Effects ofJiedu QingfeiMixture on Expressions of NE and MUC5AC in Lung Tissue of Rats with Chronic Obstructive Pulmonary Disease / 中国中医药信息杂志

ABSTRACT

Objective To explore the mechanism ofJiedu Qingfei Mixture for airway mucus hypersecretion of rat models with chronic obstructive pulmonary disease (COPD).Methods Airway instilling lipopolysaccharide combining fuming method was used to establish COPD models. Forty clean level Wistar strain rats were randomly divided into blank control group, model group,Jiedu Qingfei group, and clarithromycin group. Model group, Jiedu Qingfei group, and clarithromycin group were given normal saline,Jiedu Qingfei Mixture, and clarithromycin by gavage respectively, while the blank control group was raised normally for 30 d. All rats were killed on the 31st day for taking lung tissue (6 rats from each group were chosen randomly). Pathological changes of lung tissue and mucous glands hyperplasia were observed by HE staining method. NE and MUC5AC mRNA expression on lung tissue were detected by RT-PCR method. Protein expressions of NE and MUC5AC on pulmonary tissue and airway epithelium were detected by immunohistochemical method.Results Compared with blank control group, mucous glands hyperplasia on airway epithelium, mRNA expression of NE and MUC5AC in lung tissue, and protein expressions of NE and MUCA5C on airway epithelium in the model group significantly increased (P<0.05,P<0.01). Compared with model group, mucous glands hyperplasia on airway epithelium inJiedu Qingfei group significantly decreased (P<0.01), as same as clarithromycin group;Jiedu Qingfei group showed better effects on down-regulating NE and MUC5AC mRNA expression in lung tissue compared with clarithromycin group. MUC5AC protein expression on airway epithelium inJiedu Qingfei group significantly decreased (P<0.05), as same as clarithromycin group.Jiedu Qingfei group and clarithromycin group had no difference on NE protein expression in airway epithelium compared with model group.Conclusion Jiedu Qingfei group Mixture can reduce airway mucus hypersecretion of COPD by down-regulating MUC5AC expression through neutrophil elastase.