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Oxidative Medicine and Cellular Longevity
Volume 2018, Article ID 3804979, 17 pages
https://doi.org/10.1155/2018/3804979
Review Article

Free Radical Damage in Ischemia-Reperfusion Injury: An Obstacle in Acute Ischemic Stroke after Revascularization Therapy

1Department of Neurology, The First Hospital of Jilin University, Chang Chun 130021, China
2Clinical Trail and Research Center for Stroke, Department of Neurology, The First Hospital of Jilin University, Chang Chun 130021, China

Correspondence should be addressed to Yi Yang; moc.361@iygnayrotcod

Received 5 September 2017; Accepted 7 December 2017; Published 31 January 2018

Academic Editor: Daniela Giustarini

Copyright © 2018 Ming-Shuo Sun et al. 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.

Abstract

Acute ischemic stroke is a common cause of morbidity and mortality worldwide. Thrombolysis with recombinant tissue plasminogen activator and endovascular thrombectomy are the main revascularization therapies for acute ischemic stroke. However, ischemia-reperfusion injury after revascularization therapy can result in worsening outcomes. Among all possible pathological mechanisms of ischemia-reperfusion injury, free radical damage (mainly oxidative/nitrosative stress injury) has been found to play a key role in the process. Free radicals lead to protein dysfunction, DNA damage, and lipid peroxidation, resulting in cell death. Additionally, free radical damage has a strong connection with inducing hemorrhagic transformation and cerebral edema, which are the major complications of revascularization therapy, and mainly influencing neurological outcomes due to the disruption of the blood-brain barrier. In order to get a better clinical prognosis, more and more studies focus on the pharmaceutical and nonpharmaceutical neuroprotective therapies against free radical damage. This review discusses the pathological mechanisms of free radicals in ischemia-reperfusion injury and adjunctive neuroprotective therapies combined with revascularization therapy against free radical damage.