Role of inflammasomes in neuroinflammation after ischemic stroke.

Keun-Hwa Jung, Seung-Yong Seong
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引用次数: 1

Abstract

Ischemic stroke is a devastating disease for which there is no effective medical treatment. In the era of extensive reperfusion strategies, established neuroprotectant candidates and novel therapeutic drugs with better targets are promising for treatment of acute ischemic stroke. Such targets include the inflammasome pathway, which contributes significantly to the pathogenesis of ischemic stroke. Following ischemic stroke, damage-associated molecular patterns from damaged cells activate inflammasomes, incur inflammatory responses, and induce cell death. Therefore, inhibiting inflammasome pathways has great promise for treatment of ischemic stroke. However, the efficacy and safety of inflammasome inhibitors remain controversial, and better upstream targets are needed for effective modulation. Herein, the roles of the inflammasome in ischemic injury caused by stroke are reviewed and the potential of neuroprotectants targeting the inflammasome is discussed.

Abstract Image

炎症小体在缺血性脑卒中后神经炎症中的作用。
缺血性中风是一种毁灭性的疾病,目前尚无有效的药物治疗方法。在广泛再灌注策略的时代,已建立的候选神经保护剂和具有更好靶点的新型治疗药物有望治疗急性缺血性卒中。这些靶点包括炎性体途径,它在缺血性卒中的发病机制中起着重要作用。缺血性中风后,受损细胞的损伤相关分子模式激活炎性小体,引起炎症反应,并诱导细胞死亡。因此,抑制炎性体通路对缺血性中风的治疗具有很大的前景。然而,炎性小体抑制剂的疗效和安全性仍然存在争议,需要更好的上游靶点进行有效调节。本文综述了炎症小体在脑卒中缺血性损伤中的作用,并讨论了针对炎症小体的神经保护剂的潜力。
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