Increased Expression of Rac1 in Epilepsy Patients and Animal Models
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  • 作者:Jie Li ; Hongxia Xing ; Guohui Jiang ; Zhou Su ; Yuqing Wu ; Yi Zhang…
  • 关键词:Epilepsy ; Rac1 ; Temporal lobe epilepsy
  • 刊名:Neurochemical Research
  • 出版年:2016
  • 出版时间:April 2016
  • 年:2016
  • 卷:41
  • 期:4
  • 页码:836-843
  • 全文大小:1,333 KB
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  • 作者单位:Jie Li (1)
    Hongxia Xing (1)
    Guohui Jiang (2)
    Zhou Su (1)
    Yuqing Wu (1)
    Yi Zhang (1)
    Shuangxi Guo (1)

    1. Department of Neurology, The First Affiliated Hospital of Xinxiang Medical University, Weihui, 453100, Henan Province, China
    2. Department of Neurology, Affiliated Hospital of North Sichuan Medical University, Nanchong, 637000, Sichuan Province, China
  • 刊物类别:Biomedical and Life Sciences
  • 刊物主题:Biomedicine
    Neurosciences
    Biochemistry
    Neurology
  • 出版者:Springer Netherlands
  • ISSN:1573-6903
文摘
The mechanisms of epilepsy remain incompletely understood. Rac1 (ras-related C3 botulinum toxin substrate 1) belongs to the Rho family of small GTPases. Rac1 play important roles in cytoskeleton rearrangement and neuronal synaptic plasticity, which had also been implicated in epilepsy. However, little is known regarding the expression of Rac1 in the epileptic brain or whether Rac1-targeted interventions affect the progression of epilepsy. The aim of this study was to investigate the expression profile of Rac1 in brain tissues from patients suffering from temporal lobe epilepsy (TLE) and experimental epileptic rats and determine the possible role of Rac1 in epilepsy. We demonstrated that the expression of Rac1 is significantly increased in TLE patients and in lithium-pilocarpine epilepsy model animals compared to the corresponding controls. Rac1 inhibitor NSC23766 reduced the severity of status epilepticus during the acute stage in a lithium-pilocarpine animal model. Consistent with these results, the latent period of a PTZ kindling animal model also increased. Our results demonstrated that the increased expression of Rac1 may contribute to pathophysiology of epilepsy.

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