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创伤性脑损伤中的神经炎症反应:最新进展

Neuroinflammatory Response in the Traumatic Brain Injury: An Update.

作者信息

Kursancew Amanda C S, Faller Cristiano Julio, Bortoluzzi Daniel Paulo, Niero Luana Budny, Brandão Beatriz, Danielski Lucineia Gainski, Petronilho Fabricia, Generoso Jaqueline S

机构信息

Laboratory of Experimental Neurology, Graduate Program in Health Sciences, University of Southern Santa Catarina (UNESC), Criciúma, SC, Brazil.

Laboratory of Experimental Pathophysiology, Graduate Program in Health Sciences, University of Southern Santa Catarina (UNESC), Criciúma, SC, Brazil.

出版信息

Neurochem Res. 2024 Dec 24;50(1):64. doi: 10.1007/s11064-024-04316-4.

Abstract

The central nervous system (CNS) comprises membranes and barriers that are vital to brain homeostasis. Membranes form a robust shield around neural structures, ensuring protection and structural integrity. At the same time, barriers selectively regulate the exchange of substances between blood and brain tissue, which is essential for maintaining homeostasis. Another highlight is the glymphatic system, which cleans metabolites and waste from the brain. Traumatic brain injury (TBI) represents a significant cause of disability and mortality worldwide, resulting from the application of direct mechanical force to the head that results in a primary injury. Therefore, this review aims to elucidate the mechanisms associated with the secondary injury cascade, in which there is intense activation of glial cells, dysfunction of the glymphatic system, glutamatergic neurotoxicity, additional molecular and biochemical changes that lead to a neuroinflammatory process, and oxidative stress and in which way they can be associated with cognitive damage that is capable of lasting for an extended period.

摘要

中枢神经系统(CNS)由对脑内环境稳定至关重要的膜和屏障组成。膜在神经结构周围形成坚固的屏障,确保保护和结构完整性。同时,屏障选择性地调节血液与脑组织之间的物质交换,这对于维持体内平衡至关重要。另一个亮点是类淋巴系统,它清除大脑中的代谢物和废物。创伤性脑损伤(TBI)是全球残疾和死亡的一个重要原因,由头部受到直接机械力作用导致原发性损伤引起。因此,本综述旨在阐明与继发性损伤级联相关的机制,在继发性损伤级联中,胶质细胞强烈激活、类淋巴系统功能障碍、谷氨酸能神经毒性、导致神经炎症过程的其他分子和生化变化以及氧化应激,以及它们如何与能够长期持续的认知损伤相关联。

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