天津医药

天津医药 ›› 2020, Vol. 48 ›› Issue (5): 449-454.doi: 10.11958/20193631

• 综述 • 上一篇    下一篇

创伤性脑损伤相关神经炎症的研究进展 #br#

宋鸽 1，刘晓银 2，史新宇 2，叶益超 2，张赛 2△
  

  1. 1 天津中医药大学（邮编 301617）；2 中国人民武装警察部队特色医学中心

  • 收稿日期:2019-12-05 修回日期:2020-02-06 出版日期:2020-05-15 发布日期:2020-06-24
  • 通讯作者: 张赛 E-mail:zhangsai718@vip.126.com
  • 基金资助:
    国家自然科学基金资助项目（81671222）

Research progress on neuroinflammation related to traumatic brain injury #br#

SONG Ge1, LIU Xiao-yin2, SHI Xin-yu2, YE Yi-chao2, ZHANG Sai 2△ #br#   

  1. 1 Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China;
    2 Tianjin People's Armed Police Forces Medical Center
  • Received:2019-12-05 Revised:2020-02-06 Published:2020-05-15 Online:2020-06-24

PDF (PC)

4216

摘要： 创伤性脑损伤（TBI）发生时，外力立即造成神经系统损害。这种原发性损伤触发了体内生化级联以及新
陈代谢和细胞变化在内的继发性神经损害，称为继发性脑损伤。TBI后的神经炎症是持续的神经元损伤的关键因
素。神经炎症涉及损伤后细胞和分子调控机制，包括神经胶质（小胶质细胞和星形胶质细胞）的激活，引起脑内的炎
症介质的释放，导致周围免疫细胞的募集。了解 TBI炎症病理生理学的最新进展对于制定更有效的治疗策略至关
重要。

关键词: 脑损伤, 创伤性；神经炎症；继发性脑损伤；细胞调控机制；分子调控机制

Abstract: After the trauma brain injury occurs, the immediate neurologic damage is produced by the traumatic forces.
This primary injury triggers a secondary wave of biochemical cascades together with metabolic and cellular changes, called
secondary neural injury. The neuroinflammatory response following traumatic brain injury is known to be a key injury factor
that can drive ongoing neuronal injury.Neuroinflammation involves cellular and molecular regulatory mechanisms including
the activation of glia (microglia and astrocytes), the releasing of inflammatory mediators within the brain, and the subsequent
recruitment of peripheral immune cells. Understanding the recent progress of inflammatory pathophysiology in TBI is crucial
for the development of more effective therapeutic strategies.

中图分类号: