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目的 观察吸入糖皮质激素对大鼠支气管哮喘 (简称哮喘 )模型肺组织Clara细胞分泌蛋白 (CCSP)mRNA表达的影响。方法 用卵白蛋白 (OVA)致敏、雾化建立大鼠哮喘模型 ,以逆转录 聚合酶链反应 (RT PCR)、斑点免疫印迹法 ,分别检测大鼠激发哮喘 3天后肺组织CCSPmRNA表达水平、支气管肺泡灌洗液 (BALF)CCSP蛋白浓度及雾化吸入布地奈德的影响。结果 哮喘组大鼠肺组织CCSPmRNA表达量为 0 .5 6± 0 .0 5 ,与正常对照组 (0 .6 5± 0 .0 4 )比较差异有显著性 (P <0 .0 1) ;激素治疗组CCSPmRNA表达量为 0 .6 3± 0 .0 4 ,与哮喘组 (0 .5 6± 0 .0 5 )比较差异也有显著性 (P <0 .0 5 )。哮喘组大鼠BALF中CCSP蛋白含量为 4 9± 5 ,与正常对照组 (6 0± 5 )比较 ,差异有显著性 (P <0 .0 1) ;激素治疗组CCSP蛋白含量 (5 7± 5 )与哮喘组比较 (P <0 .0 5 ) ,BALF中嗜酸细胞比例降低 ,气道炎症反应减轻。结论 CCSPmRNA表达减少导致CCSP水平下降 ,从而促进气道炎症而参与哮喘发病。雾化吸入糖皮质激素可增加CCSPmRNA表达 ,抑制哮喘气道炎症。
Objective To observe the effect of inhaled glucocorticoid on Clara cell secretory protein (CCSP) mRNA expression in lung tissue of bronchial asthmatic rats (asthmatic model). Methods The asthma model was induced by ovalbumin (OVA) sensitization and nebulization. Reverse transcription polymerase chain reaction (RT PCR) and dot immunoblotting were used to detect the expression of CCSPmRNA, The concentration of CCSP protein in BALF and the effect of inhaled budesonide. Results The expression of CCSP mRNA in the lung tissue of asthmatic rats was 0.56 ± 0. 05, which was significantly different from that of the normal control group (0.056 ± 0.40) (P <0.01). The expression of CCSPmRNA in hormone therapy group was 0.63 ± 0.04, which was also significantly different from asthma group (0.56 ± 0.05) (P <0.05). The level of CCSP protein in BALF in asthmatic rats was 49 ± 5, which was significantly higher than that in normal control (60 ± 5) (P <0.01) 5) Compared with the asthma group (P <0.05), the proportion of eosinophils in the BALF was decreased and the airway inflammation was relieved. Conclusion The decrease of CCSP mRNA expression leads to the decrease of CCSP level, which promotes airway inflammation and participates in the pathogenesis of asthma. Inhaled glucocorticoid can increase CCSPmRNA expression and inhibit airway inflammation in asthma.