The Updated Role of Oxidative Stress in Subarachnoid Hemorrhage.

Abstract:

BACKGROUND:Subarachnoid hemorrhage (SAH) is considered as a violent disease with high rate of morbidity and mortality. Early brain injury (EBI) and delayed vasospasm are the two aspects of this disease that are becoming research hotspots. OBJECTIVE:We aim to update the role of oxidative stress in the development of EBI and delayed cerebral vasospasm after SAH. METHOD:We reviewed early researches, and mainly discussed three aspects of contents: reactive oxygen species (ROS) production, the role of oxidative stress in early brain injury and delayed vasospasm, and clinical implications. RESULTS:There are several sources for the excessive generation of oxidants after SAH such as disrupted mitochondrial respiration, upregulated enzymatic pathways, extracellular hemoglobin degradation and depressed intrinsic antioxidant systems. Neuron apoptosis induced by ROS is one vital mechanism of EBI. And extracellular hemoglobin degradation and nitric oxide synthases up-reputation are involved in the pathogenesis of delayed cerebral vasospasm. Some antioxidants show significant neuroprotection in researches. CONCLUSION:ROS production increases in SAH via mitochondria, hemoglobin or enzymatic pathway, and it plays a vital important role in SAH. It seems that antioxidant therapy will be most effective as one component in a treatment regime that attempts to address all the different pathways to EBI and vasospasm following SAH.

journal_name

Curr Drug Deliv

journal_title

Current drug delivery

authors

Yang Y,Chen S,Zhang JM

doi

10.2174/1567201813666161025115531

subject

Has Abstract

pub_date

2017-09-06 00:00:00

pages

832-842

issue

6

eissn

1567-2018

issn

1875-5704

pii

CDD-EPUB-79228

journal_volume

14

pub_type

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