Therapeutic Effect Of Ginsenoside Rg1 On Post - Traumatic Stress Disorder In Mice

Objective To investigate the possible effects of ginsenoside Rg1, an important active ingredient of ginseng, on post-traumatic stress disorder(PTSD).Methods Single prolonged stress(SPS) mouse model was established as previously reported. Different groups of PTSD mice received saline, Rg1 or sertraline(an SSRI antidepressant) treatment respectively. The sham control animals did not received SPS treatment. The injections started immediately after stress and continued daily for 8 days. On the day 8 and 10 days after stress, elevated plus maze(EPM) and forced swimming test(FST) were performed to evaluate the anxiety and depression, Immunohistochemical studies were performed after behavioral analysis to investigate neurogenesis in the hippocampus.Results We found that, the percentage of open arm entries in EPM was significantly decreased in both the Rg1-treated SPS mice and the saline-treated ones, in comparison to the sham control animals(F=11.06;t=4.505,4.564; P<0.001). As a positive control, the sertraline-treated SPS mice showed significantly increased open arm entries compared to the Rg1-treated group(t=3.44,P<0.05). In addition, similar to saline-treated SPS mice, the Rg1-treated mice showed significantly increased immobility in FST, compared to the sham control animals;again, the sertraline-treated mice showed significantly decreased immobility time in FST compared to the saline-treated ones(F=8.291,P<0.001). Besides, similar to saline-treated SPS mice, the Rg1-treated mice showed significant decrease in adult hippocampal neurogenesis, compared to the sham control animals;While the sertraline-treated mice showed significantly increase in neurogenesis compared to the saline-treated ones(F= 9.812,P<0.001).Conclusion Our results suggest that, in contrast to the anti-depressive effect of SSRI, ginsenoside Rg1 is not effective to reduce anxiety and depression, the two characteristic affective phenotypes seen in SPS animal model of PTSD. The lack of effect on hippocampal neurogenesis may explain Rg1’s invalidation on SPS-induced PTSD in mice.