Lihong Wang1, Bin Zhang2, Zhu Li1, Junhong Li1, Qing Liu3, Wuzhuang Sun1. 1. Department of Respiratory Medicine, First Hospital of Hebei Medical University China. 2. Department of Emergency, First Hospital of Hebei Medical University China. 3. Department of Respiratory Medicine, Geriatrics Hospitals in Hebei Province China.
Abstract
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.
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.
Authors: V I Peinado; J A Barberá; P Abate; J Ramírez; J Roca; S Santos; R Rodriguez-Roisin Journal: Am J Respir Crit Care Med Date: 1999-05 Impact factor: 21.405
Authors: Suellen M Curkendall; Stephan Lanes; Cynthia de Luise; Mary Rose Stang; Judith K Jones; Dewei She; Earl Goehring Journal: Eur J Epidemiol Date: 2006-11-15 Impact factor: 8.082