1. Department of Pathophysiology, Ningxia Medical University, Yinchuan 750004, China.
- Publication Type:Journal Article
- MeSH:
Apoptosis;
Caspase 3;
metabolism;
DNA Fragmentation;
Glucagon-Like Peptide 1;
metabolism;
Human Umbilical Vein Endothelial Cells;
cytology;
Humans;
MAP Kinase Signaling System;
Up-Regulation;
p38 Mitogen-Activated Protein Kinases;
metabolism
- From:
Acta Physiologica Sinica
2012;64(4):444-448
- CountryChina
- Language:Chinese
-
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.
