脂多糖诱导大鼠急性气道炎症的实验研究  

Experimental Study of Lipopolysaccharide-induced Acute Airway Inflammation in Rats

作　　者：李文军[1] 刘蔺[1] 王开绿[1] 黄玲[1] 郑晓凤[1] 

机构地区：[1]四川省绵阳市第三人民医院呼吸内科,621000

出　　处：《中国实用医药》2009年第30期6-7,共2页China Practical Medicine

摘　　要：目的细菌感染,尤其是革兰氏阴性菌感染是引起多种气道急性炎症损伤的主要因素,但其在气道急性炎症中的损伤进程仍缺乏相关研究。方法本实验利用革兰阴性杆菌类致病的抗原物质脂多糖(LPS),经大鼠气管内滴注模拟气道急性炎症损伤,分析测试LPS滴注后2、4、6d主要炎症指标的变化(包括形态学分析,支气管肺泡灌洗液(BALF)细胞计数、炎性因子水平测定)。结果LPS刺激后,气道炎症细胞浸润显著,BALF细胞总数以及分类计数均明显增加,BALF中TNF-alpha、IL-1beta、IL-8含量明显升高,以上变化均在LPS刺激后第2天达到高峰。结论LPS诱导的急性气道炎症的早期损伤可能主要由TNF-alpha介导。Objective Bacteria infection,especially gram-negative bacteria infection,is considered to be the main cause of many forms of acute airway inflammation, but its injury process is not well elucidated. Methods In the present study, we used a rat model of acute airway inflammation induced by lipopolysaccharide（LPS） ,which was administered intratracheally. And the main inflanmmtory indexes, including histology analysis, cell counts and levels of inflammatory cytokines in BALF on days 2,4,6 after LPS treatment,were measured. Results LPS could induce marked inflammatory cells infiltration in rat airways,increase cell counts in BALF, and enhance levels of TNF-alpha,IL-lbeta,IL-8 in BALF significantly. All these changes peaked on days 2 after LPS stimulation. Conclusion The early injury of LPS-indueed airway inflammation is probably mainly mediated by TNF-alpha.

关 键 词：气道炎症 炎性因子 脂多糖 

分 类 号：R56[医药卫生—呼吸系统]