p38丝裂原活化蛋白激酶信号转导通路在严重烧伤大鼠急性肺损伤中的作用  

Role of p38 mitogen-activated protein kinase signal transduction pathway in the acute lung injury of severely burned rats

作　　者：陈旭林[1] 夏照帆[1] 韦多[1] 贲道锋[1] 王广庆[1] 韩圣[1] 

机构地区：[1]第二军医大学长海医院烧伤科,上海200433

出　　处：《中华外科杂志》2004年第7期388-390,共3页Chinese Journal of Surgery

基　　金：国家自然科学基金资助项目(30271340);国家863课题资助项目(2001AA216041);军队"十五"指令性课题资助项目(01L055);上海市卫生系统百人计划课题资助项目(97BR046)

摘　　要：目的　研究 p38丝裂原活化蛋白激酶 (MAPK)信号转导通路在严重烧伤大鼠急性肺损伤中的作用。方法　健康成年的雄性SD大鼠 4 8只 ,随机分为假烫伤组、烧伤对照组和烧伤加 p38MAPK信号转导通路抑制剂 (SB2 0 35 80 )组。采用大鼠 30 %总体表面积Ⅲ度烧伤动物模型 ,观察烧伤 2 4h后肺血管通透性、肺脏含水量、肺脏病理和肺脏 p38活性等指标的改变。 结果　大鼠烧伤后2 4h肺血管通透性明显增高 (4 2 5± 4 7vs .12 1± 1 4 ,P <0 0 1) ,肺脏含水量上升 (P <0 0 5 ) ,组织病理学检查显示 :肺脏出现明显的病理损害 ,同时肺脏 p38MAPK活性明显增强。使用SB2 0 35 80能抑制肺脏 p38MAPK活性的上升 ,同时大鼠肺血管通透性明显降低 (2 4 7± 2 9vs.4 2 5± 4 7,P <0 0 1) ,肺脏含水量下降 ,肺脏的病理损害显著减轻。结论　p38MAPK的活化是严重烧伤大鼠急性肺损伤重要的发病机制之一。Objective To investigate the role of p38 mitogen-activated protein kinase (MAPK) signal transduction pathway in the acute lung injury of severely burned rats. Methods Forty-eight adult healthy rats were randomly divided into three groups: sham group, burn control group, and burn+SB203580 group. A third-degree burns over 30% total body surface area rat model was used and pulmonary capillary permeability, lung water content, pulmonary histology and p38 MAPK activity were measured at 24 hours postburn. Results Burn trauma resulted in increased pulmonary capillary leakage permeability (42.5±4.7 vs. 12.1±1.4,P<0.01), elevated lung water content(P<0.05), and worsen histologic condition. There was a significant activation of p38 MAPK at 24 hours postburn compared with control. SB203580 inhibited the activation of p38 MAPK, reduced the pulmonary capillary leakage permeability(24.7±2.9 vs. 42.5±4.7,P<0.01), decreased lung water content, and prevented burn-mediated lung injury. Conclusion The activation of p38 MAPK is one important aspect of the signaling event that contributes to burn-induced lung injury.

关 键 词：P38 丝裂原活化蛋白激酶 信号转导通路 烧伤 大鼠 急性肺损伤 

分 类 号：R641[医药卫生—外科学]