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慢性阻塞性肺病患者支气管黏膜PPAR-γ、MMP-9和iNOS的表达 被引量:1

Expressions of PPAR-γand cytokine in the bronchial mucosa of patients with chronic obstructive pulmonary disease
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摘要 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。 Objective To investigate expressions of PPAR-γ matrix metalloproteinase-9(MMP-9)and induced nitric oxide synthase(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-γ was inversely correlated with MMP-9 and iNOS(P〈0.05).Conclusions The decrease of PPAR-γ 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.
出处 《山东大学学报(医学版)》 CAS 北大核心 2009年第12期91-94,共4页 Journal of Shandong University:Health Sciences
基金 山东省自然科学基金资助项目(Y2001C01) 山东省医药卫生科技发展计划资助项目(HZ059)
关键词 肺疾病 慢性阻塞性 核转录因子PPAR-γ 基质金属蛋白酶-9 诱生型一氧化氮合酶 Chronic obstructive pulmonary disease Peroxisome proliferator-activited receptor Matrix metalloproteinase-9 Induced nitric oxide synthase
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共引文献5116

同被引文献20

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