目的:探讨荧蒽暴露对哮喘模型小鼠血液中IgE、IL-4、IL-5和肺组织中MDA、SOD、GSH-Px表达的影响。方法:选择雄性Balb/c小鼠40只,随机分为4组。A组为正常对照组,B组为哮喘模型组,C组为10μg/m3荧蒽暴露组,D组为100μg/m3C荧蒽暴露组。测定气道阻力,采用Wright-Giemsa染色和HE染色观察BALF中的嗜酸性粒细胞(EOS)的募集和肺组织病理变化,采用TBA法,黄嘌呤氧化酶法,二硫代二硝基苯甲酸法,ELISA法分别检测肺组织中丙二醛水平(MDA)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、IgE、IL-4、IL-5的表达。结果:A组的气道阻力,BALF中嗜酸性粒细胞的募集分别为3.61±0.89,(0.59±0.032)%,B组气道阻力值,BALF中EOS募集较A组显著增加(P<0.01),荧蒽暴露组气道阻力,BALF中EOS募集较模型组显著增加(P<0.01);哮喘模型组肺组织中SOD、GSH-Px的含量与正常对照组略有下降,MDA有所升高,但无统计学差异(P>0.05),荧蒽暴露组肺组织中SOD、GSH-Px的含量较哮喘模型组明显下降,MDA明显升高(P<0.01);哮喘模型组中血清中IgE、IL-4、IL-5浓度较正常对照组显著增加(P<0.01),荧蒽暴露组血清中IgE、IL-4、IL-5浓度较哮喘模型组略有增加,但无统计学差异(P>0.05);肺组织病理切片哮喘模型组中出现上皮细胞部分脱落,少量的嗜酸性粒细胞浸润在气道壁周围;荧蒽暴露组上皮细胞明显破坏、脱落,大量嗜酸性粒细胞浸润,血管周围明显水肿。结论:荧蒽暴露可加重哮喘模型小鼠的脂质过氧化反应和肺部炎性反应。 Objective: To investigate the effects of fluoranthene on the expression of IgE, IL-4 and IL-5 in blood and the expression of MDA, SOD and GSH-Px in lung tissue of asthmatic mice. Methods: Forty male Balb / c mice were randomly divided into four groups. Group A was normal control group, group B was asthma model group, group C was 10μg / m3 fluoranthene exposure group, group D was 100μg / m3C fluoranthene exposure group. The airway resistance was measured. The recruitment of eosinophils (EOS) in BALF and pathological changes of lung tissue were observed by Wright-Giemsa staining and HE staining. TBA, xanthine oxidase, The levels of malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), IgE, IL-4 and IL-5 expression. Results: The airway resistance and the eosinophil recruitment in BALF in group A were 3.61 ± 0.89 and 0.59 ± 0.032%, respectively. The airway resistance in group B was significantly higher than that in group A (P <0.01) (P <0.01). The content of SOD and GSH-Px in the lung tissue of the asthma model group decreased slightly compared with that in the normal control group, and MDA content increased (P> 0.05). The content of SOD and GSH-Px in the lung tissue of the fluoranthene-exposed group was significantly lower than that of the asthma model group and the MDA level was significantly increased (P <0.01). In the asthma model group, The concentrations of IgE, IL-4 and IL-5 in the fluoranthene-exposed group were significantly higher than those in the normal control group (P <0.01). The concentrations of IgE, IL-4 and IL- (P> 0.05). In the pathological section of lung tissue, some epithelial cells were partially shedding and a small amount of eosinophil infiltration around the airway wall. The epithelial cells in the fluoranthene-exposed group were obviously destroyed and shedding, a large number of eosinophils Infiltration, obvious perivascular edema. Conclusion: Fluoranthene exposure may increase lipid peroxidation and pulmonary inflammatory response in asthmatic mice.