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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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Autores principales: Hu, Xin, Tao, Chuanyuan, Gan, Qi, Zheng, Jun, Li, Hao, You, Chao
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4710930/
https://www.ncbi.nlm.nih.gov/pubmed/26843907
http://dx.doi.org/10.1155/2016/3215391
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author Hu, Xin
Tao, Chuanyuan
Gan, Qi
Zheng, Jun
Li, Hao
You, Chao
author_facet Hu, Xin
Tao, Chuanyuan
Gan, Qi
Zheng, Jun
Li, Hao
You, Chao
author_sort Hu, Xin
collection PubMed
description 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.
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spelling pubmed-47109302016-02-03 Oxidative Stress in Intracerebral Hemorrhage: Sources, Mechanisms, and Therapeutic Targets Hu, Xin Tao, Chuanyuan Gan, Qi Zheng, Jun Li, Hao You, Chao Oxid Med Cell Longev Review Article 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. Hindawi Publishing Corporation 2016 2015-12-30 /pmc/articles/PMC4710930/ /pubmed/26843907 http://dx.doi.org/10.1155/2016/3215391 Text en Copyright © 2016 Xin Hu et al. https://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Hu, Xin
Tao, Chuanyuan
Gan, Qi
Zheng, Jun
Li, Hao
You, Chao
Oxidative Stress in Intracerebral Hemorrhage: Sources, Mechanisms, and Therapeutic Targets
title Oxidative Stress in Intracerebral Hemorrhage: Sources, Mechanisms, and Therapeutic Targets
title_full Oxidative Stress in Intracerebral Hemorrhage: Sources, Mechanisms, and Therapeutic Targets
title_fullStr Oxidative Stress in Intracerebral Hemorrhage: Sources, Mechanisms, and Therapeutic Targets
title_full_unstemmed Oxidative Stress in Intracerebral Hemorrhage: Sources, Mechanisms, and Therapeutic Targets
title_short Oxidative Stress in Intracerebral Hemorrhage: Sources, Mechanisms, and Therapeutic Targets
title_sort oxidative stress in intracerebral hemorrhage: sources, mechanisms, and therapeutic targets
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4710930/
https://www.ncbi.nlm.nih.gov/pubmed/26843907
http://dx.doi.org/10.1155/2016/3215391
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