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

Free Radical Damage in Ischemia-Reperfusion Injury: An Obstacle in Acute Ischemic Stroke after Revascularization Therapy.
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缺血再灌注损伤中的自由基损伤:血运重建治疗后急性缺血性中风的一个障碍

DOI:
10.1155/2018/3804979
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发表时间:
2018
影响因子:
--
通讯作者:
Yang Y
Yang Y
中科院分区:
生物学2区
文献类型:
--
作者:
Sun MS;Jin H;Sun X;Huang S;Zhang FL;Guo ZN;Yang Y

文献摘要

被引文献

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急性缺血性卒中是世界范围内发病率和死亡率的常见原因。重组组织型纤溶酶原激活剂溶栓和血管内取栓术是治疗急性缺血性卒中的主要方法。然而,血运重建治疗后的缺血再灌注损伤会导致预后恶化。在缺血再灌注损伤的所有可能的病理机制中,自由基损伤(主要是氧化/亚硝化应激损伤)在这一过程中起着关键作用。自由基导致蛋白质功能障碍、DNA损伤和脂质过氧化,导致细胞死亡。此外,自由基损伤与导致出血性转化和脑水肿密切相关,这是血运重建治疗的主要并发症,主要是由于血脑屏障的破坏而影响神经预后。为了获得更好的临床预后,越来越多的研究集中在药物和非药物对自由基损伤的神经保护治疗上。本文就自由基在脑缺血再灌注损伤中的病理机制以及辅助神经保护治疗与血管重建术联合抗自由基损伤作一综述。
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.