慢性阻塞性肺病患者支气管黏膜PPARγ、MMP9和iNOS的表达

目的研究慢性阻塞性肺疾病（COPD）患者支气管黏膜中过氧化物酶增殖物激活受体 γ(PPAR γ)、基质金属蛋白酶 9(MMP 9)和诱生型一氧化氮合酶(iNOS)的表达及与气流阻塞的关系。方法根据吸烟史及肺功能检查将其受试者分为3组：吸烟伴COPD患者18例；吸烟肺功能正常组15例；不吸烟肺功能正常组15例。全部受试者经电子支气管镜取支气管黏膜标本，采用免疫组织化学法检测支气管黏膜中核转录因子PPAR γ、MMP 9和iNOS的表达，并进行相关性分析。结果①免疫组织化学染色结果：核转录因子PPAR γ在吸烟伴COPD组和吸烟肺功能正常组表达明显减少，MMP 9和iNOS在两组表达明显增多，与不吸烟肺功能正常组比较差异均有统计学意义（P＜0.01）；②相关性分析：核转录因子PPAR γ的表达与FEV1%、FEV1/FVC%呈直线正相关（P＜0.01）；MMP 9和iNOS的表达与肺功能指标呈直线负相关（P＜0.01）。COPD患者支气管黏膜中核转录因子PPAR γ的表达与MMP 9和iNOS的表达均呈直线负相关（P＜0.05）。结论COPD患者支气管黏膜中核转录因子PPAR γ表达减少导致气道的抗炎能力下降，气道内炎症细胞及炎症介质增多，导致肺组织损伤及重构，引起和加重COPD患者的气流阻塞。

Expressions of PPAR γand cytokine in the bronchial mucosa of patients with chronic obstructive pulmonary disease

Objective To investigate expressions of PPAR-γ matrix metalloproteinase-9 (MMP-9) and induced nitric oxide syn-thase (iNOS) in the bronchial mucosa of patients with chronic obstructive pulmonary disease(COPD) and to explore their correlation with airflow obstruction. Methods: Based on their smoking history and lung function, they were divided into three groups: 18 smokers with COPD, 15 smokers and 15 non-smokers with normal lung function. Expressions of PPAR-γ, MMP-9 and iNOS in the bronchial mucosa were determined by immunohistochemistry. Results ① Immunohistochemical staining showed that PPAR-γ was decreased in smokers of the COPD group and smokers of the normal lung function group, while MMP-9 and iNOS were increased in both groups compared with nonsmokers with normal lung function ( P < 0.01).② The bronchial mucosa levels of PPAR-γ was positively correlated with FEV1 % and FEV1/FVC% ( P < 0.01) , however MMP-9 and iNOS was inversely correlated with FEV1% and FEV1/FVC% ( P < 0.01). Expression of PPAR-y was inversely correlated with MMP-9 and iNOS( P < 0.05). Conclusions The decrease of PPAR-y in bronchial mucosa of patients with COPD may lead to abnormal inflammation of the airway, and thus produces or aggravates airway obstruction in patients with COPD.