中文摘要：

目的：观察甲醛对小鼠变应性鼻炎（AR）的影响。方法：48只雄性BALB/c小鼠随机分成6组,每组8只,其中A组为正常对照组;B组为单纯AR组;C组为甲醛暴露组;D、E和F组分别为甲醛低、中、高浓度（1.5、3.0、6.0mg/m3）AR组。采集外周血间接酶联免疫吸附试验法测血清中IL-4、IL-10和干扰素γ（IFN-γ）的水平,并取鼻黏膜行苏木精-伊红染色观察鼻黏膜中嗜酸粒细胞浸润情况。结果：气态甲醛暴露可导致AR小鼠挠鼻和喷嚏次数增加;B、D、E和F组小鼠外周血中IL-4和IL-10水平较A组明显升高（P〈0.05）,D、E和F组较C组明显升高（P〈0.05）;而E、F组IL-4水平较B组明显升高（P〈0.05）,D、E和F组IL-10水平明显高于B组（P〈0.05）。血清中IFN-γ水平B、D、E、F小鼠明显低于A组,B组血清中IFN-γ水平明显高于F组而低于C组,与C组相比D、E、F组外周血IFN-γ表达明显降低。鼻黏膜苏木精-伊红染色显示甲醛暴露可使AR小鼠鼻黏膜下嗜酸粒细胞数量增多。结论：气态甲醛暴露可促进Th2细胞因子表达,加重鼻黏膜中嗜酸粒细胞炎症反应,协同致敏原加重小鼠AR的症状。

英文摘要：

Objective： To observe the effect of formaldehyde inhalation on the allergic rhinitis mice model. Method：Forty-eight male BALB/C mice in six experimental group were exposure to （A） saline control; （B） Der pl ; （C） formaldehyde （3.0 mg/m^3 ）;（D） Derpl ＋ formaldehyde （1.5 mg/m^2） ; （E） Der pl ＋ formaldehyde （3.0 mg/ma） ; （F） Der pl-9 formaldehyde （6.0 mg/m^3）. The concentrations of IL-4,IL-10 and IFN-γ in the peripheral serum were measured by enzyme-linked immunosorbent assay（ELISA）. Nasal mucosal inflammation was evaluated by HE staining. Result： Formaldehyde exposure could increase the number of allergic rhinitis mice with sneezing and rubbing nose. The levels of IL-4 and IL-10 in group B, D, E and F were higher than that ingroup A （P〈0.05）. Compared with the group C, the group D, E and F could effectively increase serum IL-4 and IL-10. The concentration of IL-4 in group E and F was higher than that of group B, while the group C was lower （P〈0.05）. The concentration of IL-10 in group D, E and F was higher than that in group B （P〈0.05）. The expres- sion of IFN-7 in group B, D, E and F was lower than that in group A. While, the IFN-γ expression in group B was lower than that of group C and higher than that in group F （P〈0.05）. Moreover, the concentration of IFN-γ in group D, E and F was lower compared with group C （P〈0.05）. The nasal mucosa HE staining showed that the density of EOS increased simultaneously in formaldehyde exposure allergic rhinitis groups. Conclusion： The study showed that formaldehyde exposure can promote Th2 eytokines and eosinophil infiltration and then aggravate the allergic rhinitis symptoms.