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脑出血后的氧化应激机制与治疗靶点

Mechanisms of Oxidative Stress and Therapeutic Targets following Intracerebral Hemorrhage.

作者信息

Yao Zhenjia, Bai Qinqin, Wang Gaiqing

机构信息

Neurology, Shanxi Medical University, 030001 Taiyuan, Shanxi, China.

Neurology, Sanya Central Hospital (Hainan Third People's Hospital), 572000 Sanya, Hainan, China.

出版信息

Oxid Med Cell Longev. 2021 Feb 21;2021:8815441. doi: 10.1155/2021/8815441. eCollection 2021.

Abstract

Oxidative stress (OS) is induced by the accumulation of reactive oxygen species (ROS) following intracerebral hemorrhage (ICH) and plays an important role in secondary brain injury caused by the inflammatory response, apoptosis, autophagy, and blood-brain barrier (BBB) disruption. This review summarizes the current state of knowledge regarding the pathogenic mechanisms of brain injury after ICH, markers for detecting OS, and therapeutic strategies that target OS to mitigate brain injury.

摘要

氧化应激(OS)由脑出血(ICH)后活性氧(ROS)的积累所诱导,并在由炎症反应、细胞凋亡、自噬和血脑屏障(BBB)破坏引起的继发性脑损伤中起重要作用。本综述总结了关于脑出血后脑损伤致病机制、检测氧化应激的标志物以及针对氧化应激以减轻脑损伤的治疗策略的当前知识状态。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e66/7920740/1268018f756c/OMCL2021-8815441.001.jpg

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