尿毒症患者血清对大鼠肺微血管内皮细胞单层通透性和骨架蛋白的影响  

Effects of uremia serum on monolayer permeability and F-actin in rat pulmonary microvascular endothelial cells

作　　者：吴胜斌[1] 王应灯[1] 张薇[1] 

机构地区：[1]上海交通大学医学院附属第九人民医院肾脏内科,200011

出　　处：《中华医学杂志》2008年第47期3374-3377,共4页National Medical Journal of China

摘　　要：目的观察尿毒症患者血清对培养大鼠肺微血管内皮细胞（RPMVEC）单层通透性、肌动蛋白骨架（F-肌动蛋白）的影响，探讨尿毒症患者血清对肺微血管内皮细胞损伤的机制。方法体外培养大鼠RPMVEC并鉴定；用针头式滤器观察尿毒症患者血清对RPMVEC单层通透性的影响；F．actin用流式细胞仪测定。结果健康对照组6、12h单层通透性系数分别为（0．0382±0．0022）、（0．0393±0．0016）ml·min^-1·cm^-1·kPa^-1；尿毒症患者血清6、12h单层通透性系数分别为（0．0687±0．0014）、（0．0772±0．0031）ml·min^-1·cm^-1·kPa^-1；流式细胞仪测定F-肌动蛋白的值分别为：阴性对照组10．60±3．3、正常健康对照组1233．34±13．92、尿毒症血清组（6h）712±51、尿毒症血清组（12h）613．31±42．81；实验发现尿毒症患者血清100μl作用于RPMVEC6、12h可使RPMVEC的单层通透性增高（P〈0．01）；F-肌动蛋白解聚（P〈0．01），且二者呈负相关（r==0．927，P〈0．01）。结论尿毒症患者血清作用于RPMVEC一定时间，可引起RPMVEC单层通透性的增高与F-肌动蛋白解聚。尿毒症患者血清引起内皮单层通透性的增高的机制与F-肌动蛋白解聚密切相关。Objective To observe the effects of uremia serum on monolayer permeability and F- actin in cultured rat pulmonary microvascular endothelial cell （RPMVEC） and to investigate the mechanism of injury of RPMVEC induced by uremia serum. Methods RPMVEC was isolated and cultured from Wistar rat in vitro. The effects of serum of uremia patients on monolayer permeability of RPMVEC were observed with microfilter, and F-actin expression was evaluated by flow cytometry. Results Serum of uremia patients induced the increased permeability of RPMVEC monolayer for 6 h and 12 h（P 〈0. 01 ）, depolymerization of F-actin for 6 h and 12 h（P 〈0. 01 ） ,the increased permeability of RPMVEC monolayer induced by serum of uremia patients is significantly correlated with the depolymerization of F-actin （ r = - 0. 927, P 〈 0. 01 ）. Conclusion Serum of uremia patients may induce the elevation of permeability monolayer and the depolymerization of F-actin in RPMVEC. The elevation of permeability monolayer induced by serum of uremia patients in RPMVEC is significantly correlated with the depolymerization of F-actin.

关 键 词：尿毒症 血清 肺微血管内皮细胞 单层通透性 F-肌动蛋白 

分 类 号：R686[医药卫生—骨科学]