摘要
以脂多糖(LPS)诱导人脐静脉内皮细胞HUVECs炎症损伤,探讨肝素寡糖对炎症的影响及其分子机制。实验分为空白组(0.5%血清培养基)、模型组(LPS+0.5%血清培养基)及给药组(LPS+0.5%血清培养基+0.01、0.1、1μmol/L HDO),采用活性氧实验检测细胞内活性氧簇水平,Western blot检测VCAM-1、p38、p-p38及核转录因子NF-κB等关键蛋白的表达水平。结果显示0.01、0.1和1μmol/L的HDO可抑制100μg/m L LPS诱导的HUVECs炎症因子VCAM-1表达水平,较弱的影响细胞中NF-κB分布,并下调信号通路中关键蛋白p38和p-p38表达。结果表明,HDO可能通过抑制炎症信号通路中关键蛋白的表达水平来抑制炎症因子的表达,从而起到抗炎作用。
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-dichlorofluo- rescein 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. 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 txmol/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-KB nuclear translocation. The results all above showed that HDO could decrease the key Key regulatory proteins expression, and suppress the transcription of VCAM-1, resulting in inhibiting inflammation.
作者
张玲玲
季璇馨
刘洁茹
黄青林
何书英
ZHANG Lingling JI Xuanxin LIU Jieru HUANG Qinglin HE Shuying(School of Life Science and Technology, China Pharmaceutical University, Nanfing 210009, China)
出处
《中国药科大学学报》
CAS
CSCD
北大核心
2016年第5期619-624,共6页
Journal of China Pharmaceutical University
基金
江苏高校品牌专业建设工程资助项目(No.PPZY2015A057)
江苏高校优势学科建设工程资助项目
江苏高校优秀科技创新团队资助项目~~
关键词
肝素寡糖
内皮细胞
动脉粥样硬化
抗炎作用
脂多糖
heparin-derived oligosaccharide（HDO）
human umbilical vein endothelial cells
atherosclerosis
anti-inflammation
lipopolysaccharides
