Abstract:Objective To investigate the role of ginsenoside Rg1 in inhibiting experimental autoimmune encephalomyelitis (EAE) and its influence on T lymphocyte subsets in the spleen and cytokines in peripheral blood. Methods A mouse model of EAE was established by subcutaneous multi-point injection of MOG35-55 and pertussis toxin. The EAE mice were randomly divided into model group and low-, middle-, and high-dose ginsenoside Rg1 groups, and a normal control group was also established, with 6 mice in each group. On day 10 after first immunization, the mice were given intraperitoneal injection of ginsenoside Rg1 at different doses for 14 consecutive days. The mice were sacrificed on day 35, and the spinal cord was collected to observe pathological changes such as inflammatory cell infiltration and demyelination. Flow cytometry was used to measure Th1, Th17, and Treg subsets in the mouse spleen, and ELISA was used to measure the levels of interleukin-17A (IL-17A), interferon-γ (IFN-γ), interleukin-6 (IL-6), and interleukin-10 (IL-10) in peripheral blood. Results Compared with the model group, the low-, middle-, and high-dose ginsenoside Rg1 groups had significant reductions in the score of nerve symptoms (P<0.05), the scores of inflammatory cell infiltration and demyelination in the spinal cord (P<0.05), and the percentages of CD4+, CD8+, Th1, and Th17 lymphocyte subsets in the spleen (P<0.05) and a significant increase in the percentage of Treg (CD4+CD25+FoxP3+) (P<0.05), as well as significant reductions in the levels of IFN-γ, IL-17A, and IL-16 in peripheral blood (P<0.05) and a significant increase in the level of IL-10 (P<0.05). Ginsenoside Rg1 exerted an effect in a significant dose-dependent manner. Conclusion Ginsenoside Rg1 can significantly improve clinical symptoms and reduce demyelination and inflammatory cell infiltration in the central nervous system in EAE mice, possibly by regulating the imbalance of Th17, Th1, and Treg subsets and inhibiting the expression of inflammatory cytokines.