脂多糖诱导大鼠急性肺损伤的机制研究  

Study on Mechanism of LPS-induced Acute Lung Injure

作　　者：吴海青 李涛平[2] 徐健[2] 田芳[3] 孔德琼 

机构地区：[1]龙华新区人民医院重症医学科,广东深圳518109 [2]南方医科大学南方医院呼吸睡眠中心,广东广州510515 [3]广州开发区医院重症监护室,广东广州510730 [4]龙华新区人民医院手术室,广东深圳518109

出　　处：《现代生物医学进展》2013年第19期3648-3652,3695,共6页Progress in Modern Biomedicine

基　　金：广州开发区科技局基金项目(2010 Q-T185)

摘　　要：目的:观察NF-κB及CyPA在内毒素诱导急性肺损伤大鼠肺组织的活性变化,探索NF-κB及CyPA在内毒素诱导急性肺损伤的发病机理中的作用。方法:36只雄性SD大鼠随机分为2组:A组:正常对照组(n=18)尾静脉注射等量生理盐水;B组:内毒素组(LPS)(n=18):经尾静脉注射LPS 5 mg/kg;分别于造模后6、24、72小时,处死动物收取标本,每个时间点6只(LPS的24小时组因1只死亡固只处死5只)。分别测定肺湿重/干重、肺组织TNF-α、IL-1β、NF-κB及CyPA。结果:湿重/干重:B组各个时间点均明显高于A组(P<0.05);同一时间点的比较:B组较A组显著性升高,P<0.05;NF-κB的核内表达量及肺组织CyPA的表达各个时间点之间B组均显著高于A组,P<0.001;结论:NF-κB及CyPA在内毒素诱导大鼠急性肺损伤的发病机理中起了重要的作用。Objective： To observe the activity changes of NF-KB and CyPA in lung tissues of endotoxin- induction acute lung injury rat and explore the function of NF-KB and CyPA in the pathogenesis of endotoxin- induction acute lung injury. Methods： Randomly separate the 36 rats into 2 groups： Group A： the normal group （n=18）： given the equivalent normal saline through tail vein injection; Group B： the lipopolysaccharide group （LPS）（n=18）： given 5 mg/kg LPS through tail vein injection; When it＇s 6 hours, 24 hours and 72 hours after molding, collect the sample from the animal which is put to death, 6 samples at each time （since one of the 24-hour group of LPS dies, so only the other five are put to death）. Determine the wet weight / dry weight of the lung and TNF-α, IL-1β, NF-κB and CyPA in lung tissue. Results： W/D of Group B is obviously higher than that of Group A; There are significant differences between NF-α, IL-1β, NF-κB, CyPA of different groups by comparing them at the same point of time and that is higher in Group B. Conclusion： NF-KB and CyPA play a importent role in the pathogenesis of endotoxin- induction acute lung injury.

关 键 词：脂多糖 急性肺损伤 核转录因子-ΚB 亲环素A 

分 类 号：Q953[生物学—动物学] R563[医药卫生—呼吸系统]