新生鼠胎粪吸入综合征致急性肺损伤的发病机制研究

目的:探讨新生鼠胎粪吸入综合征致急性肺损伤的发病机制。方法:30只新生雄性SD大鼠随机分为正常对照组(N,n=10)、胎粪模型组(Mec,n=10)和胎粪+生理盐水对照组(Mec/saline,n=10),建立新生儿胎粪吸入模型,24h后采用ELISA检测3组肺组织中MPO、MDA、SOD含量,应用荧光定量PCR检测肺组织IL-1、TNF-α、IL-8、MIP的表达水平。结果:与N组比较,Mec组及Mec/saline组肺组织匀浆中MPO、MDA含量均显著性增高,3组间SOD活性无明显区别。Mec组及Mec/saline组IL-1、TNF-α及IL-8、MIP-1的表达均明显增高,与N组比较差异有统计学意义。结论:胎粪吸入综合征导致急性肺损伤过程中存在严重的氧化-抗氧化失衡,在此过程中启动的细胞因子瀑布反应加重了肺损伤。

Study on the pathogenesis of acute lung injury induced by meconium aspiration syndrome in immature rats

Objective:To investigate the pathogenesis of acute lung injury induced by meconium aspiration syndrome in immature rats.Methods:30 immature rats were randomly divided into three groups:normal group(n=10),meconium model group(Mec,n=10),meconium and saline control group(Mec/saline,n=10).After 24 hours,the activities of MPO,MDA,SOD in lung tissue were measured by ELISA,and the levels of IL-1,TNF-α,IL-8 were measured by radioimmunoassay.Results:Compared with normal group,MPO and MDA were significantly increased in Mec group and Mec/saline group,the levels of SOD in 3 groups were no significant variety.Pulmonary IL-1,TNF-α,IL-8,MIP-1 were significantly increased after meconium aspiration.Conclusion:The imbalance of oxidation-antioxidation system was exist after meconium aspiration,that induced cytokine chain reaction aggravated lung injury.