Budesonide mitigates pathological changes in animal model Of COPD through reducing neutrophil elastase expression.

OBJECTIVES This study was conducted to investigate a molecular mechanism by which budesonide inhalation may mitigate pathological responses of cigarette smoke-induced COPD. METHODS Rats were exposed to air (control) and cigarette smoke (smoking) in the presence and absence of budesonide. Cell count in bronchoalveolar lavage fluid (BALF), lung function test, mean liner intercept in lung tissue, mean alveolar number, right ventricular hypertrophy index (RVHI) and morphological changes in lungs were assessed, respectively. Alpha-1 antitrypsin (A1AT) and neutrophil elastase (NE) mRNA expression in lung tissues and their protein productions in BALF were examined as well. RESULTS Smoking rats showed significant changes in the above assessments as compared to those of the control rats (all P < 0.01 or 0.05). Budesonide applied for the smoking rat significantly decreased differential cell counts in BALF and ameliorated lung function and RVHI (P < 0.01 or 0.05) with mitigated peribronchiolar inflammation and pulmonary bullae formation in the smoke-exposed lungs. Treatment with budesonide resulted in obvious decreases in NE mRNA and protein expression levels (both P < 0.05). CONCLUSION Budesonide inhalation serves to improve lung function and right ventricular dysfunction through attenuating pulmonary inflammatory response and NE expression level in the diseased lungs.