PPARγagonist inhibits high glucose-induced production of reactive oxy-gen species by UCP2 up-regulation
10.3969/j.issn.1000-4718.2015.01.010
- VernacularTitle:PPARγ激动剂通过上调解偶联蛋白2抑制高糖介导的内皮细胞活性氧生成
- Author:
Peijian WANG
;
Qiulin WANG
;
Zhen YANG
;
Fang WANG
;
Chunhua PU
;
Wenzhang LI
;
Dengpan LIANG
;
Peng ZHOU
- Publication Type:Journal Article
- Keywords:
Peroxisome proliferator-activated receptor γ;
Uncoupling protein 2;
Oxidative stress;
Endothelial cells
- From:
Chinese Journal of Pathophysiology
2015;(1):49-53
- CountryChina
- Language:Chinese
-
Abstract:
AIM:To explore the effects of PPARγon the elevated level of reactive oxygen species ( ROS) in-duced by high glucose and its mechanism .METHODS:Human umbilical vein endothelial cells ( HUVECs) were cultured with DMEM containing high glucose (33 mmol/L D-glucose), and DMEM containing lower glucose (5.5 mmol/L D-glu-cose) was used as control .Superoxide anion and nitric oxide fluorescence probes were used to observe the effects of PPAR γagonist on ROS and NO productions in the HUVECs .The uncoupling protein 2 (UCP2) protein level in the HUVECs was detected by Western blotting .RESULTS:PPARγagonist pioglitazone inhibited the ROS generation and prevented the de-crease in NO level under high glucose condition , and these effects were reversed by pretreatment with PPARγantagonist GW9662.The results of Western blotting indicated that PPARγagonist pioglitazone up-regulated the UCP2 expression un-der high glucose condition , and this effect was also blocked by GW 9662.Inhibition of UCP2 by genipin attenuated the effect of pioglotazone on the ROS production .CONCLUSION: Activation of PPARγinhibits ROS generation under high glucose condition , and this effect may mediate by up-regulation of UCP2.
