多聚ADP-核糖聚合酶-1在放射性认知功能障碍中的研究进展  

Research progress of Poly(ADP-ribose)Polymerase-1 in the radiation-induced cognitive dysfunction

作　　者：李湘湘(综述) 张平[1] 刘芬 邹伟(审校)[1] LI Xiangxiang;ZHANG Ping;LIU Fen;ZOU Wei(Department of Neurology,Affiliated Nanhua Hospital,University of South China,Hengyang,Hunan 421002,China)

机构地区：[1]南华大学附属南华医院神经内科,湖南衡阳421002

出　　处：《现代医药卫生》2024年第12期2104-2108,共5页Journal of Modern Medicine & Health

基　　金：湖南省卫生健康委员会一般指导课题(202203074169)。

摘　　要：放射治疗后多聚ADP核糖聚合酶-1(PARP-1)的过度激活与神经炎症反应密切相关,而神经炎症是放射性认知功能障碍(RICD)的主要发病机制。该文分析了RICD中神经炎症反应的病理生理机制,包括小胶质细胞激活、星形胶质细胞的增生、少突胶质细胞的破坏、海马微环境改变和血脑屏障损伤,并对PARP-1通过这些共同机制介导神经炎症反应进而加重RICD的研究进展进行综述。最后,探讨了PARP-1抑制剂对RICD的潜在保护作用,旨在为RICD防治药物的开发提供新方向。It has been found that overactivation of Poly(ADP-ribose)Polymerase-1(PARP-1)after radiotherapy is closely related to the neuroinflammatory response,which is the main pathogenesis of radiation-induced cognitive decline(RICD).This article analyzed the pathogenic mechanisms of neuroinflammatory responses in RICD,including Microglia activation,astrocyte proliferation,oligodendrocyte destruction,hippocampal microenvironmental alterations,and blood-brain barrier damage,and reviewed the research progress on the exacerbation of RICD by PARP-1 mediating neuroinflammatory response through these common mechanisms.Finally,the potential protective effects of PARP-1 inhibitors against RICD are discussed,aiming to provide a new direction for the development RICD prevention and treatment drugs.

关 键 词：放射性认知功能障碍 多聚ADP-核糖聚合酶-1 神经炎症 电离辐射 综述 

分 类 号：R818[医药卫生—放射医学]