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目的：制作四氧化二氮（N2O4）吸入中毒致肺损伤动物模型，检测小鼠血清转化生长因子β1（TGF-β1）、肺Ⅱ型肺泡细胞表面抗原(KL-6)、肺表面活性物质相关蛋白A（SP-A）和肺表面活性物质相关蛋白D（SP-D）的变化，研究四氧化二氮吸入中毒小鼠与肺纤维化血清指标的相关性。方法实验动物为ICR小鼠,体重22~22g（n=8），随机分成对照组和中毒组(4d/7d)，将动物置于120L染毒柜制作N2O4吸入中毒致肺损伤动物模型，于4d、7d采用眼球摘除法取血，分离血清-70℃保存，ELISA法测定TGF-β1、KL-6、SP-A和SP-D含量。结果对照组血清TGF-β1(ng/L)、KL-6(mU/L)、SP-A(ng/L)和SP-D(ng/L)含量均值分别为（144.00、1177.79、41.43、22.97）；中毒组(4d)分别为（115.29、1282.08、39.22、19.95）；中毒组(7d)分别为（113.31、1069.24、38.56、19.22）。采用SPSS20.0软件，利用单因素方差分析，以P＜0.05具有统计学意义。其中中毒组与对照组之间TGF-β1、KL-6和SP-D水平差异明显，P＜0.05，SP-A水平则无显著差异。结论N2O4吸入中毒可导致TGF-β1、SP-A和SP-D水平发生改变，提示对肺功能可造成严重损伤；N2O4吸入中毒后持续监测KL-6水平在一定程度上可以反映特发性肺纤维化（IPF）的发生和发展，或可为此类IPF的早期防治提供实验依据。“,”Objective To reproduce animal model of lung injury on those inhalation of nitrogen dioxide, and detect the serum transforming growth factor-β (TGF- β1), pulmonary alveolar type II cell surface antigen (KL-6), pulmonary surfactant-associated protein A (SP-A) and pulmonary surfactant-associated protein D (SP-D). Study the serum indexes association with pulmonary fibrosis exposed to nitrogen oxides environment. Methods 8 mice were randomly divided into two groups, control group and model group. There were placed in the 120L exposed cabinet to make mice poisoned by inhalating nitrogen oxides model, and take their blood on the fourth and seventh day by eye-excised method, serum separation -70℃ preservation, detected of TGF-βELISA 1, KL-6, SP-A and SP-D content. Results Serum TGF- β1 (ng/L), KL-6 (mU/L), SP-A (ng/L) and SP-D (ng/L) were respectively 144, 1177.79, 41.43, 22.97; the model group on four-day respectively 115.29, 1282.08, 39.22, 19.95; the model group on seven-day respectively 113.31, 1069.24, 38.56, 19.22. SPSS20.0 software was adopted for the analysis with the single factor analysis of variance and statistical P<0.05. The difference carries statistical significance between the model group and the control group on TGF- β 1, KL-6 and SP-D levels ,P < 0.05, and no significant differences was found in the level of SP-A. Conclusion It can lead to impairment of lung function in short time inhalation of nitrogen oxides, and can cause serious damage of lung function; Detection of KL-6 may be helpful to reflect the development of idiopathic pulmonary fibrosis exposure to nitrogen oxides environment and can be provided certain experimental basis for early IPF.