Oxidative Stress in Intracerebral Hemorrhage: Sources, Mechanisms, and Therapeutic Targets

Intracerebral hemorrhage (ICH) is associated with the highest mortality and morbidity despite only constituting approximately 10–15% of all strokes. Complex underlying mechanisms consisting of cytotoxic, excitotoxic, and inflammatory effects of intraparenchymal blood are responsible for its highly d...

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Bibliographic Details
Published in:Oxidative medicine and cellular longevity 2016-01, Vol.2016 (2016), p.1-12
Main Authors: Li, Hao, Zheng, Jun, Gan, Qi, Tao, Chuanyuan, Hu, Xin, You, Chao
Format: Article
Language:English
Subjects:
Animals
Antioxidants
Apoptosis
Blood
Brain
Brain damage
Brain Injuries - pathology
Brain research
Cerebral Hemorrhage - metabolism
Cerebral Hemorrhage - pathology
Clinical trials
Deoxyribonucleic acid
DNA
Free radicals
Health aspects
Heme
Heme - chemistry
Hemoglobin
Hemoglobins - chemistry
Humans
Inflammation
Injuries
Intracerebral hemorrhage
Iron - chemistry
Kinases
Lipids
Mediation
Metabolism
Metabolites
Mice
Mitochondria - pathology
Mortality
NADPH Oxidases - metabolism
NF-E2-Related Factor 2 - metabolism
Nitric oxide
Nitric Oxide Synthase - metabolism
Oxidation
Oxidative Stress
Oxygen - chemistry
Prognosis
Proteins
Review
Signal Transduction
Stroke - pathology
Studies
Superoxide Dismutase - metabolism
Traumatic brain injury
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Summary:Intracerebral hemorrhage (ICH) is associated with the highest mortality and morbidity despite only constituting approximately 10–15% of all strokes. Complex underlying mechanisms consisting of cytotoxic, excitotoxic, and inflammatory effects of intraparenchymal blood are responsible for its highly damaging effects. Oxidative stress (OS) also plays an important role in brain injury after ICH but attracts less attention than other factors. Increasing evidence has demonstrated that the metabolite axis of hemoglobin-heme-iron is the key contributor to oxidative brain damage after ICH, although other factors, such as neuroinflammation and prooxidases, are involved. This review will discuss the sources, possible molecular mechanisms, and potential therapeutic targets of OS in ICH.
ISSN:1942-0900
1942-0994
DOI:10.1155/2016/3215391