Role of p38 MAPK signal pathway in attenuation of lipopolysaccharide-induced human umbilical vein endothelial cell injury by penehyclidine hydrochloride
10.3760/cma.j.issn.0254-1416.2012.01.031
- VernacularTitle:p38MAPK信号通路在盐酸戊乙奎醚减轻内毒素诱导人脐静脉内皮细胞损伤中的作用
- Author:
Jia ZHAN
;
Lixiang WANG
;
Zongze ZHANG
;
Chang CHEN
;
Kai CHEN
;
Yanlin WANG
- Publication Type:Journal Article
- Keywords:
p38 Mitogen-activated protein kinases;
Cholinergic antagonists;
Endotoxemia;
Endothelium,vascular
- From:
Chinese Journal of Anesthesiology
2012;32(1):117-119
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the role of p38 mitogen-activated protein kinase (p38 MAPK) in attenuation of lipopolysaccharide (LPS)-induced human umbilical vein endothelial cell injury by penehyclidine hydrochloride (PHC).Methods Human umbilical vein endothelial cells were provided by Medical Research Center,Wuhan University,cultured and seeded in 96-well plate (100 μl/hole) or 24-well plate (3 nl/hole) with density of 1 × 104/ml or in culture flasks (5 ml/flask) with density of 1 × 106/ml.The cells were randomly divided into 4 groups ( n =23 each):group control (group C) ; group LPS; group PHC (group P) and group PHC + LPS (group PL).The cells were exposed to LPS 1 μg/ml in groups L and PL or/and PHC 2 μg/ml in groups P and PL.LPS was added at 1 h after PHC in group PL.The cells were collected at 24 h exposure to LPS for determination of the expression of phosphorylated p38 MAPK (p-p38 MAPK) and p38 MAPK.The ratio between p-p38 MAPK and p38 MAPK was calculated.Cell viability,NO content and inducible nitric oxide synthase (iNOS) expression were also determined.Results LPS significantly decreased cell viability,increased NO content,iNOS expression,p-p38 MAPK and p-p38 MAPK/p38 MAPK ratio in group L as compared with group C.In group PL pretreatment with PHC significantly attenuated LPS-induced cell injury.Conclusion p38 MAPK pathway is involved in attenuation of LPS-induced endothelial cell injury by PHC.
