Abstract:

Ischemic stroke （IS） is a neurological disorder caused by cerebrovascular occlusion or stenosis leading to inadequate cerebral blood supply， resulting in brain tissue damage that severely affects patient survival and prognosis. Histone acetylation， a post-translational modification dynamically regulated by histone acetyltransferase （HAT） and histone deacetylase （HDAC）， influences IS pathogenesis by modulating gene expression related to microglial polarization， apoptosis， and ferroptosis. Studies demonstrate that interventions targeting histone acetylation through natural compounds， small-molecule drugs， and biopharmaceuticals can effectively mitigate neuronal damage and exert neuroprotective effects. This review focused on histone acetylation to elucidate its regulatory mechanisms in IS progression and its potential as a therapeutic target， aiming to provide theoretical foundations for the subsequent clinical IS treatment.

Key words: ischemic stroke, histones, acetylation modification, deacetylation modification

摘要：

缺血性脑卒中（ischemic stroke，IS）是一种由于脑血管阻塞或狭窄导致脑部供血不足，从而引起脑组织损害的神经系统疾病，严重影响患者的生存及预后。组蛋白乙酰化由组蛋白乙酰转移酶（histone acetyltransferase，HAT）和组蛋白去乙酰化酶（histone deacetylase，HDAC）动态调控的翻译后修饰，通过调控相关基因表达影响小胶质细胞极化、细胞凋亡及铁死亡等过程，进而干预IS的发病进程。研究表明，通过天然药物、小分子化学药物以及生物技术药物等方式干预组蛋白乙酰化可有效减轻脑细胞损伤，从而实现神经保护作用。综述了组蛋白乙酰化在IS发生发展中的调控机制及其作为IS治疗靶点的潜力，以期为后续IS的临床治疗提供理论参考。

关键词: 缺血性脑卒中, 组蛋白, 乙酰化修饰, 去乙酰化修饰