脓毒症患者血清诱导血管内皮细胞通透性相关因素研究  

Study on relationship between vascular endothelial cells hyperpermeability induced by serum of patients with sepsis and relative factors

作　　者：郑运江[1] 胡晓峰[1] 陈庆青[1] 王彩平[1] 化学胜 章韵[1] 汤耀卿[2] 

机构地区：[1]上海交通大学医学院附属新华医院崇明分院急诊科,上海202150 [2]上海交通大学医学院附属瑞金医院外科重症监护室,上海200025

出　　处：《中国临床药理学杂志》2016年第12期1059-1062,共4页The Chinese Journal of Clinical Pharmacology

基　　金：上海市卫生计生委基金资助项目(20124318);上海交通大学科技发展处基金资助项目(12XJ22016);崇明县科技发展基金资助项目(CKY2012-02)

摘　　要：目的观察脓毒症患者血清对人血管内皮细胞单层通透性的影响。方法选择45例脓毒症患者纳入试验组,根据处理方法的不同分为试验Ⅰ组(n=32,不处理)和试验Ⅱ组[(n=23,ROCK抑制药(Y27632)],同时将40例健康志愿者分为正常Ⅰ组(n=20,不处理)和正常Ⅱ组(n=20,Y27632)。分别以20%脓毒症患者血清刺激内皮细胞6 h;测定内皮细胞单层通透性,观察内皮细胞的形态分布并检测RhoA(Ras homolog A)蛋白的表达。结果与正常组相比,试验Ⅰ组的内皮细胞通透性显著升高(P<0.05),但是试验Ⅱ组预处理Y27632后,可以显著抑制内皮细胞通透性的增高(P<0.05);抑制药本身(正常Ⅱ组)对内皮细胞通透性无影响。试验Ⅰ与Ⅱ组的血清可增加内皮细胞间间隙的数量,改变细胞通透性,并能有效诱导RhoA蛋白的表达。结论脓毒症患者血清能够明显诱导血管内皮细胞通透性增高;其机制与激活Rho相关蛋白激酶/Rho相关的卷曲蛋白激酶(Rho/ROCK)信号通路、破坏内皮细胞屏障功能有关。Objective To study the effect of serum （20%） of patients with sepsis on human vascular endothelial cell （ECs） monolayer permeability. Methods Selected 45 cases of sepsis were enrolled as the experi- ment group, according to processing methods were divided into experi- ment group I （ n = 32, no treatment） and experiment group Ⅱ （ n = 23, Y27632） and 40 cases of healthy volunteers were divided into the normal group I （ n = 20, no treatment） and normal group Ⅱ （ n = 20, Y27632）, then to 20% of patients with sepsis serum stimulation endothelial cells 6 h. Determination of endothelial cell monolayer permeability observed en- dothelial cell morphology distribution and detection of RhoA （ RAS homo- log A） protein expression. Results The permeability of experiment I group was significantly higher than that of the normal group. But the higher permeability in experiment Ⅱ group was inhibited after pretreated with Y27632 and the difference was statistically significant （ P 〈 0. 05）. The inhibitor Y27632 （normal group Ⅱ ）was not effect on permeability. The serum of the patients with sepsis （two experiment groups） could increase the number of intercellular spaces, change the permeability of the endothelial cells, and effectively induced the expression of RhoA protein. Conclusion Serum of patients with sepsis significantly induced endothelial cell permeability increase. One of its mechanisms involved the regulation role of Ras homolog/Rho- associated protein kinase（ Rho / ROCK） signaling pathway, which could damage integrity of endothelial barrier function.

关 键 词：脓毒症 人血管内皮细胞 细胞通透性 

分 类 号：R97[医药卫生—药品]