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目的:观察中药防哮饮对哮喘小鼠血清白细胞介素4(IL-4)、γ-干扰素(IFN-γ)、IL-4/IFN-γ值以及肺组织病理学的变化,初步探讨该药早期干预治疗对哮喘小鼠Th1/Th2细胞亚群反应的影响及其防治哮喘的作用机理。方法:50只BALB/c健康小鼠随机分为5组:正常对照组、哮喘模型组、防哮饮小剂量组、防哮饮大剂量组、布地奈德(BUD)组。用卵白蛋白(OVA)致敏激发造模。采用双抗夹心酶联免疫吸附试验(ELISA)法检测血清IL-4、IFN-γ含量,光镜下观察肺组织病理学的变化。结果:哮喘模型组与正常对照组比较,IL-4水平显著升高、IFN-γ含量明显降低,差异均有非常显著性意义(P<0.01);与哮喘模型组比较,防哮饮大剂量组、防哮饮小剂量组及BUD组均能不同程度地降低哮喘小鼠血清IL-4水平,差异均有非常显著性意义(P<0.01);防哮饮大剂量组与BUD组比较,差异无显著性意义(P>0.05)。与哮喘模型组比较,防哮饮大剂量组及BUD组均能明显上调IFN-γ水平,差异均有非常显著性意义(P<0.01);防哮饮小剂量组IFN-γ上调不明显(P>0.05);防哮饮大剂量组与BUD组比较,差异无显著性意义(P>0.05)。哮喘小鼠肺组织病理学观察显示防哮饮小剂量组、防哮饮大剂量组分别存在不同程度的气道炎症反应;经过BUD处理的小鼠,其肺组织中支气管和微血管周围基本未见炎症细胞浸润,气道炎症基本得到抑制,和正常小鼠肺组织切片基本一致。与哮喘模型组比较,防哮饮小剂量组、防哮饮大剂量组支气管黏膜修复得较完整,其中防哮饮小剂量组气管周围仍有较多炎症细胞、PAS染色示增生的杯状细胞仍较多;防哮饮大剂量组气道及血管周围炎症浸润得到明显抑制,嗜酸性粒细胞(EOS)极少,PAS染色示杯状细胞极少,气道黏液分泌得到明显抑制。结论:中药防哮饮早期干预治疗哮喘具有抑制Th2细胞亚群优势反应,下调IL-4、上调IFN-γ表达水平,纠正Th1/Th2失衡,并能够抑制气道黏液分泌,修复气道黏膜,抑制气道及血管周围以EOS为主的炎症浸润,可能是其抑制哮喘气道炎症的重要作用机制之一。
Objective: To observe the changes of serum interleukin 4 (IL-4), interferon-γ (IFN-γ), IL-4 / IFN-γ and lung histopathology in asthmatic mice The drug early intervention on the impact of Th1 / Th2 cell subsets in asthmatic mice and its mechanism of action in the prevention and treatment of asthma. Methods: Fifty BALB / c healthy mice were randomly divided into five groups: normal control group, asthma model group, low dose anti - asthma drink group, high dose anti - asthma drink group and budesonide group. Sensitized with ovalbumin (OVA) to stimulate modeling. Serum levels of IL-4 and IFN-γ were measured by double-antibody sandwich enzyme-linked immunosorbent assay (ELISA). The pathological changes of lung were observed under light microscope. Results: Compared with the normal control group, the level of IL-4 and the level of IFN-γ in asthmatic model group were significantly decreased (P <0.01). Compared with the asthma model group, (P <0.01). Compared with BUD group, the anti-asthma drink low-dose group and BUD group all reduced the level of serum IL-4 in asthmatic mice to some extent, the difference was significant There was no significant difference (P> 0.05). Compared with the asthma model group, both IFN-γ and IFN-γ levels were significantly up-regulated in the anti-asthma drink high-dose group and the BUD group (P <0.01) P> 0.05). There was no significant difference between the high-dose anti-asthma drink group and the BUD group (P> 0.05). The histopathological observation of lung in asthmatic mice showed that there were different degrees of airway inflammation in the low-dose anti-asthma drink group and the high-dose anti-asthmatic drink group, while the bronchus and microvascular in the lung tissue of the BUD-treated mice were almost not seen Inflammatory cell infiltration, airway inflammation was basically inhibited, and normal mice lung tissue sections are basically the same. Compared with the asthma model group, bronchial mucosa repair was more complete in the low-dose anti-asthma drink group and high-dose anti-asthmatic drink group, in which there were still more inflammatory cells around the trachea in the low-dose anti-asthmatic drink group and hyperplastic goblet cells by PAS staining Still more; anti-asthma drink high-dose group of airway and perivascular inflammatory infiltration were significantly inhibited, eosinophils (EOS) very few, PAS staining showed very few goblet cells, airway mucus secretion was significantly inhibited. Conclusion: Early treatment of Asthma by asthma can inhibit the predominant Th2 cell subtype, down-regulate IL-4, up-regulate the expression of IFN-γ, correct the imbalance of Th1 / Th2, suppress airway mucus secretion and repair airway mucosa, Inhibition of airway and perivascular EOS-based inflammatory infiltration may be one of the important mechanisms of its inhibition of airway inflammation in asthma.