GLP-1 Inhibits High-Glucose-Induced Oxidative Injury of Vascular Endothelial Cells.
GLP-1 Inhibits High-Glucose-Induced Oxidative Injury of Vascular Endothelial Cells.
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GLP-1 抑制高葡萄糖诱导的血管内皮细胞氧化损伤
DOI：
10.1038/s41598-017-06712-z
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发表时间：
2017-08-14
影响因子：
4.6
通讯作者：
Guo L
中科院分区：
文献类型：
--
作者：
Li Q;Lin Y;Wang S;Zhang L;Guo L
本研究的目的是评价胰升糖素样肽-1(GLP-1)对高糖诱导的氧化应激的影响，并探讨其可能的作用机制。我们检测了人脐静脉内皮细胞(HUVECs)中活性氧(ROS)的产生、细胞凋亡、NOX4及其亚单位的表达和p47Phox的易位。用链脲佐菌素诱导雄性SD大鼠实验性2型糖尿病模型。测定空腹血糖(FBG)、空腹胰岛素(FINS)、总胆固醇(TC)、甘油三酯(TGS)和游离脂肪酸(FFA)。苏木精-伊红染色观察大鼠主动脉的组织形态。检测主动脉组织中NOX4和VCAM-1的表达。我们发现GLP-1可抑制高糖诱导的ROS生成和细胞凋亡。高糖诱导NOX4、p47Phox和RAC-1表达上调，p47Phox易位，但对GLP-1处理的细胞无影响。糖尿病组FBG、FINS、TG、TC、FFA升高，NOX4、VCAM-1水平升高。而GLP-1可减弱上述变化。GLP-1通过抑制NOX4、p47Phox和Rac-1的表达和p47Phox的转位来减轻高糖诱导的氧化应激，提示其在糖尿病血管并发症中具有临床应用价值。
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.
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影响因子：
7.7
作者：
Noyan-Ashraf MH;Momen MA;Ban K;Sadi AM;Zhou YQ;Riazi AM;Baggio LL;Henkelman RM;Husain M;Drucker DJ
通讯作者：
Drucker DJ
影响因子：
8.2
作者：
Nagashima, M.;Watanabe, T.;Terasaki, M.;Tomoyasu, M.;Nohtomi, K.;Kim-Kaneyama, J.;Miyazaki, A.;Hirano, T.
通讯作者：
Hirano, T.
影响因子：
4.8
作者：
Gorin, Y;Block, K;Abboud, HE
通讯作者：
Abboud, HE
影响因子：
7.4
作者：
Xu, Hui;Goettsch, Claudia;Li, Huige
通讯作者：
Li, Huige
C反应蛋白通过NADPH氧化酶介导的氧化应激促进单核细胞与内皮细胞的粘附
影响因子：
4
作者：
Huang, Xiuqing;Zhang, Jing;Li, Jian
通讯作者：
Li, Jian