细菌脂多糖诱导人肺动脉内皮细胞表达P-MLCK  

Expression of P-MLCK in human pulmonary arterial endothelial cell induced by lipopolysaccharide

作　　者：林闽加[1] 白建文[1] 李锦师[1] 许淑敏[1] 

机构地区：[1]同济大学东方医院急诊医学部,上海200120

出　　处：《上海交通大学学报（医学版）》2008年第4期385-387,共3页Journal of Shanghai Jiao tong University:Medical Science

基　　金：上海市自然科学基金(03ZC14078)~~

摘　　要：目的探讨细菌脂多糖(LPS)对人肺动脉内皮细胞(HPAEC)表达磷酸化肌球蛋白轻链激酶(phosphorylated myosin lightchain kinase,P-MLCK)的诱导作用。方法体外培养HPAEC,分别给予生理盐水和2μg/mL LPS孵育1 h,经免疫荧光显微镜和Western blotting检测P-MLCK。结果与生理盐水组比较,LPS刺激HPAEC后较生理盐水组细胞数量减少,细胞形态无明显改变。HPAEC在LPS刺激30、60 min后,P-MLCK表达由0.41±0.05分别增加至0.82±0.43和1.56±0.07(P<0.05,P<0.01),同时LPS 30 min组和60 min组比较有显著性差异(P<0.05);LPS刺激60 min后P-MLCK免疫反应细胞由1.25±2.1增加至16.4±4.8(P<0.01)。结论P-MLCK可能与LPS诱导的急性肺损伤所致的内皮细胞屏障功能障碍有关。Objective To study the expression of phosphorylated myosin light chain kinase（P-MLCK） in human pulmonary arterial endothelial cell（HPAEC） induced by lipopolysaccharide（LPS）. Methods HPAECs were cultured in vitro and treated with LPS（2 μg/mL） and normal saline for 1 h,respectively.Immunofluorescence method and western blotting were used to detect P-MLCK. Results Compared with normal saline group,the number of HPAECs decreased,but the morphology of cells did not change.After treatment of LPS for 30 and 60 min,the expression of P-MLCK in HPAEC increased from 0.41±0.05 to 0.82±0.43 and 1.56±0.07,respectively（P〈0.05,P〈0.01）.Between the two treatment groups（30 and 60 min）,the difference was significant（P〈0.05）.P-MLCK immunoreactive cells in HPAEC were augmented from 1.25±2.1 to 16.4±4.8 after treatment of LPS for 60 min（P〈0.01）. Conclusion P-MLCK may be related to endothelial barrier dysfunction of acute lung injury induced by LPS.

关 键 词：人肺动脉内皮细胞 细菌脂多糖 磷酸化肌球蛋白轻链激酶 

分 类 号：R563.8[医药卫生—呼吸系统] Q939.91[医药卫生—内科学]