蛋白质乳酸化(protein lactylation)是一种新发现的翻译后修饰,在脑缺血再灌注损伤中的神经保护作用正逐步受到重视。脑缺血再灌注损伤是缺血性脑卒中后再灌注治疗引起的复杂病理过程,涉及氧化应激和炎症反应等。本文综述了蛋白质乳酸化在脑缺血再灌注损伤中的神经保护机制及其研究进展。乳酸分子可以共价结合到赖氨酸残基上,影响蛋白质的功能和活性,从而在细胞代谢、基因表达调控及细胞信号传导中发挥重要作用。研究发现,蛋白质乳酸化修饰通过调控炎症和氧化应激反应,有助于减少神经元损伤和凋亡,从而发挥神经保护作用。深入研究蛋白质乳酸化修饰的生物学功能及其在脑缺血再灌注损伤中的作用机制,不仅有助于揭示脑缺血再灌注损伤的病理生理机制,还为开发新的脑缺血再灌注损伤治疗药物提供了潜在的靶点和理论依据。

Protein lactylation is a recently discovered post-translational modification, and its neuroprotective effect in cerebral ischemia-reperfusion injury has garnered increasing attention. Cerebral ischemia-reperfusion injury is a complex pathological process that occurs following reperfusion therapy after ischemic stroke, involving oxidative stress and inflammatory responses. This article reviews the neuroprotective mechanisms of protein lactylation in cerebral ischemia-reperfusion injury and highlights recent research progress. Lactate molecules can covalently bind to lysine residues and affect the function and activity of proteins, thus playing significant roles in cell metabolism, gene expression regulation, and cell signaling. Research has indicated that protein lactylation exerts neuroprotective effects by regulating inflammatory and oxidative stress responses, helping to reduce neuronal damage and apoptosis. In-depth studies of the biological functions of protein lactylation and its mechanism of action in cerebral ischemia-reperfusion injury not only aid in elucidating the pathophysiological mechanisms underlying cerebral ischemia-reperfusion injury, but also provide potential targets and theoretical basis for the development of new therapeutic drugs for cerebral ischemia-reperfusion injury.