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星形胶质细胞和小胶质细胞在创伤性脑损伤中的作用。

The contribution of astrocytes and microglia to traumatic brain injury.

作者信息

Karve Ila P, Taylor Juliet M, Crack Peter J

机构信息

Neuropharmacology Laboratory, Department of Pharmacology, University of Melbourne, Melbourne, Vic., Australia.

出版信息

Br J Pharmacol. 2016 Feb;173(4):692-702. doi: 10.1111/bph.13125. Epub 2015 Apr 24.

DOI:10.1111/bph.13125
PMID:25752446
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4742296/
Abstract

Traumatic brain injury (TBI) represents a major cause of death and disability in developed countries. Brain injuries are highly heterogeneous and can also trigger other neurological complications, including epilepsy, depression and dementia. The initial injury often leads to the development of secondary sequelae; cellular hyperexcitability, vasogenic and cytotoxic oedema, hypoxia-ischaemia, oxidative stress and inflammation, all of which influence expansion of the primary lesion. It is widely known that inflammatory events in the brain following TBI contribute to the widespread cell death and chronic tissue degeneration. Neuroinflammation is a multifaceted response involving a number of cell types, both within the CNS and in the peripheral circulation. Astrocytes and microglia, cells of the CNS, are considered key players in initiating an inflammatory response after injury. These cells are capable of secreting various cytokines, chemokines and growth factors, and following injury to the CNS, undergo changes in morphology. Ultimately, these changes can influence the local microenvironment and thus determine the extent of damage and subsequent repair. This review will focus on the roles of microglia and astrocytes following TBI, highlighting some of the key processes, pathways and mediators involved in this response. Additionally, both the beneficial and the detrimental aspects of these cellular responses will be examined using evidence from animal models and human post-mortem TBI studies.

摘要

创伤性脑损伤(TBI)是发达国家死亡和残疾的主要原因之一。脑损伤具有高度异质性,还会引发其他神经并发症,包括癫痫、抑郁和痴呆。初始损伤往往会导致继发性后遗症的发展,如细胞过度兴奋、血管源性和细胞毒性水肿、缺氧缺血、氧化应激和炎症,所有这些都会影响原发性损伤的扩展。众所周知,TBI后脑内的炎症事件会导致广泛的细胞死亡和慢性组织退化。神经炎症是一种多方面的反应,涉及中枢神经系统(CNS)内和外周循环中的多种细胞类型。星形胶质细胞和小胶质细胞作为CNS的细胞,被认为是损伤后引发炎症反应的关键因素。这些细胞能够分泌各种细胞因子、趋化因子和生长因子,并且在CNS受到损伤后,其形态会发生变化。最终,这些变化会影响局部微环境,从而决定损伤程度和后续修复情况。本综述将聚焦于TBI后小胶质细胞和星形胶质细胞的作用,突出该反应中涉及的一些关键过程、途径和介质。此外,将利用动物模型和人类TBI尸检研究的证据,探讨这些细胞反应的有益和有害方面。

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