GLP-1 Inhibits High-Glucose-Induced Oxidative Injury of Vascular Endothelial Cells

Abstract The aim of this work was to evaluate the effects of glucagon-like peptide-1 (GLP-1) on high-glucose-induced oxidative stress and investigate the possible mechanisms underlying this process. We measured reactive oxygen species (ROS) production, cell apoptosis, the expression of NOX4 and its...

Descripción completa

Guardado en:
Detalles Bibliográficos
Autores principales: Quan Li, Yajun Lin, Shu Wang, Lina Zhang, Lixin Guo
Formato: article
Lenguaje:EN
Publicado: Nature Portfolio 2017
Materias:
R
Q
Acceso en línea:https://doaj.org/article/ff1d0372db3c4ce8b14d24d2ba11d675
Etiquetas: Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
id oai:doaj.org-article:ff1d0372db3c4ce8b14d24d2ba11d675
record_format dspace
spelling oai:doaj.org-article:ff1d0372db3c4ce8b14d24d2ba11d6752021-12-02T15:05:25ZGLP-1 Inhibits High-Glucose-Induced Oxidative Injury of Vascular Endothelial Cells10.1038/s41598-017-06712-z2045-2322https://doaj.org/article/ff1d0372db3c4ce8b14d24d2ba11d6752017-08-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-06712-zhttps://doaj.org/toc/2045-2322Abstract The aim of this work was to evaluate the effects of glucagon-like peptide-1 (GLP-1) on high-glucose-induced oxidative stress and investigate the possible mechanisms underlying this process. We measured reactive oxygen species (ROS) production, cell apoptosis, the expression of NOX4 and its subunits, and p47phox translocation in human umbilical vein endothelial cells (HUVECs). An experimental type 2 diabetes model was induced using streptozotocin in male Sprague-Dawley rats. Fasting blood glucose (FBG), fasting insulin (FINS), total cholesterol (TC), triglycerides (TGs), and free fatty acid (FFA) were measured. Histomorphological analysis of the aorta was performed using hematoxylin-eosin staining. NOX4 and VCAM-1 expression in the aorta was measured. We found that high-glucose-induced ROS production and apoptosis were inhibited by GLP-1 treatment. High glucose caused upregulation of NOX4, p47phox, and Rac-1 and translocation of p47phox but had no effect on the cells pretreated with GLP-1. Furthermore, in the diabetic group, FBG, FINS, TG, TC, and FFA were increased, and NOX4 and VCAM-1 levels were also elevated. However, GLP-1 attenuated all these changes. GLP-1 ameliorated high-glucose-induced oxidative stress by inhibiting NOX4, p47phox, and Rac-1 expression and translocation of p47phox, suggesting its clinical usefulness in diabetic vascular complications.Quan LiYajun LinShu WangLina ZhangLixin GuoNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-9 (2017)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Quan Li
Yajun Lin
Shu Wang
Lina Zhang
Lixin Guo
GLP-1 Inhibits High-Glucose-Induced Oxidative Injury of Vascular Endothelial Cells
description Abstract The aim of this work was to evaluate the effects of glucagon-like peptide-1 (GLP-1) on high-glucose-induced oxidative stress and investigate the possible mechanisms underlying this process. We measured reactive oxygen species (ROS) production, cell apoptosis, the expression of NOX4 and its subunits, and p47phox translocation in human umbilical vein endothelial cells (HUVECs). An experimental type 2 diabetes model was induced using streptozotocin in male Sprague-Dawley rats. Fasting blood glucose (FBG), fasting insulin (FINS), total cholesterol (TC), triglycerides (TGs), and free fatty acid (FFA) were measured. Histomorphological analysis of the aorta was performed using hematoxylin-eosin staining. NOX4 and VCAM-1 expression in the aorta was measured. We found that high-glucose-induced ROS production and apoptosis were inhibited by GLP-1 treatment. High glucose caused upregulation of NOX4, p47phox, and Rac-1 and translocation of p47phox but had no effect on the cells pretreated with GLP-1. Furthermore, in the diabetic group, FBG, FINS, TG, TC, and FFA were increased, and NOX4 and VCAM-1 levels were also elevated. However, GLP-1 attenuated all these changes. GLP-1 ameliorated high-glucose-induced oxidative stress by inhibiting NOX4, p47phox, and Rac-1 expression and translocation of p47phox, suggesting its clinical usefulness in diabetic vascular complications.
format article
author Quan Li
Yajun Lin
Shu Wang
Lina Zhang
Lixin Guo
author_facet Quan Li
Yajun Lin
Shu Wang
Lina Zhang
Lixin Guo
author_sort Quan Li
title GLP-1 Inhibits High-Glucose-Induced Oxidative Injury of Vascular Endothelial Cells
title_short GLP-1 Inhibits High-Glucose-Induced Oxidative Injury of Vascular Endothelial Cells
title_full GLP-1 Inhibits High-Glucose-Induced Oxidative Injury of Vascular Endothelial Cells
title_fullStr GLP-1 Inhibits High-Glucose-Induced Oxidative Injury of Vascular Endothelial Cells
title_full_unstemmed GLP-1 Inhibits High-Glucose-Induced Oxidative Injury of Vascular Endothelial Cells
title_sort glp-1 inhibits high-glucose-induced oxidative injury of vascular endothelial cells
publisher Nature Portfolio
publishDate 2017
url https://doaj.org/article/ff1d0372db3c4ce8b14d24d2ba11d675
work_keys_str_mv AT quanli glp1inhibitshighglucoseinducedoxidativeinjuryofvascularendothelialcells
AT yajunlin glp1inhibitshighglucoseinducedoxidativeinjuryofvascularendothelialcells
AT shuwang glp1inhibitshighglucoseinducedoxidativeinjuryofvascularendothelialcells
AT linazhang glp1inhibitshighglucoseinducedoxidativeinjuryofvascularendothelialcells
AT lixinguo glp1inhibitshighglucoseinducedoxidativeinjuryofvascularendothelialcells
_version_ 1718388870139084800