糖皮质激素对哮喘大鼠Clara细胞分泌蛋白表达的影响

Effect of budesonide on Clara cell secretory protein and its mRNA expression in a rat model of asthma

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 investigate the effect of inhaled glucocorticoids on the expression of Clara cell secretory protein(CCSP) and its mRNA in lung tissue of a rat model of asthma Methods The rat asthmatic model was established by sensitizing and challenging SD rats with aerosolized ovalbumin (OVA). Rats were divided into a control, an asthmatic and a glucocorticoid groups. Budesonide aerosol was delivered by a jet nebulizer. The CCSP mRNA level in the lung tissue and the CCSP level in bronchoalveolar lavage fluid (BALF) were determined by RT PCR and dot immuno blotting, respectively Results The level of CCSP mRNA in the lung tissue was 0 65±0.04 in the control, 0.56±0.05 in the asthmatic and 0.63±0.04 in the glucocorticoid groups, respectively (asthma versus control, P <0.01; glucocorticoid versus asthma, P <0.05). The CCSP level in BALF was 60±5 in the control, 49±5 in the asthmatic and 57±5 in the glucocorticoid groups, respectively (asthma versus control, P <0.01; glucocorticoid versus asthma, P <0.05). Budesonide reduced the percentage of eosinophils in BALF and inhibited airway inflammation Conclusions OVA challenge in the rat model decreased CCSP mRNA, resulting in a reduction in CCSP production, which may contribute to asthmatic airway inflammation. Inhaled glucocorticoids increased the expression of CCSP mRNA in lung tissue, which may be a mechanism for the suppression of airway inflammation by glucocorticoids.