中国卒中杂志 ›› 2017, Vol. 12 ›› Issue (01): 89-93.DOI: 10.3969/j.issn.1673-5765.2017.01.018

• 综述 • 上一篇    下一篇

缺氧诱导因子-1α对脑梗死后内源性神经干细胞作用的研究进展

林亚航,陈明,段淑荣   

  1. 150001 哈尔滨哈尔滨医科大学附属第一医院神经内科
  • 收稿日期:2016-02-02 出版日期:2017-01-20 发布日期:2017-01-20
  • 通讯作者: 段淑荣duanshurongsj@163.com
  • 基金资助:

    黑龙江省自然科学基金重点项目(ZD201418)
    黑龙江省教育厅科学技术研究项目(12541337)

Research Progress of the Effects of Hypoxia Inducible Factor -1α on Endogenous Neural Stem Cells after Cerebral Infarction

  • Received:2016-02-02 Online:2017-01-20 Published:2017-01-20

摘要:

神经干细胞(neural stem cells,NSCs)治疗脑梗死无时间窗限制,无出血风险,且移植的 细胞可以分泌神经生长因子改善微环境,抑制炎症反应,减少细胞凋亡,促进神经再生,重建受损 的神经网络。缺氧诱导因子-1α(hypoxia-inducible factor-1α,HIF-1α)是脑缺血缺氧损伤中起神经 保护作用的关键因子,其在脑梗死后促进NSCs再生的作用广泛而复杂。本文将系统综述HIF-1α在脑 缺血缺氧损伤后对促进内源性NSCs增值、迁移、分化方面所起的作用,说明其可能成为临床治疗脑 梗死的有效作用靶点。

文章导读: 本文系统阐述了缺氧诱导因子-1α通过其下游信号通路促进神经干细胞的增殖和分化的机制。

关键词: 缺氧诱导因子-1α 内源性神经干细胞; 血管内皮生长因子; 细胞基质衍生因子-1α 促红细胞生成素; 脑梗死

Abstract:

Neural stem cell has been used in the treatment of cerebral infarction because of its unique functions and advantages.Treatment of cerebral infarction with neural stem cells (NSCs) has no time window limit, no bleeding risk, and the transplanted cells can secrete a large number of nerve growth factors to improve the microenvironment, inhibit inflammatory response, reduce apoptosis, promote nerve regeneration, and rebuild the damaged neural network. Hypoxia-inducible factor-1α (HIF-1α) is a key factor in the protective effects of cerebral ischemia and hypoxia, and its role in promoting the regeneration of NSCs after cerebral infarction is extensive and complex. In this paper, we will systematically review the important role of HIF-1α in promoting endogenous NSCs proliferation, migration and differentiation in the brain after cerebral ischemia and hypoxia injury, indicating that it may become the effective target of clinical treatment of cerebral infarction.

Key words: Hypoxia-inducible factor-1α; Neural stem cell; Vascular endothelial growth factor; Stromal cell-derived factor 1α; Erythropoietin; Cerebral infarction