文章摘要
李东野,刘 闯,刘伊娜,闫 艳,夏 勇,朱 红,潘德峰,尹 丽.腺病毒介导的HIF-1α基因对缺血心肌作用机制的初步探讨[J].南京医科大学学报,2007,(8):793~796
腺病毒介导的HIF-1α基因对缺血心肌作用机制的初步探讨
The initial study of mechanism about adenovirus mediated HIF-1α gene on ischemic myocardium
投稿时间:2007-01-13  
DOI:10.7655
中文关键词: 腺病毒  低氧诱导因子-1α  细胞外信号调节激酶  磷酸化细胞外信号调节激酶  核酶
英文关键词: adenovirus  hypoxia inducible factor-1α  extracellular signatregulated kinase  phosphoryl-extracellular signal-regulated kinase  ribozyme
基金项目:
作者单位
李东野 徐州医学院心血管病研究所,江苏 徐州 221002 
刘 闯  
刘伊娜  
闫 艳  
夏 勇  
朱 红  
潘德峰  
尹 丽  
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中文摘要:
      目的:研究腺病毒介导的低氧诱导因子-1α(HIF-1α) 基因转染入兔急性心肌梗死(AMI)边缘区缺血心肌后,HIF-1α?细胞外信号调节激酶(ERK)?磷酸化细胞外信号调节激酶(p-ERK)的蛋白表达情况,初步探讨HIF-1α的作用机制?方法:建立兔AMI模型,随机分为4组,分别于心肌内注入腺病毒介导的HIF-1α基因(Ad-HIF-1α)?不含HIF-1α基因腺病毒颗粒(Ad-Blank)?HIF-1α核酶基因(Rz-HIF-1α),假手术组为对照,免疫组化和免疫印迹(Western blot)方法检测HIF-1α?ERK及p-ERK的蛋白表达? 结果:AMI后1天外源性HIF-1α蛋白及p-ERK蛋白表达开始升高,7天达高峰,14?28天逐渐下降,56天时外源性HIF-1α蛋白及p-ERK蛋白均无表达,ERK在各时间点均有表达?在各组中,ERK含量基本无差异,p-ERK的蛋白含量在Ad-Blank组较Sham组升高,较Ad-HIF-1α组降低,Rz-HIF-1α组最低?结论:腺病毒介导的HIF-1α基因在缺血心肌能够有效表达,并能促进ERK的磷酸化,HIF-1α核酶基因能有效阻断缺血心肌HIF-1α的保护作用?
英文摘要:
      Objective:To study the protein expression about the HIF-1α,ERK and p-ERK on ischemic myocardium after acute myocardiac infarction(AMI) and to explore initially the mechanism about HIF-1α. Methods:Rabbits AMI model were establised, and divided into 4 groups at random, and infected with Ad-HIF-1α,Ad-Blank,Rz-HIF-1α respectively. Sham group was regarded as control. The protein expression of HIF-1α,ERK and p-ERK was detected by immunohistochemistry and Western-blot. Results:The protein expression of exogenous HIF-1α and p-ERK increased at 1d after AMI, reached the peak at 7d and decreased gradually at 14d and 28d. At 56d,the protein of HIF-1α and p-ERK was not expressed. Among four groups, there was no difference in the protein level of ERK,while p-ERK protein expression was higher in group Ad-Blank than that in group Sham, lower than that in group Ad-HIF-1α,and the protein level of p-ERK was the lowest in group Rz-HIF-1α. Conclusion:Ad-HIF-1α was transducted effectively and promote ERK phosphorylated. HIF-1α ribozyme gene can block the protective effect of HIF-1α on the ischemic myocardium.
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