海南医学院学报2017，Vol.23Issue(21)：2899-2902,4.DOI:10.13210/j.cnki.jhmu.20171025.003
GLP-1对高糖诱导内皮细胞损伤的保护作用及分子机制研究
The protective effect and molecular mechanism of GLP-1 on the high glucose-induced endothelial cell injury
摘要
Abstract
Objective:To study the protective effect and molecular mechanism of glucagon-like peptide-1 (GLP-1) on the high glucose-induced endotbelial cell injury.Methods..Endothelial cells HUVECs were cultured and divided into three groups,control group were treated with serum-free low-glucose culture medium,high glucose group were treated with serumfree culture medium containing 40mmol/L glucose and GLP-1 group were treated with serum-free culture medium containing 10mmol/L GLP 1 and 40mmol/L glucose.24 hours after treatment,the expression of apoptosis genes and autophagy genes as well as the levels of oxidative stress products and antioxidants were measured.Results:JAK2,STAT3,Bax,Caspase-9,Caspase-3,Nrf2,NQO1,HO1 and GSH-Px mRNA expression as well as ROS,gp91phox,MDA and ox-LDL levels in high glucose group of cells were significantly higher than those in control group while STSQM1,Atg 5 and LC-3 mRNA expression were significantly lower than those of control group;JAK2,STAT3,Bax,Caspase 9 and Caspase-3 mRNA expression as well as ROS,gp91phox,MDA and ox-LDL levels in GLP-1 group of cells were significantly lower than those in high glucose group while Nrf2,NQO1,HO1,GSH-Px,STSQM1,Atg-5 and LC-3mRNA expression were significantly higher than those in high glucose group.Conclusion:GLP-1 can reduce the high glucose-induced endothelial cell injury by inhibiting apoptosis,reducing oxidative stress and enhancing autophagy.关键词
胰高血糖素样肽-1/内皮细胞损伤/高糖/氧化应激/凋亡Key words
glucagon-like peptide-1/endothelial cell injury/high glucose/oxidative stress/apoptosis分类
医药卫生引用本文复制引用
王晓民,职康康,邹思力,吴永发,温兴铸,黄通,曲乐丰..GLP-1对高糖诱导内皮细胞损伤的保护作用及分子机制研究[J].海南医学院学报,2017,23(21):2899-2902,4.基金项目
国家自然科学基金面上项目基金资助项目(81570440) （81570440）
上海领军人才基金资助项目(035)Project fund funded projects on the National Natural Science Foundation of China (81570440) （035）
Shanghai leading talent fund funded project (035) （035）
