Inhibitory mechanism of exenatide on the apoptosis of endothelial cells induced by high glucose
10.3760/cma.j.issn.1000-6699.2013.09.020
- VernacularTitle:艾塞那肽抑制高糖诱导内皮细胞凋亡的作用机制
- Author:
Wei YANG
;
Lili ZHENG
;
Chong LI
;
Shan LI
;
Zhifang WANG
;
Xiaohong WANG
;
Yi ZHANG
- Publication Type:Journal Article
- Keywords:
Glucagon-like peptide-1;
Exenatide;
High glucose;
Endothelial cells;
Apoptosis
- From:
Chinese Journal of Endocrinology and Metabolism
2013;29(9):809-811
- CountryChina
- Language:Chinese
-
Abstract:
After human umbilical vein endothelial cells (HUVECs) were incubated with various concentrations of exenatide for 24,48,and 72 h under the conditions of5.5 and 33 mmol/L glucose,the cell viability was detected by MTF assay.The apoptosis rate of endothelial cells was measured by flow cytometry.Protein kinase B (Akt) phosphorylation,Bcl-2,and Bax protein expression were detected by Western blotting.The results showed that the cell viability was decreased after HUVECs were incubated with high glucose for48 and 72 h (P＜0.01).Treatment with 1,10,and 100 nmol/L exenatide for48 h significantly increased the cell viability in the presence of high glucose,in a dose-dependent manner (P＜0.01).High glucose inhibited Akt phosphorylation and Bcl-2 protein expression,stimulated Bax protein expression,with decreased Bcl-2/Bax ratio and increased apoptosis ratio of cells.After treatment with exenatide,the cell apoptosis reduced,Akt phosphorylation and Bcl-2 protein expression increased,and Bax protein expression decreased,with increased Bcl-2/Bax ratio (P ＜ 0.01).These effects of exenatide on endothelial cell were abrogated by an inhibitor of phosphotylinosital 3 kinase (PI3K) LY294002 (P ＜ 0.01),suggesting that the exenatide may regulate Bcl-2/Bax protein expression and inhibit endothelial cell apoptosis induced by high glucose through PI3k/Akt signal pathway,and thus may protect endothelial cells.
