Journal
FRONTIERS IN IMMUNOLOGY
Volume 13, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fimmu.2022.847246
Keywords
intracerebral hemorrhage; reactive oxygen species; oxidative stress; anti-oxidative stress; brain injury
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Funding
- National Natural Science Foundation of China [82071331, 81870942, 81520108011]
- National Key Research and Development Program of China [2018YFC1312200]
- Canadian Institutes of Health Sciences
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This article discusses the sources and possible molecular mechanisms of oxidative stress in causing brain injury in intracerebral hemorrhage (ICH), as well as anti-oxidative stress strategies to alleviate the devastation of ICH.
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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