出 处:《延边大学医学学报》2008年第4期235-238,共4页Journal of Medical Science Yanbian University
基 金:国家自然科学基金30560052
摘 要:[目的]探讨哮喘大鼠吸入不同时程柴油废气颗粒(DEP)后哮喘迟发相反应的变化情况,即DEP吸入对哮喘大鼠的影响.[方法]取雄性Wistar大鼠随机分为6个组,A组给予生理盐水攻击,B组给予卵蛋白攻击,C,D,E,F组先给予卵蛋白攻击,再分别吸入DEP 1,2,3,4周.攻击结束1周后用生理盐水激发A组大鼠30 min,用卵蛋白激发其余各组大鼠30 min,24 h后行乙酰胆碱激发试验,测定气道阻力,比较每组大鼠被乙酰胆碱激发后最终气道阻力与基础气道阻力比值的变化,即气道反应性的变化,并观察肺泡灌洗液中嗜酸性粒细胞数的变化,检测血清IgE水平和肺组织中IL-5,IFN-γ水平并观察病理变化等.[结果]A组未发生气道高反应性,其余各组大鼠气道阻力比值均较A组增高,且E,F组较B组明显增高,差异均有统计学意义;DEP的吸入时程与气道阻力比值呈正相关(r=0.886).B,C, D,E,F组肺泡灌洗液中嗜酸性粒细胞数、血清IgE及肺组织IL-5水平均显著高于A组,且E,F组嗜酸性粒细胞数显著高于B组,D,E,F组肺组织中IL-5水平明显高于B组.差异均有统计学意义,DEP的吸入时程与IL-5水平呈正相关(r=0.583);B,C,D,E,F组肺组织IFN-γ水平与A组比较明显降低,E, F组较B组明显降低,差异均有统计学意义,DEP的吸入时程与IFN-γ水平呈负相关(r=-0.550).肺组织病理观察表明,A组大鼠气道上皮细胞完整,气道周围未见炎症细胞浸润,以纤毛柱状上皮细胞为主,仅有少量的杯状细胞,基底膜未见纤维化;随着DEP吸入时程的延长,大鼠气道逐渐出现上皮细胞的坏死、中断及脱落,杯状细胞增生,气道周围炎症细胞浸润及基底膜纤维化等改变.[结论]柴油废气颗粒的吸入通过促进Th2淋巴细胞活性,加重哮喘大鼠迟发相反应.OBJECTIVE To investigate the effects of diesel exhaust particles (DEP) inhaled to late asthmatic reaction in the rats. METHODS Male Wistar rats were randomly divided into 6 groups. Group A was sensitizated with saline and group B with ovalbumin, and group C, D, E and F were respectively challenged with ovalhumin, then inhaled DEP for 1 week, 2 weeks, 3 weeks and 4 weeks. After 1 week of end of DEP inhalation, group A was challenged with saline for 30 minutes, and the other groups with ovalbumin for 30 minutes, and acetycholin provocatin test was taken after 24 hours, then the airway resistances of all groups were determined. The airway reactivity were compared in each group, and the changes of eosinophil count, the levels of IgE of IL-5 and IFN-γ were determined, and the pathologic change was observed. RESULTS There was no airways hyperresponsiveness in the control group, and the airways hyperresponsiveness was significantly different between the control group and the other groups, and that of group B was higher than that of group E and group F, respectively, and increase gradually with the inhalation of the DEP (r = 0. 886). The eosinophil count, the levels of IgE and and IL-5 of group B, C, D, E and F in brouchialveolar lavage fluid were significantly greater than that of group A, and the eosinophil count of group E, F and the levels of IL-5 of group D,E and F were higher than that of group B, respectively. The degree of airway hyperresponsiveness depended on the inhalation time of DEP(r=0. 583). The levels of IFN-γ of group B, C,D,E and F were, significantly reduced when compared with group A, and that of group E and F were significantly decreased when compared to group B, and the level of IFN-γ density depending on the inhalation time of dep(r=-0. 550). The lung pathology showed the epithelial shedding, infiltration of peribronchial inflammatory cells and fibrosis on the basement membrane gradually. CONCLUSION Inhaled DEP caused asthmatic inflammatory changes by Th 2 lymphocyte, and increas
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