过氧化物酶体增殖体激活受体γ和Toll样受体-4在慢性阻塞性肺疾病患者肺血管重塑中的作用机制及相关性分析  

Mechanism and relationship of PPAR-γ and TLR4 to lung revascularization in patients with chronic obstructive pulmonary disease

作　　者：伏俊[1] 房三友[1] 闻寅[1] 王道峰[1] 朱晓兰[1] 戎霞君[2] 

机构地区：[1]泰兴市人民医院呼吸内科,江苏省225400 [2]上海瑞金医院呼吸内科

出　　处：《中华临床医师杂志（电子版）》2014年第14期32-35,共4页Chinese Journal of Clinicians(Electronic Edition)

摘　　要：目的探讨过氧化物酶体增殖体激活受体γ(PPAR-γ)和Toll样受体-4(TLR4)在慢性阻塞性肺疾病(COPD)患者肺血管重塑中的作用机制以及PPAR-γ和TLR4的表达与肺血管重塑的相关性。方法取86例因患有肺鳞癌进行肺叶切除的男性患者癌旁组织标本,其中COPD组40例,非COPD组(作为对照)46例。采用病理图像分析系统测算肺动脉管壁面积/管总面积(WA%)、管壁厚度/血管外径(WT%)。用免疫组织化学法检测PPAR-γ和TLR4在肺血管平滑肌细胞中的表达,并对其与血管重塑程度进行相关性分析。结果 COPD组肺血管炎症程度WA%、WT%显著高于非COPD组(P<0.01);肺血管平滑肌细胞TLR4的表达水平明显高于非COPD组(P<0.01),PPAR-γ的表达水平明显低于非COPD组(P<0.01);COPD组PPAR-γ和TLR4表达水平与血管WA%和WT%呈显著的相关关系(P<0.01)。结论 COPD患者存在肺血管重塑,COPD患者肺血管重塑可能是由于抑制炎症因子产生的PPAR-γ水平减少,TLR4水平增高,导致肺部抗炎能力降低,肺部炎症加重,释放的炎症因子导致血管内膜增生、肺部血管内径狭窄、血管平滑肌增生等,最终导致肺部血管重塑。Objective To explore the mechanism and relationship ofPPAR-γ and TLR4 to lung revascularization in patients with chronic obstructive pulmonary disease（COPD）. Methods Lung tissues from patients with COPD（COPD group, n=40）and those without COPD（non-COPD group, n=46） were obtained from surgically resected specimens. The ratio of the thickness of the wall to the external diameter of the pulmonary arterioles（WT%） and the ratio of the area of the wall to that of the pulmonary arterioles（WA%） were analyzed by computer-based image analysis system. Immunohistochemical technique was applied to investigate the expressions of PPAR-γ and TLR4 in vascular smooth muscle cells. Results The inflammatory infiltration degree, WA%, WT% were significantly higher than that of control group（P〈0.01）. Compared with controt group, the expressions of PPAR-γ in vascular smooth muscle cells were decreased significantly（P〈0.01）, and the expressions of TLR4 in vascular smooth muscle cells were increased significantly（P〈0.01）, the expressions of PPAR-γ and TLR4 had significant correlation with WA% and WT%. Multiple linear regression analysis showed that PPAR-γ and TLR4 were main influence factors of pulmonary vascular remodeling （WA%, WT%） （P〈0.01）. Conclusions COPD patients with pulmonary vascular remodeling, levels of TLR4 increase and levels of PPAR-）, reduce are the reason of pulmonary vascular remodeling. The ability of lung inflammation reduce, enhancing lung inflammation, and than the release of inflammatory cytokines cause intimal hyperplasia, pulmonary vessel diameter stenosis and vascular smooth muscle proliferation, eventually leading to pulmonary vascular remodeling.

关 键 词：肺疾病 慢性阻塞性 过氧化物酶体增殖物激活受体 TOLL样受体4 血管 重塑 

分 类 号：R563.9[医药卫生—呼吸系统]