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反义血管紧张素Ⅱ受体Ⅰ_B基因转移对大鼠颈动脉损伤后新生内膜的影响
引用本文:欧阳平!广州,许顶立!广州,黄洪莲,刘伊丽!广州,侯玉清!广州,宋后燕,戴云.反义血管紧张素Ⅱ受体Ⅰ_B基因转移对大鼠颈动脉损伤后新生内膜的影响[J].中华心血管病杂志,1999(5).
作者姓名:欧阳平!广州  许顶立!广州  黄洪莲  刘伊丽!广州  侯玉清!广州  宋后燕  戴云
作者单位:第一军医大学南方医院心内科(欧阳平!510515广州,许顶立!510515广州,刘伊丽!510515广州,侯玉清!510515广州),第一军医大学基础部(黄洪莲,戴云),上海医科大学分子遗传研究室(宋后燕)
摘    要:目的 探讨腺病毒载体介导的大鼠反义血管紧张素Ⅱ受体ⅠB(AT1B)RNA转移对大鼠颈动脉损伤后新生内膜的影响。方法 利用重组腺病毒载体将大鼠反义AT1B RNA转移至大鼠颈动脉球囊损伤模型中 ,2 1天后观察其对新生内膜形成的影响。结果 用腺病毒载体转导大鼠反义AT1BRNA至大鼠球囊损伤的颈动脉 ,与对照组相比 ,2 1天后损伤血管新生内膜 /中层面积比降低了 4 7%(P <0 0 0 1)。结论 反义AT1BRNA对血管成形术后再狭窄可能有一定的预防作用。

关 键 词:受体  血管紧张素  哺乳动物腺病毒属  血管内膜  基因疗法

Effects of adenoviral vector-mediated rat antisense AT_(1B) gene transfer on neointima proliferation after rat carotid artery injury
OUYANG Ping,XU Dingli,HUANG Honglian,et al..Effects of adenoviral vector-mediated rat antisense AT_(1B) gene transfer on neointima proliferation after rat carotid artery injury[J].Chinese Journal of Cardiology,1999(5).
Authors:OUYANG Ping  XU Dingli  HUANG Honglian  
Institution:OUYANG Ping,XU Dingli,HUANG Honglian,et al. Department of Cardiology,Nanfang Hospital,First Military Medical University,PLA,Guangzhou 510515
Abstract:Objective To study the effects of rat angiotensin II receptor I B (antisense AT 1B ) gene transfer mediated by adenoviral vector on neointimal proliferation after rat carotid injury.Methods Antisense (AT 1B ) gene was transducted into the carotid artery by adenoviral vector after carotid balloon injury and the restenosis model was established in SD rat. Neointima/media area ratio in local artery at day 21 after gene transfer was measured.Results Rat antisense AT 1B gene was succesfully transducted into the carotid artery after carotid balloon injury. Neointima/media area ratio was significantly reduced (47%, P <0.01) compared with the control group at day 21 after gene transfer.Conclusion The results suggest the possibility that antisense AT 1B gene transfer is a potential therapeutic approach to prevent neointimal hyperplasia.
Keywords:antisense AT    1B      adenovirus vector    restenosis neointima hyperplasia    gene therapy  
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