雷公藤甲素对哮喘小鼠白介素13和嗜酸性粒细胞趋化因子表达的影响

目的观察雷公藤甲素(TL)对哮喘小鼠肺组织中白介素13(IL-13)和嗜酸性粒细胞趋化因子(Eotaxin)表达的影响,探讨TL治疗哮喘的作用机理。方法40只雄性昆明小鼠随机分成4组:正常对照组、哮喘未治疗组、地塞米松治疗组及TL治疗组,以卵清蛋白致敏和激发方法建立哮喘小鼠动物模型并给予相应治疗。24 d后处死小鼠,检测各组支气管肺泡灌洗液(BALF)中白细胞总数及嗜酸性粒细胞(Eos)计数;采用逆转录-聚合酶链反应(RT-PCR)方法检测各组小鼠肺组织匀浆中IL-13、eotaxin mRNA的表达量;采用免疫组化法检测各组小鼠肺组织切片中IL-13、eotaxin蛋白的表达水平;并探讨他们之间的关系。结果哮喘未治疗组小鼠肺组织IL-13、eotaxin mRNA及蛋白的表达量均明显高于正常对照组(P<0.01),TL治疗组及地塞米松治疗组低于哮喘未治疗组(P<0.01或<0.05)。肺组织IL-13蛋白的表达与BALF中的白细胞总数、Eos计数及肺组织eotaxin蛋白的表达呈正相关(r分别为0.513、0.604、0.625,P<0.01)。肺组织eotaxin蛋白的表达与BALF中的白细胞总数、Eos计数呈正相关(r分别为0.679、0.718,P<0.01)。结论TL抑制哮喘气道炎症的机制可能与其抑制肺组织中IL-13及eotaxin的表达有关。

Effects of triptolide on the expression of IL-13 and eotaxin in asthmatic mice

Objective To investigate the role of triptolide in the expression of IL-13 and eotaxin in ovalbumin-challenged asthmatic mice,exploring the potential mechanism of triptolide in the therapy of asthma.Methods40 healthy Kunming male mice were randomly divided into 4 groups: control group(group A),asthmatic group(group B),dexamethasone group(group C) and triptolide group(group D).The asthmatic model was established with the treatment of ovalbumin.24 days after the experiment started,the mice were executed.The numbers of total leukocytes and eosinophils in bronchoalveolar lavage fluid(BALF) were counted by optical microscope.RT-PCR was employed to detect the mRNA of IL-13 and eotaxin from the lung tissue.Immunohistochemistry was used to measure the protein expression of IL-13 and eotaxin.ResultsThe mRNA and protein levels of IL-13 and eotaxin in group B was significantly increased compared with those in group A,C and D(P<0.01 or P<0.05).IL-13 protein expression significantly associated with the numbers of total leukocytes or eosinphils in BALF and with the expression of eotaxin protein from the lung tissue(r=0.513,0.604,0.625,P<0.01,respectively). There was a positive association between expression of eotaxin protein and total leukocyte or eosinophil counts in the BALF(r= 0.679,0.718,P<0.01, respectively).ConclusionTriptolide may inhibit asthmatic airway inflammation partially through inhibiting the expression of IL-13 and eotaxin.