MRP1 expression and bronchial epithelial function in lipopolysaccharide-induced rat model of chronic obstructive pulmonary disease
Received:October 29, 2013  
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DOI:10.3969/j.issn.1005-4847.2014.03.006
KeyWord:Lipopolysaccharide;Chronic obstructive pulmonary disease;Multidrug resistance-associated protein 1;Function;Expression;Rat
                    
AuthorInstitution
汪珊珊 安徽中医药大学药学院, 合肥
汪电雷 安徽中医药大学药学院, 合肥
陶秀华 安徽中人科技有限责任公司药理组, 合肥
汪辰吟 安徽中医药大学药学院, 合肥
陈金佩 安徽中医药大学药学院, 合肥
杨丽丽 安徽中医药大学药学院, 合肥
曹银 安徽合肥市精神病医院药剂科, 合肥
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Abstract:
      Objective To study the impact of establishment of lipopolysaccharide (LPS)-induced rat model of chronic obstructive pulmonary disease(COPD)on the function of multidrug resistance-associated protein 1(MRP1)in the rat bronchial epithelium. Methods Using intratracheal instillation of LPS to establish COPD rat model. 8-week old healthy male Wistar rats were divided into 3 groups (10 rats in each group): (1) Normal control;(2) Modeling for 14 days after LPS instillation; (3) Modeling for 28 days after LPS instillation. Pulmonary function and the concentration of phenol red in bronchoalveolar lavage fluid (BALF) and plasma were measured. The ratio of phenol red concentration in BALF/plasma was used as an index of the MRP1 function in the rat bronchial epithelium and the expression of MRP1 in the bronchial epithelium was also observed by immunohistochemistry. Results Compared with the normal group, the pulmonary functions of the rats in the model groups were significantly reduced along with the modeling progress. After intravenous administration of phenol red, the ratio of phenol red concentration in BALF/plasma was gradually reduced, and the expression of MRP1 in the bronchial epithelium was significantly decreased. Conclusions COPD rat model can be established by intratracheal LPS instillation, and the function of MRP1 in bronchial epithelium was gradually reduced along with the modeling progress.
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