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Title: [Effect of budesonide on Clara cell secretory protein and its mRNA expression in a rat model of asthma].
Author: Luo F, Wang Z, Liu X, Liu C, Zhang X, Wang W.
Journal: Zhonghua Jie He He Hu Xi Za Zhi; 2002 Sep; 25(9):538-41. PubMed ID: 12423562.
Abstract:
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.

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