AMPK信号通路在脑缺血再灌注损伤中的作用及相关药物的研究进展

    Role of AMPK Signaling Pathway in Cerebral Ischemia-reperfusion Injury and Research Progress of Related Drugs

    • 摘要: 脑缺血再灌注损伤是由于脑缺血后恢复血流灌注伴随的氧化应激激活、细胞自噬、炎症反应、细胞凋亡等一系列有害的生理反应导致的损伤。随着对脑缺血再灌注损伤研究的深入,发现AMPK信号传导通路在其中发挥重要作用。本文就近年来APMK信号通路调控炎症反应、细胞自噬、线粒体损伤以及氧化应激而影响脑缺血再灌注损伤以及药物干预作用研究进行综述,为研究脑缺血再灌注损伤及其药物的开发应用提供理论基础。

       

      Abstract: Cerebral ischemia-reperfusion injury arises from a cascade of deleterious physiological responses, including the activation of oxidative stress, autophagy, inflammatory reactions, and apoptosis, which occur upon the restoration of blood perfusion following cerebral ischemia. With the further study of cerebral ischemia-reperfusion injury, AMPK signaling pathway is found to play an important role in it. This article reviews the recent studies on the effects of AMPK signaling pathway on cerebral ischemia-reperfusion injury and drug intervention by regulating inflammation reactions, autophagy, mitochondrial injury and oxidative stress, and provides a theoretical basis for the study of cerebral ischemia-reperfusion injury and the development and application of its drugs.

       

    /

    返回文章
    返回