睡眠剥夺是导致神经炎症、氧化应激及认知功能障碍的重要诱因，其机制与星形胶质细胞的活化密 切相关。星形胶质细胞作为中枢神经系统的关键调控者，通过A1/A2极化表型在睡眠剥夺中发挥双重作 用：A1型通过释放促炎因子和神经毒素加剧神经炎症及突触损伤，而A2型则通过分泌神经营养因子和抗 炎介质促进神经修复。本文系统综述了睡眠剥夺中星形胶质细胞的活化机制及相关信号通路：NF-κB通 路、MAPK通路在、SHH通路和JAK-STAT通路。研究表明，慢性睡眠剥夺通过炎症介质积累及星形胶质 细胞过度激活导致认知障碍，而调控其极化表型（如抑制A1型或增强A2型）可能成为干预睡眠剥夺相关 神经损伤的新策略。未来需进一步解析星形胶质细胞极化的时空特异性及信号网络交互作用，为靶向治 疗提供理论依据。

Sleep deprivation (SD) is a significant contributor to neuroinflammation, oxidative stress, and cognitive dysfunction, with its mechanisms closely linked to astrocyte activation. As key regulators of the central nervous system, astrocytes exhibit dual roles in SD through A1/A2 polarized phenotypes: A1 astrocytes exacerbate neuroinflammation and synaptic damage by releasing pro-inflammatory factors and neurotoxins, whereas A2 astrocytes promote neural repair via secretion of neurotrophic factors and anti-inflammatory mediators. This review systematically summarizes the activation mechanisms of astrocytes in SD and related signaling pathways, including NF-κB, MAPK, SHH and JAK-STAT. Chronic SD induces cognitive impairment through the accumulation of inflammatory mediators and hyperactivation of astrocytes, while modulating their polarization phenotypes (e.g., suppressing A1 or enhancing A2) may serve as novel strategies for intervening in SD-related neural injuries. Future studies should further elucidate the spatiotemporal specificity of astrocyte polarization and interactions within signaling networks to provide a theoretical basis for targeted therapies.