牛蒡子苷元抗哮喘小鼠气道炎症作用及机理研究

The effection and mechanism of arctigenin in airway inflammation in bronchial asthma rats

目的:观察牛蒡子苷元对哮喘小鼠气道炎症的影响并探究相关作用机制。方法:将30只雌性BALB/c小鼠随机分为正常对照组、模型组和牛蒡子苷元组。采用卵清白蛋白与氢氧化铝致敏,并雾化吸入卵清蛋白激发制备小鼠支气管哮喘模型,81天后检测小鼠支气管肺泡灌洗液中细胞总数和炎症细胞数;采用HE染色在光镜下观察各组小鼠肺组织病理学变化;采用RT-PCR和Western blot分别对肺组织E选择素的mRNA和蛋白表达进行测定;采用Western blot对肺组织中NF-κB p65活化水平(p-NF-κB p65/total NF-κB p65)进行检测。结果:与模型组相比,牛蒡子苷元组小鼠BALF中细胞总数、嗜酸性粒细胞数、中性粒细胞和巨噬细胞数明显降低;小鼠肺组织病理变化明显减轻;此外,与模型组相比,牛蒡子苷元组哮喘小鼠肺组织E选择素mRNA和蛋白的表达降低,哮喘小鼠的NF-κB p65活化水平显著下降。结论:牛蒡子苷元10 mg/kg可能通过抑制NF-κB的活化从而降低OVA诱导的哮喘小鼠气道炎症水平,为牛蒡子苷元进一步应用于哮喘的治疗奠定了一定的实验基础。

Objective： To observe the role of arctigenin in airway inflammation in a murine model of OVA-induced asthma,and to study its mechanism. Methods： Thirty female BALB / c mice were randomly divided into 3 groups： Control group,model group and the ATG group. The total numbers of cells and the inflammatory cells counts in BALF were measured after 81 days’ intervention. Hematoxylin and eosin（ H＆E）staining was used to observe pathological alterations in lungs. The mRNA and protein expression of E-selectin was analyzed by RT-PCR and western blot respectively. The activation of NF-κB p65（ p-NF-κB p65 / total NF-κB p65） was also detected by western blot. Results： Compared with the model group,the total cell counts,eosinophils counts,neutrophil counts and macrophages counts in BALF were markedly reduced; alteration in lungs was obviously alleviated; In addition,compared with the model group,the mRNA and protein expressions of E-selectin in lungs were reduced significantly in ATG group,and the level of NF-κB p65 activation in lungs were decreased obviously. Conclusion： OVA-induced airway inflammation was significantly inhibited by ATG（ 10 mg / kg） possibly through in activation of NF-κB in mice.Thus lay a theoretical foundation for ATG to cure asthma.