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.
作者
李湘湘(综述)
张平
刘芬
邹伟(审校)
LI Xiangxiang;ZHANG Ping;LIU Fen;ZOU Wei(Department of Neurology,Affiliated Nanhua Hospital,University of South China,Hengyang,Hunan 421002,China)
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)。
