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Received Sep 5, 2017; Accepted Dec 7, 2017
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1. Introduction
Acute ischemic stroke is a leading cause of death and disability worldwide [1–3]. Because of the growth of the older global population, ischemic stroke incidence has increased in recent decades [4]. Acute ischemic stroke contributes to a loss of brain function mainly due to a reduction in cerebral blood flow. Currently, intravenous administration of tissue plasminogen activator (tPA) and endovascular thrombectomy are the two main treatment strategies for acute ischemic stroke [5–7]. Currently, intravenous recombinant tissue plasminogen activator (tPA) is the most effective treatment strategy for acute ischemic stroke and remains the first-choice treatment in clinics worldwide. However, there are limitations in the clinical use of intravenous tPA. First, intravenous administration of tPA must be restricted to a strict time window: within 4.5 hours between the last time the patient exhibited normal behavior and the intravenous treatment. The treatment time window is so narrow that only a small number of patients are eligible for intravenous tPA [8]. Besides, the low successful recanalization rate also influences the rate of a favourable outcome [9]. Additionally, complications such as hemorrhagic transformation and fatal edema are severe and can sometimes aggravate the disease [10].
Successful recanalization of the responsible cerebral vessels which lead to blood reflow is the primary target after the onset of acute ischemic stroke. However, there are also possible complications after revascularization, among which cerebral ischemia-reperfusion injury is one of the most serious. Ischemia-reperfusion injury is a common and inevitable problem after revascularization therapy. Although successful recanalization leads to the restoration of cerebral circulation, a fair amount of patients still do not improve in terms of symptoms and function [11, 12]. Cerebral ischemia-reperfusion injury is defined as a biochemical cascade that causes deteriorative effects in ischemic brain tissue, which compromises and antagonizes the beneficial effect of recanalization [13–15]. During the cerebral ischemia reperfusion phase, the pathophysiological mechanisms include the release of excitotoxic neurotransmitters, intracellular Ca2+ accumulation, free radical damage, neuron apoptosis, neuroinflammation, and lipolysis [16–22]. Among these complex pathophysiological mechanisms, free radical damage to...