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

Frontiers in Immunology

卷:13

Yan Zhang¹  Suliman Khan¹  Yang Liu¹  Mengzhou Xue¹  Guofeng Wu³  V. Wee Yong⁴ 

[1] Academy of Medical Science, Zhengzhou University, Zhengzhou, China;

[2] Department of Cerebrovascular Diseases, The Second Affiliated Hospital of Zhengzhou University, Zhengzhou, China;

[3] Department of Emergency, Affiliated Hospital of Guizhou Medical University, Guiyang, China;

[4] Hotchkiss Brain Institute and Department of Clinical Neurosciences, University of Calgary, Calgary, AB, Canada;

关键词: intracerebral hemorrhage;    reactive oxygen species;    oxidative stress;    anti-oxidative stress;    brain injury;   

DOI  :  10.3389/fimmu.2022.847246

来源: DOAJ

【 摘 要 】

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.

【 授权许可】

Unknown