| ObjectiveTo investigate distribution,expression and interaction of peroxisome proliferators-activatedreceptor-γ(PPAR-γ),matrixmetalloproteinase-9(MMP-9)and induced nitric oxide synthase(iNOS) in the bronchial mucosa of patients with chronic obstructive pulmonary disease(COPD) and its correlation with airflow obstruction, further investigate pathogenesy of chronic obstructive pulmonary disease.Methods1.The bronchial mucosa were obtained from 48 patients with lung location disease at QiLuHospitalrepirationclinic service and sickroom,Shandong University.Bronchial mucosa were quickly put into paraform to fix,gradient alcoholic dehydration,paraffin imbedding,to make 2μm blade for immunohistochemistry.Inquest their habits of smoking history and history,undertake pulmonary function test.,to sign informed consent.According to their habits of smoking history,COPD history,and lung function,they were divided into three groups.18 smokers with COPD,15 smokers and 15 nonsmokers with normal lung function.2.The expression and distribute of PPAR-γ,MMP-9 and iNOS in the bronchial mucosa were detected by immunohistochemistry,and the correlative was conduced, under microscope to analysis positive staining result by automatic image analysis system.3.Data were analyzed by using a statistical software program(SPSS for Windows, version 11.5,SPSS Inc),using mean±standardized deviate to express all data. Student t was used for analyzing two sets difference.Pearson correlation analysis were used for analyzing linear correlation,P＜0.05 has statistics discrepancy.Results1.The change index of pulmonary functionDifference was significant of smokers with COPD in FEV1 percentage,FVC percentage and FEV1/FVC percentage compared with smokers and nonsmokers with normal lung function(P＜0.05)2.Immunohistochemistry staining resultPPAR-γwas diminished expressed in bronchial epithelial cells and alveolar macrophages in smokers with COPD group and smokers with normal lung function group(0.137±0.029,0.149±0.031),between the two groups has no statistics discrepancy;compared with nonsmokers with normal lung function(0.218±0.023),with the significant difference(P＜0.01).MMP-9 was higher expressed in bronchial epithelial cells and alveolar macrophages in smokers with COPD group and smokers with normal lung function group(0.194±0.059,0.189±0.038),iNOS also was higher expressed in bronchial epithelial cells and alveolar macrophages in smokers with COPD group and smokers with normal lung function group(0.188±0.030,0.186±0.035),between the two groups has no statistics discrepancy;MMP-9 and iNOS were diminished expressed in bronchial epithelial cells and alveolar macrophages in nonsmokers with normal lung function(0.108±0.022,0.128±0.034),compared with before two groups,with the significant difference(P＜0.01).3.The correlative analysisThe bronchial mucosa levels of PPAR-γwas positively correlated with FEV1 percentage and FEV1/FVC percentage respectively(r=0.592,r=0.425,P＜0.01).The bronchial mucosa levels of MMP-9 was inversely correlated with FEV1 percentageandFEV1/FVC percentage respectively(r=-0.458,r=-0.463,P＜0.01).The bronchial mucosa levels of iNOS was inversely correlated with FEV1 percentage and FEV1/FVC percentage respectively(r=-0.493,r=-0.477,P＜0.01).The expression of PPAR-γwas inversely correlated with MMP-9(r=-0.363,P＜0.05) and iNOS(r= -0.431,P＜0.05).Conclusions1.Decrease- expression of PPAR-γin bronchial mucosa patients with COPD may lead to the abnormal inflammation of airway.Inflammation cells was increased, released more inflammatory factors,which may causes and aggravates the airway obstruction in patients with COPD.2.Detect expression of PPAR-γ,MMP-9 and iNOS in bronchial mucosa patients with COPD may judgement pathogenetic condition of the patients.3.To induce expression of PPAR-γin self body with COPD,or using PPAR-γexcitomotor to enhance its activity,may able to anti-inflammatory and improve lung function with COPD.
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