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脑出血后的氧化应激：从分子机制到治疗靶点。

Oxidative Stress Following Intracerebral Hemorrhage: From Molecular Mechanisms to Therapeutic Targets.

机构信息

Department of Cerebrovascular Diseases, The Second Affiliated Hospital of Zhengzhou University, Zhengzhou, China.

Academy of Medical Science, Zhengzhou University, Zhengzhou, China.

出版信息

Front Immunol. 2022 Mar 9;13:847246. doi: 10.3389/fimmu.2022.847246. eCollection 2022.

DOI:10.3389/fimmu.2022.847246
PMID:35355999
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8959663/
Abstract

Intracerebral hemorrhage (ICH) is a highly fatal disease with mortality rate of approximately 50%. Oxidative stress (OS) is a prominent cause of brain injury in ICH. Important sources of reactive oxygen species after hemorrhage are mitochondria dysfunction, degradated products of erythrocytes, excitotoxic glutamate, activated microglia and infiltrated neutrophils. OS harms the central nervous system after ICH mainly through impacting inflammation, killing brain cells and exacerbating damage of the blood brain barrier. This review discusses the sources and the possible molecular mechanisms of OS in producing brain injury in ICH, and anti-OS strategies to ameliorate the devastation of ICH.

摘要

脑出血（ICH）是一种死亡率约为 50%的高致命性疾病。氧化应激（OS）是 ICH 中脑损伤的一个突出原因。出血后活性氧的重要来源是线粒体功能障碍、红细胞降解产物、兴奋性谷氨酸、激活的小胶质细胞和浸润的中性粒细胞。OS 主要通过影响炎症、杀死脑细胞和加剧血脑屏障损伤，在 ICH 后对中枢神经系统造成损害。本文综述了 ICH 中 OS 产生脑损伤的来源和可能的分子机制，以及抗 OS 策略来改善 ICH 的破坏。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aecc/8959663/8e837d0f9e45/fimmu-13-847246-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aecc/8959663/6d94f495dcca/fimmu-13-847246-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aecc/8959663/8e837d0f9e45/fimmu-13-847246-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aecc/8959663/6d94f495dcca/fimmu-13-847246-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aecc/8959663/8e837d0f9e45/fimmu-13-847246-g002.jpg

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[3]
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[4]
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[5]
Spermidine Exerts Neuroprotective Effects Following Intracerebral Hemorrhage in Mice Through Anti-Inflammation and Blood-Brain Barrier Protection.

J Inflamm Res. 2025-6-7

[6]
Traditional Chinese Medicine and Ferroptosis in Intracerebral Hemorrhage: A Potential Therapeutic Approach.

Drug Des Devel Ther. 2025-6-4

[7]
Matrix metalloproteinase‑9 in hemorrhagic transformation after acute ischemic stroke (Review).

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[8]
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[9]
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本文引用的文献

[1]
Modes of Brain Cell Death Following Intracerebral Hemorrhage.

Front Cell Neurosci. 2022-2-3

[2]
Gap Junctions and Hemichannels Composed of Connexins and Pannexins Mediate the Secondary Brain Injury Following Intracerebral Hemorrhage.

Biology (Basel). 2021-12-25

[3]
Plasma obtained following murine hindlimb ischemic conditioning protects against oxidative stress in zebrafish models through activation of nrf2a and downregulation of duox.

PLoS One. 2021

[4]
Effect of Deferoxamine on Outcome According to Baseline Hematoma Volume: A Post Hoc Analysis of the i-DEF Trial.

Stroke. 2022-4

[5]
Central Nervous System Tissue Regeneration after Intracerebral Hemorrhage: The Next Frontier.

Cells. 2021-9-23

[6]
Neuroprotection of minocycline by inhibition of extracellular matrix metalloproteinase inducer expression following intracerebral hemorrhage in mice.

Neurosci Lett. 2021-11-1

[7]
The combination of deferoxamine and minocycline strengthens neuroprotective effect on acute intracerebral hemorrhage in rats.

Neurol Res. 2021-10

[8]
Safety and efficacy of remote ischemic conditioning for the treatment of intracerebral hemorrhage: A proof-of-concept randomized controlled trial.

Int J Stroke. 2022-4

[9]
Intracerebral haemorrhage: from clinical settings to animal models.

Stroke Vasc Neurol. 2020-12

[10]
Neuroinflammation in intracerebral haemorrhage: immunotherapies with potential for translation.

Lancet Neurol. 2020-12

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