›› 2008, Vol. 3 ›› Issue (06): 460-464.

• 综述 • 上一篇    

酪氨酸激酶A和酪氨酸激酶B与 脑缺血缺氧性损伤

肖力,何俐   

  1. 610041 四川省成都市 四川大学华西医院神 经内科
  • 收稿日期:2008-05-20 修回日期:1900-01-01 出版日期:2008-06-20 发布日期:2008-06-20
  • 通讯作者: 何俐

  • Received:2008-05-20 Revised:1900-01-01 Online:2008-06-20 Published:2008-06-20

摘要: 酪氨酸激酶A(TrkA)和酪氨酸激酶B(TrkB)是神经营养因子的高亲和力受体,通过与其 特异性配体(神经生长因子和脑源性神经营养因子)结合,发挥对脑缺血缺氧性损伤的保护作用。 它们与脑缺血缺氧的关系已成为近年来一个研究热点。本文从TrkA和TrkB在脑缺血缺氧性损伤后的 表达、作用及其保护机制方面进行综述。

关键词: 缺血缺氧性; 脑; 受体; TrkA; 受体; TrkB

Abstract: Tyrosine kinase A(TrkA) and tyrosine kinase B(TrkB) are high-affinity receptors of neurotrophic factor, and they can protect the brain against hypoxic/ischemic injury via combining to their specific ligand (nerve growth factor, NGF and brain –derived neurotrophic factor, BDNF). In recent years, the relationship between TrkA and TrkB with cerebral hypoxic/ischemic injury has become a hot spot for many researchers. In this paper, we review the expression, function and mechanism of protection of TrkA and TrkB in cerebral hypoxic/ischemic injury.

Key words: Hypoxia-ischemia; brain; Receptor; tyrosine kinase A(TrkA); Receptor; tyrosine kinase B(TrkB)