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

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, excit...

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Published inFrontiers in immunology Vol. 13; p. 847246
Main Authors Zhang, Yan, Khan, Suliman, Liu, Yang, Wu, Guofeng, Yong, V Wee, Xue, Mengzhou
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Media S.A 09.03.2022
Subjects
Animals
anti-oxidative stress
Brain Injuries - etiology
brain injury
Cerebral Hemorrhage
Disease Models, Animal
Immunology
intracerebral hemorrhage
oxidative stress
Oxidative Stress - physiology
Reactive Oxygen Species
intracerebral hemorrhage
brain injury
anti-oxidative stress
oxidative stress
reactive oxygen species
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Summary: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.
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This article was submitted to Multiple Sclerosis and Neuroimmunology, a section of the journal Frontiers in Immunology
Edited by: Qing-Wu Yang, Xinqiao Hospital, China
Reviewed by: Xunming Ji, Capital Medical University, China; Alina Gonzales-Quevedo, Instituto de Neurología y Neurocirugía, La Habana, Cuba
ISSN:1664-3224
1664-3224
DOI:10.3389/fimmu.2022.847246