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中华神经创伤外科电子杂志 ›› 2019, Vol. 05 ›› Issue (03) : 179 -181. doi: 10.3877/cma.j.issn.2095-9141.2019.03.012

所属专题: 文献

综述

CXCL12与创伤性颅脑损伤后神经细胞凋亡的相关性
张慧艳1, 冀兵2,()   
  1. 1. 030001 太原,山西医科大学第一临床医学院
    2. 030001 太原,山西医科大学第一医院急诊科
  • 收稿日期:2019-03-05 出版日期:2019-06-15
  • 通信作者: 冀兵
  • 基金资助:
    国家临床重点专科建设项目(2013-544)

Research progress on the relationship between CXCL12 and nerve cell apoptosis after traumatic brain injury

Huiyan Zhang1, Bing Ji2,()   

  1. 1. First School of Clinical Medicine, Shanxi Medical Univercity, Taiyuan 030001, China
    2. Department of Emergency, The First Hospital of Shanxi Medical Univercity, Taiyuan 030001, China
  • Received:2019-03-05 Published:2019-06-15
  • Corresponding author: Bing Ji
  • About author:
    Corresponding author: Ji Bing, Email:
引用本文:

张慧艳, 冀兵. CXCL12与创伤性颅脑损伤后神经细胞凋亡的相关性[J]. 中华神经创伤外科电子杂志, 2019, 05(03): 179-181.

Huiyan Zhang, Bing Ji. Research progress on the relationship between CXCL12 and nerve cell apoptosis after traumatic brain injury[J]. Chinese Journal of Neurotraumatic Surgery(Electronic Edition), 2019, 05(03): 179-181.

创伤性颅脑损伤(TBI)后的神经细胞凋亡是继发性TBI中最严重的病理生理变化,是临床上致残、致死率高的重要原因。有效控制神经细胞凋亡是治疗TBI的关键,直接关系到TBI患者的预后。CXCL12是一类具有趋化活性的细胞因子,在中枢神经系统有广泛的表达,在神经保护、神经功能调节、神经细胞发生和神经炎症反应中起着关键作用。随着研究的不断深入,发现CXCL12与TBI后神经细胞凋亡有着密切的联系。本文就CXCL12与TBI后神经细胞凋亡关系的研究进展展开综述。

Nerve cell apoptosis after traumatic brain injury (TBI) is the most serious pathophysiological change in secondary brain injury and an important cause of high clinical disability and mortality. Effective control of nerve cell apoptosis has become a key target for the treatment of TBI, which is directly related to the prognosis of patients with TBI. CXCL12 is a kind of chemoactive cytokine, which is widely expressed in the central nervous system and plays a key role in neurogenesis, neuroprotection, neuronal function regulation and neuroinflammatory response. With the development of research, CXCL12 was found to be closely related to nerve cell apoptosis after TBI. This paper reviews the research progress of CXCL12 and nerve cell apoptosis after TBI.

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