过氧化物酶体增殖物γ在COPD肺高压大鼠血管重塑中作用.docVIP

过氧化物酶体增殖物γ在COPD肺高压大鼠血管重塑中作用 　　【摘要】目的：探讨罗格列酮对COPD肺高压大鼠气道炎症及血管重塑中的作用及其机制。方法：36只wistar大鼠随机分为肺高压组（A组）、治疗组(B组)和空白对照组（C组），前两组以烟熏、低氧和脂多糖（LPS）建立慢性支气管炎肺动脉高压病的大鼠模型，B组第3周起，同时给以盐酸罗格列酮治疗，C组给予生理盐水模拟造模和治疗。比较各组大鼠肺动脉压力和结构变化，并分析PPARγ与血管重建的相关性。结果 ：A组肺血管压力（mPAP和RVSP）和重塑程度(MA%和MT%)均高于D组显著增高(P均＜0.05)。经罗格列酮治疗后，B组上述指标均较A组明显下降(P均＜0.05)。A、B、C组肺组织的PPARγ mRNA水平依次升高（P 　　【关键词】肺高压；慢性支气管炎；重塑；血管；过氧化物酶增殖物激活受体γ 　　The effects of peroxisome proliferators-activated receptor γ (PPARγ) agonist on vascular remodeling in pulmonary hypertension with COPD 　　Wang ChenWang XinTang HuapingHan WeiCao Jilan 　　【Abstract】Objective To explore the effects of peroxisome proliferators-activated receptor γ (PPARγ) agonist on vascular remodeling in pulmonary hypertension with COPD. Methods36 wistarrats were divided into 3 groups：pulmonary hypertension group（Group A）,Rosiglitazone group(Group B) and controlled group(Group C). The mPAP and RVSP were detected after pulmonary artery catheterization, while MA% and MT% of the pulmonary vascular wall were measured in histological sections. PPARγ mRNA in lung tissue was assessed by RT-PCR. ResultsThe pressure (mPAP and RVSP）and remodeling (MA%和MT%) of pulmonary vessels in group A were aggravated than in group C (P＜0.05) and were extenuated with rosiglitazone (P＜0.05). PPARγ mRNA were increased in turn of group A, group B and group C. ConclusionRosiglitazone alleviates the pulmonary artery remodeling and pulmonary hypertension by up-regulating transcription of PPARγ. 　　【keyword】pulmonary hypertension； chronic bronchitis；remodeling； vascular; peroxisome proliferator- activated receptor γ 　　【中图分类号】R85【文献标识码】A【文章编号】1005-0515(2011)04-0036-02 　　肺血管重塑和血管收缩是COPD肺动脉高压形成和维持的关键环节[1]。过氧化物酶增殖物激活受体γ（peroxisome proliferator-activted receptor γ, PPARγ）参与了COPD的气道炎症和重塑过程，但其在COPD肺高压中的作用研究尚少。本研究在COPD肺高压大鼠的动物模型上，观察 PPARγ在肺组织的表达及对血管重塑的作用。 　　1 材料和方法 　　1.1 材料: 　　1.1. 1 动物：雄性wistar大鼠36只，购自青岛市药检所，6-8周龄，体重220±20g，SPF级饲养。 　　1.1. 2 试剂：香烟(哈德门,青岛卷烟厂)；盐酸罗格列酮（文迪雅，4mg/片）；LPS（美国Sigma公司）；IL-8 ELISA测定试剂盒