铁死亡参与脑卒中后缺血再灌注损伤的作用机制

Mechanism of ferroptosis involved in ischemia/reperfusion injury after stroke

铁死亡的核心特征是细胞内高水平铁催化自由基的形成,不饱和脂肪酸积累和铁诱导的脂质活性氧积累,引起氧化应激造成DNA、蛋白质和脂质损伤。既往研究表明,缺血性脑卒中后神经元细胞发生铁死亡,抑制铁死亡对神经元细胞具有保护作用。本综述从铁死亡、缺血性脑卒中、神经炎症角度探讨铁死亡与卒中后脑缺血再灌注损伤的相关性,丰富缺血性脑卒中的干预靶点。

The core characteristics of ferroptosis are the formation of free radicals catalyzed by high-level iron in cells,the accumulation of unsaturated fatty acids and the iron-dependent accumulation of lipid reactive oxygen species,which cause oxidative damage and eventually lead to DNA,protein and lipid damage.Previous studies have shown that ferroptosis occurs in neurons cell after ischemic stroke,and inhibiting ferroptosis has a protective effect on neurons.This review will explore the correlation between ferroptosis and cerebral ischemia-reperfusion injury from the perspectives of ferroptosis,ischemic stroke and neuroinflammation,to enrich the intervention targets of ischemic stroke.