中华临床医师杂志（电子版）
中華臨床醫師雜誌（電子版）
중화림상의사잡지（전자판）
CHINESE JOURNAL OF CLINICIANS(ELECTRONIC VERSION)
2013年
22期
10035-10040
,共6页
李海燕%成炜%丛金鹏%于文成
李海燕%成煒%叢金鵬%于文成
리해연%성위%총금붕%우문성
肺疾病,慢性阻塞性%过氧化物酶体增殖物激活受体%基质金属蛋白酶9%肺血管重塑
肺疾病,慢性阻塞性%過氧化物酶體增殖物激活受體%基質金屬蛋白酶9%肺血管重塑
폐질병,만성조새성%과양화물매체증식물격활수체%기질금속단백매9%폐혈관중소
Pulmonary disease,chronic obstructive%Peroxisome proliferator-activated receptors%Matrix metalloproteinase 9%Pulmonary vascular remodeling
目的：探讨PPARγ、MMP-9在慢性阻塞性肺疾病（COPD）患者肺血管炎症和肺血管重塑中的作用。方法收集手术切除有吸烟史的男性鳞癌患者的肺组织。按其肺功能将30例患者分成对照组和COPD 组，每组15例。术前行肺功能检查和心脏超声检查估测肺动脉收缩压（PASP），取无癌细胞浸润的外周肺组织应用HE染色和多利亚蓝-立春红S染色及图像分析，检测肺小动脉管壁面积/血管总面积、管腔面积/血管总面积、内膜面积/血管总面积及血管旁胶原纤维面积。应用免疫组织化学方法检测肺血管内皮细胞PPARγ、MMP-9表达，并进行相关分析。结果（1）与对照组比较，COPD组肺小动脉管壁充血水肿，炎性细胞浸润明显增多，管腔面积减小，内膜面积、管壁面积与血管总面积之比值增大，血管旁胶原纤维面积增加。（2）COPD组肺血管内皮细胞PPARγ表达水平显著低于对照组（P＜0.01），MMP-9的表达水平显著高于对照组（P＜0.01）。（3）相关分析显示肺血管内皮细胞 PPARγ表达与 MMP-9表达呈负相关（r＝-0.85，P＜0.01）； PPARγ表达与炎性细胞及肺小动脉肌化动脉比例、血管旁胶原纤维面积成负相关（r 分别＝-0.604、-0.759、-0.862，P＜0.01）；MMP-9表达与炎性细胞及肺小动脉肌化动脉比例、血管旁胶原纤维面积成正相关（r分别＝0.524、0.961、0.954，P＜0.01）；吸烟指数与肺小动脉肌化动脉比例成正相关（r＝0.889，P＜0.01）。结论吸烟者和 COPD 患者均存在不同程度的肺血管炎症反应和肺血管重塑，在此过程中，MMP-9可能通过加剧肺血管炎症反应，促使血管壁细胞外基质的代谢紊乱，参与肺血管重塑过程，PPARγ可能通过抵抗炎症反应，减轻血管损伤，从而发挥抗重塑的作用。
目的：探討PPARγ、MMP-9在慢性阻塞性肺疾病（COPD）患者肺血管炎癥和肺血管重塑中的作用。方法收集手術切除有吸煙史的男性鱗癌患者的肺組織。按其肺功能將30例患者分成對照組和COPD 組，每組15例。術前行肺功能檢查和心髒超聲檢查估測肺動脈收縮壓（PASP），取無癌細胞浸潤的外週肺組織應用HE染色和多利亞藍-立春紅S染色及圖像分析，檢測肺小動脈管壁麵積/血管總麵積、管腔麵積/血管總麵積、內膜麵積/血管總麵積及血管徬膠原纖維麵積。應用免疫組織化學方法檢測肺血管內皮細胞PPARγ、MMP-9錶達，併進行相關分析。結果（1）與對照組比較，COPD組肺小動脈管壁充血水腫，炎性細胞浸潤明顯增多，管腔麵積減小，內膜麵積、管壁麵積與血管總麵積之比值增大，血管徬膠原纖維麵積增加。（2）COPD組肺血管內皮細胞PPARγ錶達水平顯著低于對照組（P＜0.01），MMP-9的錶達水平顯著高于對照組（P＜0.01）。（3）相關分析顯示肺血管內皮細胞 PPARγ錶達與 MMP-9錶達呈負相關（r＝-0.85，P＜0.01）； PPARγ錶達與炎性細胞及肺小動脈肌化動脈比例、血管徬膠原纖維麵積成負相關（r 分彆＝-0.604、-0.759、-0.862，P＜0.01）；MMP-9錶達與炎性細胞及肺小動脈肌化動脈比例、血管徬膠原纖維麵積成正相關（r分彆＝0.524、0.961、0.954，P＜0.01）；吸煙指數與肺小動脈肌化動脈比例成正相關（r＝0.889，P＜0.01）。結論吸煙者和 COPD 患者均存在不同程度的肺血管炎癥反應和肺血管重塑，在此過程中，MMP-9可能通過加劇肺血管炎癥反應，促使血管壁細胞外基質的代謝紊亂，參與肺血管重塑過程，PPARγ可能通過牴抗炎癥反應，減輕血管損傷，從而髮揮抗重塑的作用。
목적：탐토PPARγ、MMP-9재만성조새성폐질병（COPD）환자폐혈관염증화폐혈관중소중적작용。방법수집수술절제유흡연사적남성린암환자적폐조직。안기폐공능장30례환자분성대조조화COPD 조，매조15례。술전행폐공능검사화심장초성검사고측폐동맥수축압（PASP），취무암세포침윤적외주폐조직응용HE염색화다리아람-립춘홍S염색급도상분석，검측폐소동맥관벽면적/혈관총면적、관강면적/혈관총면적、내막면적/혈관총면적급혈관방효원섬유면적。응용면역조직화학방법검측폐혈관내피세포PPARγ、MMP-9표체，병진행상관분석。결과（1）여대조조비교，COPD조폐소동맥관벽충혈수종，염성세포침윤명현증다，관강면적감소，내막면적、관벽면적여혈관총면적지비치증대，혈관방효원섬유면적증가。（2）COPD조폐혈관내피세포PPARγ표체수평현저저우대조조（P＜0.01），MMP-9적표체수평현저고우대조조（P＜0.01）。（3）상관분석현시폐혈관내피세포 PPARγ표체여 MMP-9표체정부상관（r＝-0.85，P＜0.01）； PPARγ표체여염성세포급폐소동맥기화동맥비례、혈관방효원섬유면적성부상관（r 분별＝-0.604、-0.759、-0.862，P＜0.01）；MMP-9표체여염성세포급폐소동맥기화동맥비례、혈관방효원섬유면적성정상관（r분별＝0.524、0.961、0.954，P＜0.01）；흡연지수여폐소동맥기화동맥비례성정상관（r＝0.889，P＜0.01）。결론흡연자화 COPD 환자균존재불동정도적폐혈관염증반응화폐혈관중소，재차과정중，MMP-9가능통과가극폐혈관염증반응，촉사혈관벽세포외기질적대사문란，삼여폐혈관중소과정，PPARγ가능통과저항염증반응，감경혈관손상，종이발휘항중소적작용。
Objective In order to investigate the effect of peroxisome proliferators activated receptor gamma and matrix metalloproteinase-9 in pulmonary vascular inflammation and remodeling in patients with chronic obstructive pulmonary disease(COPD) by detecting the expression of PPARγand MMP-9 of pulmonary vascular endothelial cells. Methods Lung specimens were collected from the male patients who with lung carcinoma and smoking history and need to be operated in thoracic surgery, 30 patients were divided into 2 groups, control group:patients with normal pulmonary function (non-COPD group) and patients with COPD(COPD group), each of 15 cases, matched with age. Air flow obstruction was determined by pulmonary function test and pulmonary artery pressure were examined by continuous wave Doppler echocardiographic measurement of the tricuspid regurgitant jet, and the smoking index were recorded in all patients before the operations. The remodeling of pulmonary artery remodeling was observed with HE staining under microscope and triple strains, lumen area, arteries walls, intimal area, muscular arteries, partial muscular arteries, non partial muscular arteries were measured, the expression of PPARγ and MMP-9 of pulmonary vascular endothelial cells were measured by means of immunohisto-chemistry, analysis were made. Results (1)Compared with control group, arteries walls of COPD group congested and swelled, inflammation cells increased, the thickness of intimal layer, walls of intra-acinar pulmonary muscular arteries was significantly higher, the area of its lumen was narrow and the proportion of their muscular arteries was higher, the area of collagen fibrils was increased. (2)The expression of PPARγin control group was higher than that in COPD group (P<0.01), and the expression of MMP-9 in COPD group was higher than that in control group. (3)Correlation analysis:An negative correlations were showed with the expression of PPARγand MMP-9(r=-0.85, P<0.01). The expression of PPARγ and inflammation cells, the pulmonary artery of the artery muscle ratio, the area of collagen fibrils, negative correlation was showed negative correlations (r=-0.604, -0.759, -0.862, P<0.01); An positive correlations were showed in the expression of MMP-9 and inflammation cells, pulmonary artery of the artery muscle ratio, the area of collagen fibrils (r=0.524, 0.961, 0.954, P<0.01 ); the artery wall area and the area of collagen fibrils showed positive correlations (r=0.878, P<0.01). An positive correlation was showed with the smoking index and the ratio of muscular arteries (r=0.889, P<0.01). Conclusion Patients with smoking and COPD have pulmonary vascular inflammation and remodeling, MMP-9 of pulmonary vascular endothelial cells may be involved in the inflammation and remodeling process, but PPARγmay be involved in the anti-inflammation and anti-remodeling process.
