四氧化二氮吸入致肺损伤病理学改变及SMAD蛋白表达研究

目的:复制四氧化二氮(N2O4)吸入致肺损伤动物模型,检测SMAD2/3和SMAD7的蛋白表达和肺病理学变化,研究其致肺纤维化的损伤机制。方法:实验动物为ICR小鼠,体质量22～22 g,随机分成正常对照组(n=8)和中毒组(n=24),分时相(1、4、7 d,n=8)取肺组织HE染色观察肺纤维化情况,采用免疫组化方法检测SMAD2/3和SMAD7的蛋白表达情况。结果:N2O4中毒后,各组动物的肺部出现水肿和出血,部分肺组织出现纤维组织增生;肺泡SMAD2/3胞浆染色,表达较弱;肺泡SMAD7核染色,表达较强。结论:N2O4吸入致肺损伤后可出现纤维化,SMAD2/3和SMAD7参与了其病变过程,并可能在肺纤维化发生发展过程中发挥重要作用。

Pathological changes and SMAD proteins expression of lung injury induced by nitrogen tetroxide

Objective：To imitate pulmonary injury animal models by inhaling nitrogen tetroxide,and investigate the correlation between SMAD proteins expression and pulmonary fibrosis.Methods： ICR mice,weight 20～22 g each,intoxicated by inhaling nitrogen tetroxide,and divided into the control group（n=8） and the intoxicated group（n=24）.The morphological changes of pulmonary fibrosis was observed by pathologists at different time points（1,4,7 d,n=8）.And SMAD proteins expression were determined by immunohistochemistry at different time points（24 h/48 h/72 h,n=8）.Results： After animal models were intoxicated,all animals had the lung edema and hemorrhage,and partial fibrosis in lung tissue.SMAD2/3 was weakly expressed in some alveolar epithelial cytoplasm,but SMAD7 was strongly expressed in their nuclei.Conclusion：Pulmonary fibrosis can be developed after inhaling nitrogen tetroxide,and SMAD proteins can play an important role in the pulmonary fibrosis process.