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

Abstract

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.

• Authors: Yan Zhang, Suliman Khan, Yang Liu, Guofeng Wu, V Wee Yong, Mengzhou Xue
• Journal: Frontiers in immunology (Front Immunol) Vol. 13 Pg. 847246 ( 2022) ISSN: 1664-3224 [Electronic] Switzerland
• PMID: 35355999 (Publication Type: Journal Article, Review, Research Support, Non-U.S. Gov't)
• Copyright: Copyright © 2022 Zhang, Khan, Liu, Wu, Yong and Xue.

Chemical References

• Reactive Oxygen Species

Topics

• Animals
• Brain Injuries (etiology)
• Cerebral Hemorrhage
• Disease Models, Animal
• Oxidative Stress (physiology)
• Reactive Oxygen Species