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.