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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。
Objective: To investigate the pathogenesis of acute lung injury induced by meconium aspiration syndrome in neonatal rats. Methods: Thirty newborn male Sprague-Dawley rats were randomly divided into normal control group (n = 10), meconium model group (n = 10) and meconium + saline control group ). The neonatal model of meconium aspiration was established. The levels of MPO, MDA and SOD in lung tissue were detected by ELISA after 24 hours. The expression of IL-1, TNF-α, IL-8 and MIP in lung tissues were detected by real- . Results: Compared with N group, the contents of MPO and MDA in lung homogenate of Mec group and Mec / saline group were significantly increased, while there was no significant difference between the three groups. The levels of IL-1, TNF-α, IL-8 and MIP-1 in Mec and Mec / saline groups were significantly higher than those in N group. CONCLUSIONS: There is a serious oxidative-antioxidant imbalance in meconium aspiration syndrome during acute lung injury, and a cascade of cytokines initiated during this process aggravates lung injury.