转位蛋白18kDa在癫痫相关神经炎症中的研究进展

Research progress of translocator protein 18kDa in neuroinflammation induced by epilepsy

目前仍有1/3的癫痫患者对抗癫痫发作药物(Anti-seizure medications,ASMs)耐药,而ASMs只能缓解症状,无法彻底治愈,因此从癫痫的发病机制着手研发新型的ASMs成了现如今急需解决的社会问题。越来越多的研究证实神经炎症参与癫痫的发生和发展,转位蛋白分子18 kDa(Translocator protein 18 kDa,TSPO)也被认为是神经炎症的标志物,贯穿神经炎症反应的始终。目前TSPO在癫痫引发神经炎症中的作用机制众说纷纭,缺乏总结与概述。本文对TSPO在神经炎症及其在癫痫引发神经炎症作用的相关研究进展作一综述,旨在为寻找治疗癫痫的相关靶点与通路提供新思路。

Currently,approximately one-third of epilepsy patients exhibit resistance to anti-seizure medications(Anti-seizure medications,ASMs),which can only alleviate symptoms,but cannot completely cure the condition.Consequently,the development of new ASMs from an understanding of epilepsy pathogenesis has emerged as an urgent social issue.The role of neuroinflammation in various neurological diseases has garnered significant attention as a popular research topic both domestically and internationally.Numerous studies have corroborated the involvement of neuroinflammation in the onset and progression of epilepsy.The biological target,Translocator protein 18 kDa(TSPO),is considered as a marker of neuroinflammation and is intricately involved in the entire neuroinflammatory response.Investigating the function of TSPO in epilepsy neuroinflammation can potentially uncover new treatment targets.At present,the exact mechanism of TSPO in epilepsy neuroinflammation remains unclear,thus necessitating a comprehensive summary and overview.This article reviewed the advancements made in TSPO research within the realm of neuroinflammation and its role in epileptic neuroinflammation,aiming to contribute novel insights for the identification of related targets and pathways for epilepsy treatment.