布地奈德对哮喘小鼠气道上皮细胞闭锁蛋白表达的影响

发布时间：2018-10-10 07:12

【摘要】：目的观察哮喘小鼠气道上皮细胞闭锁蛋白的表达及布地奈德对其表达的影响。方法将24只雌性BALB/c小鼠随机分为哮喘模型组、布地奈德组及对照组,每组8只。对照组用生理盐水,哮喘模型组和布地奈德组用卵清蛋白腹腔注射致敏及雾化吸入激发建立哮喘模型,布地奈德组每次激发前1 h吸入布地奈德混悬液1 mg,连续14 d。对照组和哮喘模型组用等量生理盐水代替布地奈德,吸入方法和时间同布地奈德组。小鼠末次激发24 h后,计数支气管肺泡灌洗液(BALF)中的嗜酸性粒细胞(EOS),HE和PAS染色观察支气管及周围肺组织的病理改变、杯状细胞增生和黏液分泌;电镜观察气道上皮的超微结构;免疫组织化学和荧光定量PCR检测气道上皮occludin的表达。结果与对照组比较,哮喘模型组小鼠BALF中EOS计数、气道上皮杯状细胞数及病理学评分明显增高;支气管肺组织occludin蛋白表达明显减弱,差异均有统计学意义(P0.01)。与哮喘模型组比较,布地奈德组EOS和杯状细胞计数及病理学评分明显降低,occludin蛋白表达增强,差异均有统计学意义(P0.01)。哮喘模型组气道上皮细胞间的连接结构不完整,细胞间隙增宽,而布地奈德组上述表现较哮喘组减轻。结论布地奈德能上调哮喘小鼠气道上皮occludin的表达、促进受损气道上皮的修复,可能是吸入型糖皮质激素治疗哮喘的机制之一。
[Abstract]:Objective to observe the expression of atresia protein in airway epithelial cells of asthmatic mice and the effect of budesonide on it. Methods 24 female BALB/c mice were randomly divided into asthma model group, budesonide group and control group. The asthmatic model was induced by intraperitoneal injection of ovalbumin and inhaled by atomization inhalation in the asthmatic model group and budesonide group. The budesonide group inhaled budesonide suspension 1 mg, for 14 days. The control group and asthma model group were treated with the same amount of saline instead of budesonide, the inhalation method and time were the same as those in the budesonide group. The eosinophilic granulocytes in (BALF) of bronchoalveolar lavage fluid (BALF) were counted for 24 h after the last stimulation. The pathological changes, goblet cell proliferation and mucus secretion were observed by PAS and eosinophils in bronchoalveolar lavage fluid (BALF), and the ultrastructure of airway epithelium was observed by electron microscope. Immunohistochemistry and fluorescence quantitative PCR were used to detect the expression of occludin in airway epithelium. Results compared with the control group, the number of EOS in BALF, the number of goblet cells in airway epithelium and the pathological score in asthmatic model group were significantly increased, and the expression of occludin protein in bronchopulmonary tissue was significantly decreased (P0.01). Compared with asthmatic model group, budesonide group significantly decreased the expression of cludin protein in EOS, goblet cell count and pathological score (P0.01). The airway epithelial cells in asthmatic model group were not well connected and the intercellular gap was widened, while the above findings in budesonide group were less than those in asthma group. Conclusion budesonide can up-regulate the expression of occludin in airway epithelium of asthmatic mice and promote the repair of damaged airway epithelium, which may be one of the mechanisms of inhaled glucocorticoid in the treatment of asthma.
【作者单位】：四川省乐山市人民医院呼吸内科;泸州医学院附属医院呼吸一科;
【基金】：四川省卫生厅科研项目(No:110341)
【分类号】：R562.25

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