中文摘要：

目的研究肿瘤坏死因子（TNF）-α对哮喘小鼠支气管肺泡灌洗液（BALF）中白三烯D4（uD4）和E4（LTF4）表达的影响，从而探讨其在哮喘发病过程中作用机制。方法48只雌性BALB／c小鼠随机均分为6组：正常对照（A）组，哮喘模型（B）组，TNF-α（0．1μg/kg）腹腔注射给药（C1）组，TNF-α（0．4μg/∥kg）腹腔注射给药（C2）组，TNF-α（0．1μg/kg）雾化吸入给药（D1）组，TNF-α（0．4μg/kg）雾化吸人给药（D2）组。建立哮喘小鼠模型，苏木精-伊红（HE）染色观察肺组织病理变化，收集BALF进行炎性细胞计数，酶联免疫疫吸附（ELISA）法检测其LTD4和LTFA水平。结果①HE染色显示B、C、D组气道炎症明显改变，C、D组BALF中炎性细胞计数、嗜酸性粒细胞（EOS）明显高于B组（P〈0．05）；②ELISA法结果显示BALF中LTD4和LTE4水平：B、C、D组高于A组（P〈0．01），C、D组明显高于B组（P〈0．05），C2组明显高于C1组（P〈0．05），D2组明显高于D1组（P〈0．05），但C1组和D1组之间、C2和D2组之间比较，差异无统计学意义。结论TNF-α可引起肺内炎性介质LTIM和LTE4产生增加，同时引起EOS和其他炎性细胞在气道和肺组织局部募集、浸润，维持和加重了哮喘病理改变，这可能是哮喘炎症状态持续存在的发生机制之一。

英文摘要：

Objective To investigate the expression of leukotriene D4 and leukotriene E4 in the bronchoalveolar lavage fluid （BALF） in asthma mice model and to explore the role of tumor necrosis factor α （TNF-α） played in asthma pathogenesis. Methods Forty-eight BALB/c mice were randomly assigned into normal control （A group） , asthma（ B group）, inhaled low dose TNF-α （ C1 group）, inhaled high dose TNF-α （ C2 group）, injected low dose TNF-α（D1 group）and injected high dose TNF-α groups（D2 group）（n = 8 each）. The mice were sensitized with ovalbumin to establish the asthmatic model. The histological changes were evaluated by hematoxylin and eosin staining, BALF were collected, the total cell and the cell differentials were counted, and the levels of leukotriene D4 and leukotriene FA were measured by enzyme-linked immunosorbent assay. SPSS 17.0 software was used to analyze the data. Results ①Typical inflammatory changes were shown in asthma group and TNF-α intervention groups The total cells, EOS amounts of TNF-α intervention group were significantly higher than those of asthma group. ② The expression of LTD4 and LTE4 in BALF ： B group, C group and D group were significantly higher than that in A group（P 〈0. 01 ）, C group and D group were significantly higher than B group（P 〈0. 05）, C2 group were significantly higher than C1 group（ P 〈 0. 05 ）, D2 group were significantly higher than D1 group（ P 〈 0. 05 ）, but no statistical significance were obtained between C1 group and D1 group, C2 group and D2 group. Conclusion TNF-α can significantly increase the expression of LTD4 and LTE4 in BALF in asthmatic mice, promote asthma attack and deteriorate airway inflammation. It may be one of the mechanism of TNF-α involved in asthma.