Abstract：
Cerebral ischemia-reperfusion injury involves a series of pathophysiological processes that occur when blood supply is restored after cerebral vascular obstruction, leading to neuronal damage. The AMPK/ERK1/2 signaling pathway has been identified as crucial in this process, although the exact mechanisms underlying the induction of ischemia-reperfusion injury remain unclear. In this study, we investigated the involvement of the AMPK/ERK1/2 signaling pathway in neuronal oxidative stress damage following cerebral ischemia-reperfusion by establishing animal and cell models. Our experimental results demonstrated that cerebral ischemia-reperfusion leads to oxidative stress damage, including cell apoptosis and mitochondrial dysfunction. Moreover, further experiments showed that inhibition of AMPK and ERK1/2 activity, using U0126 and Compound C respectively, could alleviate oxidative stress-induced cellular injury, improve mitochondrial morphology and function, reduce reactive oxygen species levels, increase superoxide dismutase levels, and suppress apoptosis. These findings clearly indicate the critical role of the AMPK/ERK1/2 signaling pathway in regulating oxidative stress damage and cerebral ischemia-reperfusion injury. The discoveries in this study provide a theoretical basis for further research and development of neuroprotective therapeutic strategies targeting the AMPK/ERK1/2 signaling pathway.
摘要：
脑缺血再灌注损伤涉及脑血管阻塞后血液供应恢复所发生的一系列病理生理过程,导致神经元损伤.AMPK/ERK1/2信号通路在这一过程中至关重要,虽然诱导缺血再灌注损伤的确切机制尚不清楚。在这项研究中,我们通过建立动物和细胞模型研究了AMPK/ERK1/2信号通路在脑缺血再灌注后神经元氧化应激损伤中的作用。我们的实验结果表明，脑缺血再灌注导致氧化应激损伤，包括细胞凋亡和线粒体功能障碍。此外，进一步的实验表明，抑制AMPK和ERK1/2活性，分别使用U0126和化合物C，可以减轻氧化应激诱导的细胞损伤，改善线粒体形态和功能，降低活性氧的水平，增加超氧化物歧化酶水平，并抑制细胞凋亡。这些发现清楚地表明AMPK/ERK1/2信号通路在调节氧化应激损伤和脑缺血再灌注损伤中的关键作用。本研究的发现为进一步研究和开发针对AMPK/ERK1/2信号通路的神经保护治疗策略提供了理论基础。
