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。
Tyrosine kinase A(TrkA) and tyrosine kinase B(TrkB) are high-affi nity receptors of neurotrophic factor, and they can protect the brain against hypoxic/ischemic injury via combining to their specif ic 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.
出处
《中国卒中杂志》
2008年第6期460-464,共5页
Chinese Journal of Stroke
关键词
缺血缺氧性
脑
受体
TrkA
受体
TrkB
Hypoxia-ischemia, brain
Receptor, tyrosine kinase A(TrkA)
Receptor, tyrosine kinase B(TrkB)