Luo Fengming, Wang Zengli, Liu Xiaojing, Liu Chuntao, Zhang Xiaohong, Wang Wenzhi
Department of Respiratory Disease, Huaxi Hospital of Sichuan University, Chengdu 610041, China.
Zhonghua Jie He He Hu Xi Za Zhi. 2002 Sep;25(9):538-41.
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.
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.
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.
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.
探讨吸入糖皮质激素对哮喘大鼠模型肺组织中克拉拉细胞分泌蛋白（CCSP）及其mRNA表达的影响。
通过用雾化卵清蛋白（OVA）致敏和激发SD大鼠建立大鼠哮喘模型。将大鼠分为对照组、哮喘组和糖皮质激素组。用喷射雾化器给予布地奈德气雾剂。分别通过逆转录聚合酶链反应（RT-PCR）和斑点免疫印迹法测定肺组织中CCSP mRNA水平和支气管肺泡灌洗液（BALF）中CCSP水平。
对照组肺组织中CCSP mRNA水平为0.65±0.04，哮喘组为0.56±0.05，糖皮质激素组为0.63±0.04（哮喘组与对照组相比，P<0.01；糖皮质激素组与哮喘组相比，P<0.05）。BALF中CCSP水平对照组为60±5，哮喘组为49±5，糖皮质激素组为57±5（哮喘组与对照组相比，P<0.01；糖皮质激素组与哮喘组相比，P<0.05）。布地奈德降低了BALF中嗜酸性粒细胞的百分比并抑制了气道炎症。
大鼠模型中OVA激发降低了CCSP mRNA水平，导致CCSP产生减少，这可能导致哮喘气道炎症。吸入糖皮质激素增加了肺组织中CCSP mRNA的表达，这可能是糖皮质激素抑制气道炎症的机制之一。
