大鼠胸主动脉损伤后罗格列酮对血管再狭窄及基质金属蛋白酶-9表达的影响  

Effects of rosiglitazone on vascular restenosis and expression of matrix metalloproteinase-9 in aorta-injured rats

作　　者：贾国洪[1] 李绍冰[1] 王春梅[1] 姜玲玲[2] 

机构地区：[1]河北省人民医院老年心血管病区,石家庄050051 [2]河北医科大学生物化学教研室

出　　处：《临床心血管病杂志》2006年第4期231-233,共3页Journal of Clinical Cardiology

基　　金：河北省科技厅攻关项目(No:4276421)

摘　　要：目的:通过观察罗格列酮对大鼠胸主动脉损伤后管腔狭窄、基质金属蛋白酶9(MMP9)和磷酸化细胞外信号调节激酶(pERK)1、pERK2表达的影响,探讨罗格列酮减轻血管再狭窄的分子生物学机制。方法:90只SD大鼠随机均分为假手术组、损伤组和罗格列酮组。苏木精伊红染色观察血管管腔面积和内膜面积变化;原位杂交方法检测MMP9mRNA的表达;免疫组化方法检测MMP9及pERK1、pERK2蛋白表达;以放射免疫法测定血浆血栓素B2(TXB2)。结果:罗格列酮组管腔面积较损伤组增加、内膜面积较损伤组减少(均P<0.05)。罗格列酮组MMP9mRNA及蛋白和pERK1、pERK2蛋白表达较损伤组显著减少(P<0.05)。罗格列酮组TXB2的血浆浓度较损伤组显著减少(P<0.05)。结论:罗格列酮能减轻术后血管再狭窄的发生,其机制可能与通过影响信号转导通路pERK1、pERK2而抑制大鼠胸主动脉损伤后MMP9mRNA及蛋白表达,同时降低血浆中TXB2浓度有关。Objective：To investigate the effects of rosiglitazone on vascular restenosis and explore its cellular mechanism. Method：Ninety SD rats were divided into three groups randomly： sham group, angioplasty group and rosiglitazone group. Thoracic aortas were isolated for observation of morphological changes by macroscope and HE stanining method. The protein expressions of matrix metalloproteinase-9 （MMP-9） and phosphate extracellular signal-regulated kinase 1/2 （pERK1/2） were measured by immunohistochemical, and the mRNA expressionin of MMP9 were measured by situ hybridization technique. The level of plasma TXB2 was measured with radioimmunoassay. Result：Compared with the angioplasty group, the intima area was smaller in the rosiglitazone group（ P 〈0.05） ,and the lumen area was larger （ P 〈0.05）. The protein and mRNA expression of MMP-9 and pERK1/ 2 were remarkably lower in rosiglitazone group （ P 〈0.05）. Compared with angioplasty group, the concerntration of plasma TXB2 was remarkably lower in rosiglitazone group. Conclusion：Rosiglitazone may attenuate restenodsis by suppressing expression of MMP-9 through pERK1/2 signal transduction pathway, and decreasing the release of TXA2 in aorta injured rats.

关 键 词：罗格列酮 血管再狭窄 基质金属蛋白酶-9 血栓素A2 

分 类 号：R345[医药卫生—基础医学]