【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。更多还原

【Abstract】 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.更多还原