Effect of ginsenoside Rb1 on central oxidative stress of rats with postoperative fatigue syndrome / 中草药

ABSTRACT

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.