柴油废气颗粒对哮喘大鼠气道趋化因子Eotaxin表达的影响

Effects of Diesel Exhaust Particle on Expression of Eotaxin in Asthmatic Rats

目的分析空气污染物的柴油废气颗粒(DEP)吸入对哮喘模型大鼠的气道嗜酸粒细胞趋化因子表达的影响。方法以SD雄性大鼠为实验动物,利用卵白蛋白(OVA)制备哮喘模型,之后再给予雾化吸入DEP各1、2及3周。每只大鼠均于最后一次吸入结束后次日处死,取支气管组织和肺泡灌洗液,ELISA法和定量PCR分别检测CCL11、CCL24、CCL26的基因和蛋白表达水平。结果随着DEP吸入时间的延长,CCL24和CCL26的基因和蛋白表达均逐渐上升,与对照组相比差异有统计学意义。而CCL11的基因和蛋白表达在DEP吸入后无明显变化。结论柴油DEP吸入加重哮喘大鼠的气道高反应性,与DEP刺激CCL24和CCL26趋化因子表达部分相关。

Objective To investigate the effects of diesel exhaust parti cles（DEP） on the production of CCL11,CCL24 and CCL26 in asthmatic rats. Methods Fifty SD rats were randomly divided into five groups.Group A was an normal con trol group.The rats in group B,C,D,and E were sensitized and challenged by o valbumin（OVA） to establish asthma model.Then the rats in the group C,D,E were inhaled DEP for 1,2,3 weeks,respectively.Lung tissue and brouchoalv eolar lavage fluid（BALF） were collected for detection of CCL11,CCL24,and CCL 26 expression by ELISA and q-RT-PCR.Results The transcripti on of CCL 24,CCL26 gene and the production of CCL24 and CCL26 protein increased significantly comp ared with the control group（P0.05）,and were positively associated with the DE P inhalation time.However,CCL11 gene and protein expression were not changed s ignificantly compared with the control.Conclusion The exposur e to DEP can indu ce the production of CCL24 and CCL26 in the asthmaic rats,which might aggravate airway hyperresponsiveness.