多发性硬化（multiple sclerosis，MS）是一种自身免疫性炎症性脱髓鞘疾病。神经炎症、氧化应激、髓 鞘脱失及细胞凋亡是 MS 重要的发病机制。磷脂酰肌醇 3-激酶/蛋白激酶 B（phosphatidylinositol 3-kinase/ Protein Kinase B，PI3K/Akt）信号通路与上述病理生理过程密切相关。目前，针对MS的免疫抑制治疗以疾 病修饰疗法为主，主要以降低复发率和短期恶化为目的，尚无法治愈该疾病，随着对MS病理机制的深入研 究，新的发病机制与治疗靶点也亟待探索。本文以“多发性硬化、PI3K/Akt信号通路、炎症反应、氧化应激、 细胞凋亡”为关键词，检索2004～2024年“Pubmed、中国知网、web of science”数据库中的相关文献，对PI3K/ Akt信号通路与MS神经炎症，氧化应激，脱髓鞘和细胞凋亡的关系研究进展进行综述，旨在为MS的治疗提 供新思路。

Multiple sclerosis (MS) is an autoimmune inflammatory demyelinating disease. Neuroinflammation, oxidative stress, demyelination, and apoptosis are important pathogenesis of MS. The phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) signaling pathway is closely related to the above pathophysiological processes. Currently, the immunosuppressive treatment for MS mainly focuses on disease-modifying therapies, aiming to reduce relapse rates and short-term exacerbations. However, it cannot cure the disease. With in-depth research into the pathological mechanism of MS, new pathogenic mechanisms and therapeutic targets urgently need to be explored. This paper takes“multiple sclerosis, PI3K/Akt signaling pathway, inflammatory response, oxidative stress, apoptosis”s keywords and retrieves relevant literature from the“Pubmed, China National Knowledge Infrastructure, and Web of Science”databases between 2004 and 2024. It reviews the research progress on the relationship between the PI3K/Akt signaling pathway and MS neuroinflammation, oxidative stress, demyelination, and apoptosis, aiming to provide new ideas for the treatment of MS.