丙戊酸钠在脑卒中后的保护作用机制研究进展

Research progress on protective mechanism of sodium valproate after stroke

脑卒中是一种常见的神经系统疾病,导致大量的神经功能损伤和残疾。尽管目前已有多种治疗手段,但仍然缺乏对脑卒中后具有保护作用的有效药物。近年来,丙戊酸钠作为一种广谱抗癫痫药物,其潜在的神经保护作用引起了人们的关注。研究表明,丙戊酸钠通过抑制脑卒中后的炎症介质表达、抑制组蛋白去乙酰化酶、抑制小胶质细胞和星形胶质细胞的活化,减轻脑卒中后炎症反应;调节相关基因、增强脑内抑制性神经递质γ-氨基丁酸的含量,抑制细胞凋亡,调节与细胞凋亡有关的信号通路,如丝裂原活化蛋白激酶/细胞外调节蛋白激酶(MAPK/ERK)信号通路、c-Jun氨基末端激酶(JNK)信号通路,抑制细胞凋亡;诱导热休克蛋白(HSPs),如HSP70的表达,对脑卒中后的神经组织起到保护作用。本文对近年来丙戊酸钠在脑卒中后的保护作用机制的研究进展进行综述。

Stroke is a common neurological disorder that leads to significant neurological damage and disability.Although there are currently multiple treatment options available,there is still a lack of effective drugs that have a protective effect after stroke.In recent years,sodium valproate,as a broad-spectrum antiepileptic drug,has attracted attention for its potential neuroprotective effects.Research has shown that sodium valproate can alleviate the inflammatory reaction after stroke by inhibiting the expression of inflammatory mediators,inhibiting histone deacetylase,and inhibiting the activation of microglia and astrocytes;it can regulate related genes and enhance the content of inhibitory neurotransmittersγ-aminobutyric acid in the brain,inhibit cell apoptosis,regulate signaling pathways related to cell apoptosis,such as mitogen-activated protein kinase/extracellular regulated protein kinase(MAPK/ERK)signaling pathway,and c-Jun N-terminal kinase(JNK)signaling pathway,which can inhibit cell apoptosis;and it can induce the expression of heat shock proteins(HSPs),such as HSP70,which can protect the nervous tissue after stroke.This paper will review the research progress on the protective mechanism of sodium valproate after stroke in recent years.