期刊文献+

二氧化硫暴露对哮喘大鼠速发相反应影响 被引量:6

Effects of sulfur dioxide on the immediate asthma reaction in rats
原文传递
导出
摘要 目的探讨二氧化硫(SO2)暴露对哮喘大鼠速发相反应的影响。方法选择Wistar雄性大鼠40只,随机分为4组,每组各10只;A组为正常对照组,B组为哮喘模型组,C组为SO2低质量浓度(15 mg/m3)哮喘组,D组为SO2高质量浓度(30 mg/m3)哮喘组。每只大鼠染毒结束1周后处死,测量每只大鼠的气道阻力30 min的变化,观察肺组织病理形态学变化,采用酶联免疫吸附试验法测定血清中白细胞介素(IL)-13和IgE的水平。结果①B组大鼠的气道阻力明显高于A组,差异有统计学意义(P<0.01),C、D组大鼠的气道阻力较B组明显升高,差异有统计学意义(P<0.01);②B组大鼠血清中IL-13和IgE的水平较A组明显增高,差异有统计学意义(P<0.01),C、D组大鼠血清中IL-13和IgE的水平与B组比较差异无统计学意义(P>0.05);③肺组织病理切片实验组大鼠支气管上皮细胞部分脱落或全部脱落,大量的嗜酸性粒细胞和淋巴细胞浸润,也出现单核细胞的浸润,杯状细胞大量增生,并充填上皮细胞的位置,有大量的黏液分泌,可见黏液栓,基底膜出现纤维化。结论 SO2可加重哮喘大鼠气道高反应性和肺部变态炎症反应。 Objective To investigate the effects of different concentrations of sulfur dioxide(SO2) on the immediate asthma reaction in rats.Methods 40 Wistar rats were randomly divided into 4 groups,a control group(group A),an asthma model group(Group B),a low SO2 concentration group(group C,15 mg/m^3) and a high SO2 concentration group(group D,30 mg/m^3).The rats were executed one week after the exposure ended,and the changes of airway resistance in each rat was evaluated for 30 min.The pathological changes of lungs were observed.The levels of IgE and interleukin-13(IL-13) of the serum were detected by ELISA.Results ①The airway resistance:group B was higher than that of group A(P〈0.01),group C and D were higher than that of group B(P〈0.01).②The expression of IL-13:group B was gradually higher than that of group A(P〈0.01),while no significant differences were found among group C,D and group B(P〈0.05).The concentration of IgE in group B was higher than that of group A(P〉0.05),but no significant differences were observed among group B and group C,D(P〉0.05).③The pathological changes of lung showed the epithelial shedding,infiltration of inflammatory cells in peribronchial and partly fibrosis on the basement membrane.Conclusion SO2 exposure may exacerbate immediate asthma reaction in rats.
出处 《中国职业医学》 CAS 北大核心 2010年第5期376-378,共3页 China Occupational Medicine
关键词 二氧化硫 气道高反应性 白细胞介素-13 免疫球蛋白E(IgE) Sulfur dioxide Immediate asthma reaction(IAR) Interleukin-13(IL-13) Immunoglobulin E(IgE)
  • 相关文献

参考文献8

  • 1WARNER J O. Worldwide variation in the prevalence of atopic syruptoms: what does it all mean [ J ]. Thorax, 1999,54 : S46 - S51.
  • 2DELFINO R J,QUINTANA P J,FLORO J,et al. Association of FEV1 in asthmatic children with personal and microenvironmental exposure to airborne particulate matter[ J ]. Environ Health Perspect, 2004,112 (8) :932 -941.
  • 3ZHU M M, ZHOU Q H, ZHU M H, et al. Effects of nebulized ketamine on allergen-induced airway h and inflammation in actively sensitized Brown-Norway rats[ J ]. J Inflamm (Lond), 2007,4 : 10.
  • 4MAKELA M J, KANEHIRO A, BORISH L, et al. IL-10 is necessary for the expression of airway hyperresponsiveness but not pulmonary inflammation after allergic sensitization[ J]. Proc Natl Acad Sci USA, 2000,97 (11 ) :6007 -6012.
  • 5POSTMA D S, BLEECKER E R, AMELUNG P j, et al. Genetic susceptibility to asthma-bronchial hyperresponsiveness eoinherited with a major gene for atopy[ J]. N Engl J Med,1995,333(14) :894 -900.
  • 6WILLS-KARP M, LUYIMBAZI J, XU X, et al. Interleukin-13 : central mediator of allergic asthma[J]. Science,1998,282(5397) :2258 -2261.
  • 7COHN L,TEPPER J S, BOTrOMLY K. IL-4-independent induction of airway hyperrespon-siveness by Th2, but not Thl, cells [ J]. J Immunol,1998,161 (8) :3813 -3816,.
  • 8ZHU Z, HOMER R J, WANG Z, et al. Pulmonary expression of interleukin-13 causes inflammation, mucus hypersecretion, subepithelial fibrosis,physiologic abnormalities, and eotaxin production [ J]. J Clin Invest, 1999,103 ( 8 ) :779 - 788.

同被引文献107

引证文献6

二级引证文献25

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部