化疗所致认知障碍（CICI）是抗肿瘤药物的主要不良反应之一，降低了癌症幸存者的生活质量。大量的实验和临床研究表明，化疗药物产生大量的活性氧物种（ROS），导致氧化应激、神经炎症、血脑屏障（BBB）破坏和神经细胞死亡，最终导致CICI。尽管在探索CICI不同病理机制方面取得了进展，但尚未开发出有效的治疗方法来防止CICI的进展。Nrf2是主要的转录因子，调控细胞氧化还原平衡和与炎症相关的基因表达。新兴的证据表明，上调Nrf2及其靶基因可以抑制氧化应激和神经炎症，恢复BBB完整性，增加神经生成。本综述讨论了Nrf2在CICI中的作用，以及其对氧化应激、炎症、神经毒性的应对方式，以及可能用于增强CICI中Nrf2活化的潜在Nrf2激活剂。© 2023. 作者，以Springer Science+Business Media, LLC的专有许可，属于Springer Nature。

Chemotherapy-induced cognitive impairment (CICI) is one of the major adverse effects of antineoplastic drugs, which decrease the quality of life in cancer survivors. Extensive experimental and clinical research suggests that chemotherapeutic drugs generate an enormous amount of reactive oxygen species (ROS), contributing to oxidative stress, neuroinflammation, blood-brain barrier (BBB) disruption, and neuronal death, eventually leading to CICI. Despite the progress in exploring different pathological mechanisms of CICI, effective treatment to prevent CICI progression has not been developed yet. Nrf2 is the principal transcription factor that regulates cellular redox balance and inflammation-related gene expression. Emerging evidence suggests that upregulation of Nrf2 and its target genes could suppress oxidative stress, and neuroinflammation, restore BBB integrity, and increase neurogenesis. This review discusses the role of Nrf2 in CICI, how it responds to oxidative stress, inflammation, neurotoxicity, and potential Nrf2 activators that could be used to enhance Nrf2 activation in CICI.© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.