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人参皂苷Rg1对SHR大鼠纹状体GDNFmRNA基因表达和多巴胺含量的影响(1)
http://www.100md.com 2012年4月1日 胡颖,林忠东,郑飞霞,施旭来
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     摘 要:目的:探讨人参皂苷Rg1对SHR大鼠纹状体GDNFmRNA基因表达和多巴胺含量的影响。方法:将SHR大鼠随机分为模型对照组(MC组)、盐酸哌甲酯控释片组(MPH组)和人参皂苷Rg1组(Rg1组)。各组按设计剂量给药14天后,取纹状体组织,采用高效液相法检测多巴胺(DA)的含量、原位杂交法检测GDNFmRNA的基因表达。结果:盐酸哌甲酯控释片组和人参皂苷Rg1组的纹状体神经元的细胞膜及细胞浆GDNFmRNA基因表达明显增强,模型对照组未见明显表达;盐酸哌甲酯控释片组和人参皂苷Rg1组与模型对照组比较,纹状体多巴胺的含量显著升高。结论:人参皂苷Rg1可能通过促进纹状体GDNFmRNA的基因表达和增加多巴胺的含量而起到治疗ADHD的作用。

    关键词:人参皂苷Rg1;注意缺陷多动障碍;胶质细胞源性神经营养因子;多巴胺;大鼠

    中图分类号:R285.5

    文献标识码:A

    文章编号:1673-7717(2012)04-0862-03

    Effect of Ginsenosides Rg1 on GDNFmRNA Expression and DA Content in Striate Body of SHR Rats

    HU Ying,LIN Zhong-dong,ZHENG Fei-xia,SHI Xu-lai

    (Department of Neurology,Yueying Children's Hospital Affiliated to Wenzhou Medical College,Wenzhou 325000,Zhejiang,China)

    Abstract:Objective:To investigate effects of ginsenosides Rg1 on the GDNFmRNA expression and the DA content in striate body of the SHR rats.Methods:SHR rats were randomized into model group(MC group),methylphenidate hydrochloride controlled-release tablets group(MPH group) and ginsenosides Rg1 group(Rg1 group).The rats received gastric gavage of corresponding drugs according to the experimental design for 14 days.HPLC was used to detected the contents of DA and GDNFmRNA,which were observed by the technique of in situ hybridization in striate body after treatment.Results:The gene of GDNFmRNA was higher expressed in striate body neuronal cell membrane of rats in MPH group and ginsenosides Rg1 group,but it did not significantly expressed in model group.The contents of DA in striate body in rats of MPH group and ginsenosides Rg1 group were significantly higher than that of model group.Conclusions:Ginsenosides Rg1 can increase the expression of GDNFmRNA and the content of DA in striate body,which may be one of the mechanisms of ADHD treatment.

    Key words:Ginsenosides Rg1;attention deficit disorder with hyperactivity;GDNF;dopamine;rats

    注意缺陷多动障碍(attention deficit hyperactivity disorder,ADHD)是指以儿童活动过度、明显的注意力不集中、冲动控制力差而影响其社会功能为临床表现的一种行为障碍。ADHD发病机制非常复杂,在神经生化方面,脑内多巴胺(DA)功能缺陷学说最受支持,研究发现胶质细胞源性神经营养因子(glial cell-line derived neurotrophic factor, GDNF)对多巴胺能神经元有特异性营养作用,是一种有效的多巴胺能神经营养因子[1] ......

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