Effect of propofol on interleukin-1β-induced increase in monolayer permeability of human umbilical vein endothelial cells
10.3760/cma.j.issn.0254-1416.2013.04.022
- VernacularTitle:异丙酚对IL-1β诱导人脐静脉内皮细胞通透性增高的影响
- Author:
Mingliang JIN
;
Liming JIA
;
Zhiqiang PEI
;
Dong PU
;
Jianying DING
;
Miao WU
- Publication Type:Journal Article
- Keywords:
Propofol;
Interleukin-1β;
Endothelial cell;
Permeability
- From:
Chinese Journal of Anesthesiology
2013;(4):473-476
- CountryChina
- Language:Chinese
-
Abstract:
Objective To evaluate the effect of propofol on interleukin-1β (IL-1β)-induced increase in monolayer permeability of human umbilical vein endothelial cells (HUVECs).Methods Primary HUVECs were cultured and purified by immuno-magnetic separation.The expression of VE-cadherin in endothelial cells was determined by immunofluorescence.The HUVEC monolayer permeability was detected by the Transwell system.The cells were seeded on the upper chamber (2 × 105 cells/well) and cultured for 3 days after confluence.The cells were treated in two ways.The cells were randomly divided into 6 groups (n =36 each) and 5 of the 6 groups treated with 1,2,5,10 and 20 ng/ml IL-1β for 24 h except for control group.The cells were also randomly divided into 5 groups (n =30 each) and 4 of the 5 groups were pretreated with 0,10,50 and 100 μmol/L propofol for 30 min,and then treated with 10 ng/ml IL-1β for 24 h except for control group.The cells were radomly divided into 3 groups (n =18 each) and 2 of the 3 groups were pretreated with 50 μmol/L propofol for 30 min,and then treated with 10 ng/ml IL-1β for 24 h or 30 min.The expression of occludin protien,p38 mitogen activiated protienkinase (p38 MAPK) and phosphorylated p38 MAPK (p-p38 MAPK) was determined by Western blot.Results Compared with control group,5,10 and 20 ng/ml IL-1β significantly increased HUVEC monolayer permeability in a concentration-dependent manner (P ＜ 0.05 or 0.01).10,50 and 100 μmol/L propofol inhibited IL-1 β-induced increase in the permeability of HUVEC monolayer permeability in a concentration-dependent manner (P ＜ 0.01).IL-1β could down-regulate HUVEC occludin protein expression,and activate p38MAPK signaling pathway,and propofol inhibited IL-1β-induced down-regulation of HUVEC occludin protein expression and activation of p38 MAPK signaling pathway (P ＜ 0.01).Conclusion Propofol can alleviate IL-1β-induced increase in the permeability of HUVEC monolayer via inhibiting activation of p38 MAPK signaling pathway.
