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CD151对大鼠心肌梗死后血管新生及心功能的影响 被引量:14

Gene transfer of CD151 enhanced myocardial angiogenesis and improved cardiac function in rats with experimental myocardial infarction
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摘要 目的观察CD151基因对心肌梗死后大鼠梗死心肌微血管密度和心功能的影响,以明确CD151体内促血管新生作用。方法结扎大鼠冠状动脉左前降支建立心肌梗死模型。构建PAAVCD151重组质粒,分点注射至梗死心肌及周围进行基因转染。另外设置心肌内不转染及转染PAAVGFP心肌梗死对照组。4周后测定心肌微血管密度及心功能。结果心肌注射PAAVCD151转染后心肌中CD151蛋白表达明显高于对照组(P<0.01)。转染CD151组心肌微血管密度[(385.4±79.9)N/MM2]明显高于对照组[(240.8±40.3)N/MM2](P<0.01)。心脏收缩功能指标射血分数、短轴缩短率、左室内压最大上升和下降速率等参数亦明显高于对照组(P<0.01)。结论CD151在体内具有明确的促血管生成作用,通过促进缺血心肌的血运重建起到保护心脏功能的作用。 Objective To investigate the effects of in vivo CD151 gene transfer on angiogenesis and heart function in rats with myocardial infarction. Methods Acute myocardial infarction (AMI) was induced in male Spague-Dawley (SD) rats by left anterior descending coronary artery ligation. The surviving rats randomly received myocardial injection of saline (MI control ), pAAV-CD151 and pAAV-GFP (n = 12/group). Sham-operated rats without myocardial injection ( n = 12) were taken as normal control. Four weeks later, heart function and the expression of CD151 were measured. Micro vessels density (MVD) in infarct myocardium was observed by factor Ⅷ related antigen immunochemical staining. Results The expression of CD151 ( 1.98 ± 0. 23 vs. 0. 91 ± 0. 09, P 〈 0. 01 ) and MVD counting [ ( 385.4 ± 79.9 ) vs. (252.5 ±43.0 )n/mm^2 ,P 〈 0. 01 ] in pAAV-CD151 treated MI rats were significantly higher than that in MI control group, similarly, EF (64. 0 ± 8.7 ) % vs. (41.5 ± 5.0) %, P 〈 0. 01 ] and dp/dtmax ( 6620. 2 ± 884. 6 vs. 5545.5 ±693.0, P 〈0. 01 ) were also significantly increased post pAAV-CD151 treatment. These parameters were not affected by pAAV-GFP treatment. Conclusion CD151 in vivo gene transfer for rats with acute myocardial infarction enhanced myocardial angiogenesis and improved left ventricular function.
出处 《中华心血管病杂志》 CAS CSCD 北大核心 2006年第2期159-163,共5页 Chinese Journal of Cardiology
基金 国家自然科学基金资助项目(30270563)
关键词 心肌梗塞 新生血管化 生理性 CD151 Myocardial infarction Neovascularization,physiologic CD151
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参考文献8

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二级参考文献9

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