Effect of Glucagon-like Peptide-1 on High-Glucose-induced Oxidative Stress and Cell Apoptosis in Human Endothelial Cells and Its Underlying Mechanism. Issue 2 (August 2015)

• Record Type: Journal Article
• Authors: Wang, Rehua; Lu, Lihong; Guo, Yansong; Lin, Feng; Chen, Haifeng; Chen, Wei; Chen, Minsheng
• Is Part Of: Journal of cardiovascular pharmacology. Volume 66:Issue 2(2015)
• Publication Date: 2015-08
• Subjects: glucagon-like peptide-1 -- high glucose -- human umbilical vein endothelial cell -- oxidative stress -- apoptosis -- atherosclerosis; Cardiovascular Diseases -- drug therapy -- Periodicals; Cardiovascular System -- drug effects -- Periodicals; Cardiovascular pharmacology -- Periodicals; Cardiovascular agents -- Periodicals; Cardiovascular agents; Cardiovascular pharmacology; Periodicals; 615.7105
• DOI: 10.1097/FJC.0000000000000255
• Languages: English
• ISSNs: 0160-2446

Abstract

Abstract : Abstract: Glucagon-like peptide-1 (GLP-1) has been demonstrated to play an important role in type 2 diabetes mellitus, leading to cardiovascular diseases. This study aimed to examine the GLP-1 regulation of high-glucose-induced oxidative stress and cell apoptosis in human umbilical vein endothelial cells (HUVECs) and its underlying mechanism. HUVECs were isolated from healthy umbilical cords and cultured. GLP-1 and the GLP-1R antagonist, exendin (9–39), were used to pretreat the cells. The expression of NADPH oxidase subunits gp91 and p22 phox messenger RNA was detected by real-time quantitative polymerase chain reaction. Reactive oxygen species production was detected with flow cytometry and fluorescence microscopy. Lucigenin assay was used to measure the NADPH oxidase activity. The terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling assay was used to investigate endothelial cell apoptosis. Apoptosis proteins were detected by immunoblotting. GLP-1 decreased high-glucose-induced oxidative stress, the expression of gp91 and p22phox messenger RNAs, and NADPH oxidase activation. Exendin (9–39) antagonized the effects of GLP-1 on high-glucose-induced oxidative stress. GLP-1 also increased HUVEC's high-glucose-induced proliferation and inhibited apoptosis. GLP-1 inhibited high-glucose-induced oxidative stress and cell apoptosis in HUVECs through GLP-1R–dependent and GLP-1 (9–36)–related pathways. GLP-1 suppressed high-glucose-induced oxidative stress and consequently may have an antiatherosclerosis effect on diabetes mellitus patients.