基础医学与临床 ›› 2011, Vol. 31 ›› Issue (2): 222-224.

• 短篇综述 • 上一篇    

疼痛的分子生物学研究新进展

马璐璐1,刘薇1,黄宇光2   

  1. 1. 北京协和医院麻醉科
    2. 中国医学科学院 北京协和医学院 北京协和医院 麻醉科
  • 收稿日期:2010-01-18 修回日期:2010-05-26 出版日期:2011-02-05 发布日期:2011-03-14
  • 通讯作者: 黄宇光 E-mail:pumchhyg@yahoo.com.cn
  • 基金资助:
    院校级基金

Update in molecular mechanism of pain

MA Lu-lu 1,LIU Wei 2,HUANG Yu-guang 1   

  1. 1. PUMC Hospital, CAMS & PUMC
    2.
  • Received:2010-01-18 Revised:2010-05-26 Online:2011-02-05 Published:2011-03-14
  • Contact: HUANG Yu-guang E-mail:pumchhyg@yahoo.com.cn

摘要: 疼痛做为一种慢性疾病,威胁着全球数百万患者,而目前的治疗方法效果欠佳且副作用较多。目前已证实胶质细胞的激活,参与突触前/后神经元细胞间的信号传导, 并促进细胞因子、化学趋化因子、前炎性因子和肿瘤坏死因子的释放和激酶通路的信号传导,最终导致神经元超兴奋性,临床上则表现为痛觉过敏或痛觉异常。因此对疼痛发病机制,尤其是分子生物学机制的认识将为我们寻找新的疼痛靶向治疗方法提供希望。

Abstract: Neuropathic pain is a chronic condition affecting millions of people worldwide, and current treatments are often inadequate, ineffective or associated with potential severe side effects. A great deal of researches in the past decade have demonstrated the activation of glial constitutes a vital signaling network between pre-synaptic neurons and post-synaptic neurons, contributing to the release of cytokines、chemotaxin、proinflammatory factors and tumor necrosis factor, facilating the kinase pathways and finally leading to the activation of neurons. Clinical manifestations include hyperalgesia and allodynia. However further understanding of pain mechanism, especially molecular mechanism will help us find the new target therapy for pain.

Key words: pain,sodium channel,microglia,Extracellular signal-regulated MAP kinases

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