Effect of heparin-derived oligosaccharide on lipopolysaccharides-induced inflammation in HUVECs and its molecular mechanisms
10.11665/j.issn.1000-5048.20160520
- VernacularTitle:肝素寡糖对脂多糖诱导人脐静脉内皮细胞炎症的影响及分子机制研究
- Author:
Lingling ZHANG
1
;
Xuanxin JI
;
Jieru LIU
;
Qinglin HUANG
;
Shuying HE
Author Information
1. 中国药科大学生命科学与技术学院
- Publication Type:Journal Article
- Keywords:
heparin-derived oligosaccharide(HDO);
human umbilical vein endothelial cells;
atherosclerosis;
anti-inflammation;
lipopolysaccharides
- From:
Journal of China Pharmaceutical University
2016;47(5):619-624
- CountryChina
- Language:Chinese
-
Abstract:
In this study, the effect of heparin-derived oligosaccharide(HDO)on lipopolysaccharides(LPS)-induced inflammation in human umbilical vein endothelial cells(HUVECs)and the molecular mechanisms were investigated. The generation of intracellular reactive oxygen species(ROS)was detected by 20, 70-dichlorofluorescein diacetate(DCFH-DA). Experiment is divided into blank group(0. 5% serum medium), model group(LPS+0. 5% serum medium)and HDO dosing group(LPS+0. 5% serum medium +0. 01, 0. 1, 1mol/L HDO). The intracellular reactive oxygen species level was detected by reactive oxygen species experiment, the level of key regulatory proteins p38 and p-p38 in MAPK pathways and VCAM-1 were determined by Western blot. The results showed that HDO at 0. 01, 0. 1 and 1 μmol/L could inhibit the expression of VCAM-1 in HUVECs induced by 100 μg/mL LPS, and reduce the expression of key regulatory proteins p38 and p-p38, but could not obviously affect NF-κB nuclear translocation. The results all above showed that HDO could decrease the key regulatory proteins expression, and suppress the transcription of VCAM-1, resulting in inhibiting inflammation.
