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目的:探讨哮喘小鼠发病过程中白细胞介素32(IL-32)及肿瘤坏死因子-α(TNF-α)在肺内表达的变化及布地奈德的干预作用。方法:将30只健康雌性BALB/c小鼠随机分为3组:卵蛋白(OVA)致敏并激发的哮喘模型组(A组),OVA致敏、激发并予布地奈德吸入治疗组(B组)及正常对照组(C组),每组10只。观察卵蛋白激发及布地奈德干预后哮喘小鼠气道的病理变化;免疫组织化学染色观察IL-32及TNF-α表达的变化。结果:IL-32及TNF-α在对照组中呈低表达,在哮喘组中表达明显增加,使用布地奈德干预后,IL-32及TNF-α的表达明显降低(P<0.05),且二者表达量均与气道壁厚度呈正相关(r=0.716,P<0.05;r=0.459,P<0.05)。结论:IL-32及TNF-α可能参与了哮喘小鼠气道重塑过程,布地奈德干预改善哮喘小鼠的气道重塑可能与降低IL-32及TNF-α的表达有关。
Objective: To investigate the changes of interleukin 32 (IL-32) and tumor necrosis factor-α (TNF-α) expression in the lung and the intervention of budesonide in asthmatic mice. Methods: Thirty healthy female BALB / c mice were randomly divided into three groups: asthma model group (group A) sensitized and challenged with ovalbumin (OVA), sensitized by OVA, challenged with budesonide inhalation therapy group B group) and normal control group (C group), 10 rats in each group. The pathological changes of airway in asthmatic mice were observed after ovalbumin stimulation and budesonide intervention. The expressions of IL-32 and TNF-α were observed by immunohistochemical staining. Results: The expression of IL-32 and TNF-α was low in the control group and significantly increased in the asthmatic group. The expression of IL-32 and TNF-α was significantly decreased after the intervention of budesonide (P <0.05) Both expression levels were positively correlated with airway wall thickness (r = 0.716, P <0.05; r = 0.459, P <0.05). Conclusion: IL-32 and TNF-α may be involved in the process of airway remodeling in asthmatic mice. Budesonide may improve airway remodeling in asthmatic mice and decrease the expression of IL-32 and TNF-α.