内毒素性急性肺损伤小鼠肺组织中炎症介质的表达

Expression of inflammatory media in acute lung injury induced by endotoxin in mice

目的探讨内毒素性急性肺损伤过程中两类炎性介质的相互关系及其变化规律。方法腹腔注射脂多糖(LPS)(20mg/kg)建立小鼠急性肺损伤模型。用放射免疫(ELISA)法分别测定各组各时相点肺组织匀浆上清液中TNF-α、IL-8、IL-10 3种细胞因子的含量,同时观察肺组织形态学改变,进行肺湿/干重比(W/D)测定。结果与对照组比较,ALI组各时相点小鼠肺组织中3种炎症因子水平及W/D值均明显上升,差异有统计学意义(P<0.05),表达峰值时间:TNF-α为4h,IL-8为2h,而IL-10为8h。结论内毒素性急性肺损伤过程中相继发生了促炎反应和抗炎反应,促炎/抗炎失衡,炎症反应失控,可能是内毒素肺损伤的重要机制。

Objective To investigate the correlation between the two inflammatory media and their kinetic changes in endotoxininduced acute lung injury. Methods The ALI model was set up by intraperineal injection of lipopolysaccharide （LPS）. The changes of TNF-α,IL-8, IL-10 levels in the pulmonary tissues were detected by ELISA at different times. Besides, the following changes were observed： lung wet/dry weight ratio, lung histological manifestations. Results The levels of inflammatory media and W/D in ALI group were higher obviously than those in control mice, the expression of TNF-α was seen to peak at 4h and IL-8 at 2h,IL-10 at 8h in lung tissue after challenge. Conclusion Pro-inflammatory response and ant-inflammatory response occurred successively af- ter injecting LPS, the unbalance between them may be the mechanism of LPS-induced acute lung injury.