内毒素血症时小鼠肺局部致炎及抗炎因子与急性肺损伤的关系  

Pulmonary cytokine production in mice and its relation to endotoxininduced acute lung injury

作　　者：陈永华[1] 蒋建新[1] 谢国旗[1] 张宇[1] 邱俊[1] 刘大维[1] 周继红[1] 朱佩芳[1] 

机构地区：[1]第三军医大学大坪医院野战外科研究所四室,重庆400042

出　　处：《中国危重病急救医学》2000年第6期331-333,共3页Chinese Critical Care Medicine

基　　金：国家自然科学基金!资助项目 (38970 833);军队医药卫生杰出中青年基金

摘　　要：目的 :探讨内毒素血症休克时肺部失控性炎症反应致炎及抗炎因子的变化规律及其与急性肺损伤的关系。方法 :建立小鼠内毒素肺损伤动物模型 ,分别采用小鼠肿瘤坏死因子α( TNFα)、白介素 6 ( IL 6 )、IL 4、IL 10酶联免疫吸附法 ( EL ISA)试剂盒检测肺组织匀浆液内上述细胞因子含量 ,同时观察肺损伤程度及动物 2 4小时内的存活率。结果 :注射内毒素 ( L PS)后 1小时 ,1m g/ kg和 10 mg/ kg两种剂量组 TNFα和IL 6即显著升高 ,并分别于伤后 1和 3小时达峰值 ;2组 IL 10及低剂量组 IL 4于伤后 1小时开始升高 ,而高剂量组 IL 4在注射内毒素后 1小时无明显变化 ,至 3小时显著升高。低剂量组 IL 4于 3小时达峰值 ,2组IL 10及高剂量组 IL 4则于伤后 5小时增加达峰值。高剂量组致炎及抗炎因子升高的幅度都显著高于低剂量组 ,且高剂量组两类细胞因子直至伤后 8小时仍显著高于正常对照组。致炎及抗炎因子升高的幅度与内毒素肺损伤的严重程度相平行。结论 :内毒素肺损伤后致炎与抗炎介质相继产生 ,两者相互作用的失衡是导致内毒素肺损伤的重要机制。因此 ,在内毒素肺损伤的防治中应考虑到局部抗炎与致炎反应的综合作用。Objective:To observe the kinetic changes in proand antiinflammatory cytokines in pulmonary tissue and their relation to endotoxininduced acute lung injury.Methods:A murine model of endotoxininduced lung injury was reproduced by injection of different doses of lipopolysaccharide(LPS,E.coli 026∶B6) via tail veins.The levels of tumor necrosis factorα(TNFα),interleukin6(IL6),IL4,IL10 in lung homogenates were measured by enzymelinked immunosorbent assay.Results:TNFα and IL6 levels in lung tissue were produced primarily after the LPS challenge.TNFα and IL6 levels were significantly increased at 1 hour and decreased at 8 hours in low dose group compared with the controls,whereas in high dose group they increased continuously till 8 hours and were markedly higher than those in low dose group.Otherwise,antiinflammatory cytokines including IL4 and IL10 levels elevated at 3 hours and peaked at 5 hours which were produced later than proinflammatory mediators,such as TNFα and IL6 .The levels of IL4 and IL10 in high dose group were markedly higher than those in low dose group.The alterations of proand antiinflammatory cytokines were shown to be paralleled with lung structure damage and the fatal outcome.Conclusions:Local proand antiinflammatory cytokines in lung could produced successively after the infusion of LPS,the unbalance between them may contribute to the immune dysfunction and lead to acute lung injury.

关 键 词：肺损伤 内毒素血症 TNF-Α TL-6 TL-4 

分 类 号：R655.3[医药卫生—外科学]