多动症大鼠前额叶皮质中Nf1对BDNF的调节作用
投稿时间:2017-03-02  修订日期:2017-03-06  点此下载全文
引用本文:何保梅,吴丽慧.多动症大鼠前额叶皮质中Nf1对BDNF的调节作用[J].医学研究杂志,2017,46(11):54-57
DOI: 10.11969/j.issn.1673-548X.2017.11.014
摘要点击次数: 918
全文下载次数: 663
作者单位E-mail
何保梅 325000 杭州, 浙江省人民医院、杭州医学院附属人民医院  
吴丽慧 325000 杭州, 浙江省人民医院、杭州医学院附属人民医院 jaemny@163.com 
基金项目:国家自然科学基金资助项目(81271505,81571359);国家卫生部浙江省联合重点科研项目(WKJ2012-2-018)
中文摘要:目的 探讨神经纤维素(neurofibromin 1,Nf1)对脑源性神经营养因子(BDNF)表达的调节在多动症(ADHD)发病机制中的作用。方法 选用SHR大鼠作为多动症动物模型,WKY大鼠作为对照。应用RT-PCR、蛋白印记法检测Nf1和BDNF的mRNA、蛋白质水平;将Nf1过表达质粒共转染至PC12H及7919细胞,检测Nf1过表达后BDNF水平以探索Nf1与BDNF作用关系;用Image-pro Plus软件进行定量分析。结果 与WKY大鼠相较,SHR动物模型脑前额叶皮质中Nf1、BDNF水平均偏低(P=0.000);过表达Nf1可使BDNF水平上调(PC12H细胞P=0.000,7919细胞P<0.05)。结论 SHR前额叶皮质中Nf1、BDNF水平偏低,Nf1对BDNF有正性调控作用。前额叶皮质中Nf1对BDNF的调控作用可能参与多动症的发病机制。
中文关键词:多动症  Nf1  脑源性神经营养因子  SHR  WKY大鼠
 
Nf1 and BDNF Dysregulation in the Prefrontal Cortex Involved in the Pathogenesis of Attention Deficit Hyperactivity
Abstract:Objective To investigate the interaction between the Nf1 (Neurofibromin 1)and the BDNF (brain derived neurotrophic factor) in the mechanism of attention deficit hyperactivity disorder (ADHD).Methods Spontaneously hypertensive rats were chosen as the experimental group and WKY servesd as control. RT-PCR, Western-blot were used to detect the mRNA and protein expression levels of Nf1 and BDNF. To explore their relationship, BDNF expression levels were detected after Nf1 expression plasmid transferred and transfection in PC12H and CBRH-7919 cells.Results were quantified by Image-pro plus software.Results In the PFC of ADHD model rats SHR, Nf1 expression was abnormally degressive(P=0.000), in common with the expression of BDNF(P=0.000). Ectopic expression of Nf1 further encouraged the expression of BDNF (PC12H:P=0.000,7919:P<0.05).Conclusion Nf1 expression was significantly lower in PFC of SHR than control, and positively correlated with the levels of BDNF. These findings show that in the prefrontal cortex, Nf1-BDNF dysregulation may be involved in the pathomechanism of ADHD.
keywords:ADHD  Nf1  BDNF  SHR  WKY
查看全文  查看/发表评论  下载PDF阅读器

京公网安备 11010502037822号