论文部分内容阅读
目的探讨空气污染物中柴油废气课粒(diesel exhaust particle,DEP)吸入对哮喘模型大鼠的气道反应性和免疫学指标的影响。方法选择Wistar大鼠60只,随机分为对照组(A组)、模型组(B组)、实验组(C组、D组、E组、F组),每组各10只。每只大鼠染毒结束后次日处死,并测定每只大鼠气道阻力(RL)30min的变化;采用酶联免疫吸附试验(ELISA)测定血清IgE和肺组织中白介素-5(IL-5)和γ-干扰素(IFN-γ)浓度的变化。结果抗原激发后,B组的气道阻力(7.069±0.632)比A组(3.567±0.211)明显增高;E、F组的气道阻力(8.879±0.616),(11.009±0.693)比B组(7.069±0.632)明显增高(F=156.187,P<0.01);气道阻力增高与DEP吸入时间呈相关性(r=0.948,P<0.01);B组血清中IgE(25.003±1.172)的浓度较A组(20.242±2.143)明显增加(F=2.490,P<0.01);C、E组肺组织中IL-5浓度(17.078±5.235),(18.618±4.228)较B组(12.788±2.827)明显增高(F=4.263,P<0.01);而肺组织中IFN-γ浓度在各组之间比较差异均无统计学意义(F=1.193,P>0.05)。结论柴油废气颗粒吸入可加重哮喘大鼠的气道高反应性,促进血清IgE介导及肺组织中IL-5分泌增加的气道炎症反应。
Objective To investigate the effects of diesel exhaust particulate (DEP) inhalation on airway responsiveness and immunological parameters in asthmatic rats. Methods Sixty Wistar rats were randomly divided into control group (A group), model group (B group), experimental group (C group, D group, E group and F group), with 10 rats in each group. Each rat was sacrificed on the next day after the end of the exposure and the airway resistance (RL) of each rat was measured for 30 min. Serum IgE levels and IL-5 levels were measured by enzyme-linked immunosorbent assay (ELISA) 5) and γ-interferon (IFN-γ) concentrations. Results The airway resistance (7.069 ± 0.632) in group B was significantly higher than that in group A (3.567 ± 0.211) after antigen challenge. The airway resistance (8.879 ± 0.616) and (11.009 ± 0.693) in group E and F were significantly higher than those in group B 7.069 ± 0.632) (F = 156.187, P <0.01). The increase of airway resistance was correlated with DEP inhalation time (r = 0.948, P <0.01). The serum IgE concentration of group B (25.003 ± 1.172) The level of IL-5 in group C and E was significantly higher than that in group B (12.788 ± 2.827) (17.078 ± 5.235) and (18.618 ± 4.228) respectively in group A (20.242 ± 2.143) (F = 2.490, P <0.01) (F = 4.263, P <0.01). However, there was no significant difference in the concentration of IFN-γ between the two groups (F = 1.193, P> 0.05). Conclusion Diesel exhaust particulate inhalation may aggravate airway hyperresponsiveness in asthmatic rats and promote serum IgE-mediated airway inflammatory response with increased IL-5 secretion in lung tissue.