活化过氧化物酶体增殖激活物受体γ对烟熏肺气肿大鼠肺血管炎症的影响  

Effect of activated peroxisome proliferator-activated receptor gamma on pulmonary vascular inflammation in a rat model of emphysema

作　　者：薛茜[1] 尹燕[1] 韩丹[1] 侯刚[1] 王秋月[1] 康健[1] 

机构地区：[1]中国医科大学附属第一医院呼吸疾病研究所,辽宁沈阳110001

出　　处：《中国现代医学杂志》2014年第5期33-38,共6页China Journal of Modern Medicine

摘　　要：目的观察过氧化物酶体增殖激活物受体γ(PPARγ)活化后对烟熏肺气肿大鼠肺血管炎症的影响。方法将40只SPF级雄性大鼠按照随机数字表法分为空白组、模型组、罗格列酮组(R组)、罗格列酮+BADGE组(RB组),每组10只。采用烟熏12周的方法复制肺气肿大鼠模型。观察4组大鼠肺血管的变化,免疫组织化学检测PPARγ和金属基质蛋白酶9(MMP-9)在肺血管上的表达。多组间比较采用单因素方差分析,组间两两比较采用SNK-q检验,采用直线相关分析进行相关性检验。结果模型组和RB组大鼠肺血管中大量炎症细胞浸润,血管重塑明显,肺血管炎症细胞浸润程度模型组(212.35±21.24)/0.01 mm2和RB组(200.37±32.35)/0.01 mm2明显高于空白组(26.81±4.93)/0.01 mm2和R组(101.23±22.44)/0.01 mm2(均P<0.01),肺血管重塑程度模型组(1.65±0.53)和RB组(1.49±0.63)明显高于空白组(0.25±0.04)和R组(0.53±0.05)(均P<0.01),肺血管炎症细胞浸润和肺血管重塑呈正相关(r=0.903,P<0.01);肺血管上PPARγ蛋白(平均光密度值)表达R组(0.311±0.022)明显高于模型组(0.234±0.013)、RB组(0.237±0.012)和空白组(0.279±0.003)(均P<0.01),MMP-9表达模型组(0.418±0.014)和RB组(0.411±0.011)明显高于空白组(0.356±0.021)和R组(0.376±0.004)(均P<0.01),PPARγ与MMP-9表达呈负相关(r=-0.643,P<0.01)。结论烟熏肺气肿大鼠肺血管炎症和血管重塑明显,活化PPARγ有抑制MMP-9、减轻肺血管炎症和血管重塑作用。[Objective] To study the protective effect of activated peroxisome proliferator-activated receptor gamma on pulmonary vascular inflammation in a rat model of emphysema. [Methods] 40 male Wistar rats were randomly divided into 4 groups, 10 each, a control group, a pulmonary emphysema model group, a Rosiglitazone-treatment group （group R）, and a Rosiglitazone ± BADGE treatment group （group RB）. The rat model of emphysema was established by daily exposure cigarette smoke. After 12 weeks the pathological and morphometric changes in the pulmonary arterioles were analyzed. PPARy and MMP-9 protein were detected by immunohistochemical method. Analysis of variance, pair wise comparison between groups using SNK-q test, Pearson linear correlations were carried out statistical analysis. [Results] Plenty of inflammatory cells were infiltrated in the pulmonary vessels in model group and group RB, as the remodeling of arterioles did. The ratio of small vasculars inflammation （212.35 ± 21.24） / 0.01 mrn2 in model group （200.37± 32.35）/0.01 mm2 in group RB was obviously higher than the control （26.81 ± 4.93）/0.01 mm2 and R group （101.23 ± 22.44）/0.01 mm2 （all P〈O.O1）. The ratio of pulmonary vascular remodeling of model group （1.65 ± 0.53）, RB group （1.49 ± 0.63） was higher than of control （0.25 ±0.04） and group R （0.53± 0.05） （all P〈0.01）. The degree of vascular inflammation positively correlated the degree of vessel remodeling （r=0.903, P〈0.01）. The expression of PPAR gamma protein （the average optieal density） （0.234 ± 0.013） in model group and （0.237± 0.012） in group RB was lower compared with the control （0.279 ± 0.003） and R group （0.3tl ± 0.022） （all P〈0.01）, however, the expression of MMP-9 in model group （0.418 ± 0.014） and （0.411 ± 0.011） in RB group was significantly higher than that the R group （0.376 ±0.004） and eontrol （0.356 ±0.021） （all P〈0.01）. The PPAR gamma level negatively correlated the le

关 键 词：肺气肿 血管炎 炎症 过氧化物酶体增殖激活物受体y 金属基质蛋白酶9 

分 类 号：R563.3[医药卫生—呼吸系统] R364.5[医药卫生—内科学]