目的 研究4周的跑台运动结合生慧汤对睡眠剥夺大鼠SIRT1/NF-κB信号通路及相关炎症因子的调节作用，探讨其改善睡眠剥夺大鼠学习记忆可能的作用机制。方法 将48只睡眠剥夺模型大鼠随机均分为空白对照组（CON组）、有氧运动组（EX组）、完全睡眠剥夺组（TSD组）、完全睡眠剥夺 + 有氧运动组（TSD + EX组）、完全睡眠剥夺 + 生慧汤 + 有氧运动组（TSD + SHT + EX组）、完全睡眠剥夺+生慧汤组（TSD + SHT组）。EX组、TSD + EX组进行4周的跑台运动、TSD + SHT + EX组同时给与4周的跑台运动及生慧汤之后，采用多平台水环境法建立大鼠完全睡眠剥夺模型，TSD组、TSD + EX组、TSD + SHT组、TSD + SHT + EX组进行72 h的睡眠剥夺。睡眠剥夺结束后采用Morris水迷宫评价大鼠的学习记忆，采用Western blot（免疫印迹试验）检测大鼠海马中SIRT1、IκBα（NF-κB的抑制蛋白）、AC-NF-κB p65（乙酰化NF-κB p65）蛋白表达水平，采用实时荧光定量PCR技术和ELISA（酶联免疫吸附剂测定）分别检测海马和血清中TNF-α（肿瘤坏死因子-α）、IL-6（白细胞介素-6）、IL-1β（白细胞介素-1β）mRNA表达水平，采用HE染色（苏木精-伊红染色法）观察大鼠海马的神经元形态。结果 与CON组比较，TSD组大鼠上平台潜伏期和游泳总路程显著增加，初次抵达平台时间显著延长，目标象限停留时间显著减少；SIRT1、IκBα表达显著降低、AC-NF-κB p65表达显著升高；海马及血清中TNF-α、IL-6、IL-1β表达水平显著升高。与TSD组比较，TSD + EX组、TSD + SHT组、TSD + SHT + EX组大鼠平台潜伏期和游泳总路程显著减少，初次抵达平台时间缩短，目标象限停留时间增加；SIRT1、IκBα表达升高、AC-NF-κB p65表达降低；海马及血清中TNF-α、IL-6、IL-1βmRNA表达水平显著降低；TSD + SHT + EX组、TSD + EX组、TSD + SHT组海马神经元细胞排列较规则，数量增加，细胞核饱满。结论 4周的有氧运动结合生慧汤可抑制神经元损伤，改善睡眠剥夺引起的大鼠学习记忆能力，其机制可能与SIRT1/NF-κB信号通路中的关键蛋白及TNF-α、IL-6、IL-1β等炎症因子表达有关。

Objective To explore the possible mechanism of 4 weeks of treadmill exercise combined with Shenghui Decoction on the regulation of SIRT1/NF-κB signaling pathway and related inflammatory factors in sleep deprived rats to improve learning memory in sleep deprived rats.Methods Forty-eight sleep deprived model rats were randomly and equally divided into blank control group (CON group), aerobic exercise group (EX group), complete sleep deprived group (TSD group), complete sleep deprived+aerobic exercise group (TSD + EX group), complete sleep deprived + Shenghui Decoction + aerobic exercise group (TSD + SHT + EX group), and complete sleep deprived + Shenghui Decoction group (TSD + SHT group). After 4 weeks of treadmill exercise in the TSD and TSD + EX groups, and 4 weeks of running table exercise and raw wisdom soup in the TSD + SHT + EX group, the complete sleep deprived model was established using the multi-platform water environment method, and 72 h of sleep deprivation was performed in the TSD, TSD+EX, TSD+SHT, and TSD +SHT+EX groups. After the end of sleep deprivation, the learning memory of rats was evaluated by Morris water maze, and the expression levels of SIRT1, IκBα (inhibitory protein of NF-κB) and AC-NF-κB p65 (acetylated NF-κB p65) proteins were detected in the hippocampus of rats by Western blot (immunoblotting test), using real-time fluorescence quantitative PCR technique and ELISA (enzyme-linked immunosorbent assay) were used to detect the mRNA expression levels of TNF-α (tumor necrosis factor-α), IL-6 (interleukin-6) and IL-1β (interleukin-1β) in hippocampus and serum, respectively, and HE staining (hematoxylin-eosin staining method) was used to observe the neuronal morphology of rat hippocampus.Results Compared with the CON group, the platform latency, the total distance of swimming and the first arrival time of rats in the TSD group increased significantly, target quadrant dwell time decreased significantly; the expression of SIRT1 and IκBα decreased significantly, and the expression of AC-NF-κB p65 increased significantly; the expression of TNF-α, IL-6 and IL-1β in the hippocampus and serum increased significantly. Compared with the TSD group, the platform latency, the total distance of swimming and the first arrival time of rats reduced and the target quadrant dwell time increased of rats in the TSD + EX group, TSD + SHT group and TSD + SHT + EX group; SIRT1 and IκBα expression was increased, AC-NF-κB p65 expression was decreased; TNF-α, IL-6 and IL-1β mRNA expression levels in hippocampus and serum were significantly increased. The hippocampal neuron cells in the TSD + SHT + EX group, TSD + EX group and TSD + SHT group hippocampal neuron cells were more orderly arranged with number increased, and the nuclei were full.Conclusion Four weeks of aerobic exercise combined with Shenghui Decoction inhibits neuronal damage and improves sleep deprivation-induced learning memory ability in rats, and the mechanism may be related to the expression of key proteins in the SIRT1/NF-κB signaling pathway and inflammatory factors such as TNF-α, IL-6, and IL-1β.