Improvement of ginsenoside Rb1 on inflammation of central nervous system in postoperative fatigue syndrome rats / 中草药

ABSTRACT

Objective: To explore the inflammatory factor and inflammation signal pathway in hippocampus of postoperative fatigue syndrome (POFS) rats, and to investigate the central mechanism of POFS and the anti-fatigue effect of ginsenoside Rb1. Methods: Ninety-six male SD rats were randomly divided into control, POFS, and ginsengoside Rb1 intervention groups (ginsengoside Rb1 groups), and each group was divided into subgroups by postoperative 1, 3, 5, and 7 d. The fatigue was assessed with open field test. The mRNA levels of inflammatory cytokines in hippocampus were measured by real-time quantitative PCR. The activation of p38MAPK enzyme was examined by Western blotting and immunohistochemisty. The translocation of NF-κB/p65 in nuclear was measured by Western blotting and immunohistofluorescence. Results: On postoperative day 1 and day 3, compared with the control group, the journey of rats in the POFS group declined (P < 0.01), while resting time increased (P < 0.01), the level of inflammation cytokines added, the expression of p-p38MAPK protein was enhanced and the ratio of NF-κB/p65 cytoplasm/NF-κB/p65/nuclear was also elevated (P < 0.05). Compared with the POFS group, the resting time of rats decreased (P < 0.05) on postoperative day 1 and day 5.On day 1 and day 3 after surgery, the journey of rats was enhanced (P < 0.01), the level of inflammation cytokines was declined and the ratio of NF-κB/p65 cytoplasm/NF-κB/p65/nuclear was decreased (P < 0.05). The levels of p-p38MAPK in postoperative day 3, day 5, and day 7 were also declined (P < 0.05). The results of immunohistochemisty and immunohistofluorescence were accordance with Western blotting. Conclusion: The inflammatory cytokine in hippocampus of POFS rats is increased and the inflammation signal pathway is activated. Ginsenoside Rb1 has some improvement effects on central fatigue in POFS rats. Key words