目的 观察人参皂苷Rb₁对术后疲劳综合征大鼠中枢氧化应激的影响，探讨其抗疲劳机制。方法 采用70%中段小肠切除端吻合术法建立术后疲劳综合征大鼠模型。术前将大鼠按体质量随机分为对照组、模型组和人参皂苷Rb₁（10 mg/kg）组，每组再按术后第1、3、7、10天各时间点分为4小组，术前1 h给药，连续给药至各小组相应时间点。术后第2～7天大鼠进行水迷宫实验，第1、3、7、10天检测大鼠最大抓力及脑内丙二醛（MDA）的量、超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶（GSH-Px）活性，电镜观察海马CA1区超微结构变化。结果 与对照组相比，模型组大鼠最大抓力在第3、7、10天明显下降（P＜0.05），在水迷宫实验中总平均逃避潜伏期明显延长（P＜0.05），穿越平台次数明显减少（P＜0.05）；与模型组相比，人参皂苷Rb₁组大鼠上述行为学指标得到明显改善（P＜0.05）。与对照组相比，模型组大鼠脑内MDA的量、SOD活性在术后第1、3天明显上升（P＜0.05），GSH-Px活性在术后第7天明显上升（P＜0.05）；与模型组相比，人参皂苷Rb₁组大鼠MDA的量明显下降（P＜0.05），SOD、GSH-Px活性明显上升（P＜0.05）。电镜观察可见人参皂苷Rb₁组大鼠海马CA1区神经元超微结构得到改善。结论 手术导致中枢氧化应激状态改变，人参皂苷Rb₁可通过增强中枢抗氧化酶活性减弱氧化应激损伤，保护中枢神经元，这可能是其抗术后疲劳的机制之一。

Objective To investigate the central oxidative stress characteristics of rats with postoperative fatigue syndrome (POFS) and the antifatigue mechanism of ginsenosides Rb₁. Methods Rat models of POFS were established by using the 70% middle part of small bowel resection method. Ninety-six SD rats were randomly divided into control, model, and ginsenoside Rb₁ (GRb₁, 10 mg/kg) groups by weight. Rats in each group were administered 1 h before operation and were then divided into four subgroups at days 1, 3, 7, and 10. Morris water-maze test was done on postoperative days 2—7. Meanwhile, grasping test, malondialdehyde (MDA) content, superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) activities were detected on postperative days 1, 3, 7, and 10 and the ultrastructure of hippocampal CA1 area was observed through electron microscope. Results Compared with the control group, the maximum grip of model rats had an obvious decline on days 3, 7, and 10 (P < 0.05). The total average escape latency was significantly extended (P < 0.05) and the platform crossing times were significantly reduced (P < 0.05). Compared with the model group, the above indexes of rats in GRb₁ group were effectively improved after the intervention (P < 0.05). Compared with the control group, on postoperative days 1 and 3, the MDA content was obviously increased (P < 0.05) and SOD activity was obviously raised (P < 0.05). On postoperative day 7, GSH-Px activity was obviously raised (P < 0.05). After the intervention of GRb₁, the MDA content was effectively decreased (P < 0.05), SOD and GSH-Px activities were effectively improved (P < 0.05). Electron microscope showed that the ultrastructure of hippocampal CA1 area of rats in GRb₁ group was significantly improved. Conclusion Surgical stress leads to the state change of central oxidative stress; GRb₁ could reduce the damage of oxidative stress by strengthening the activity of central anti-oxidant enzymes, so as to protecte central neurons, which may be one of the mechanisms against POFS.

国家自然科学基金资助项目（81070702，81171857）；浙江省卫生厅支撑学科项目（11-ZC24）；浙江省医药卫生平台重点资助计划项目（2011ZDA018）；浙江省中医药科学研究基金计划项目（2011ZB087）