The preclinical efficacy of Panax ginseng in multiple sclerosis: a systematic review and meta-analysis with a perspective on clinical translation

Background Multiple sclerosis (MS) is a chronic autoimmune neurodegenerative disorder with limited disease-modifying therapies. Panax ginseng (P. ginseng), a traditional medicine with anti-inflammatory properties, is a proposed therapeutic agent. This systematic review and meta-analysis evaluated preclinical and clinical evidence regarding the therapeutic efficacy of P. ginseng in MS models and patients.Methods We searched MEDLINE, ScienceDirect, Scopus, Web of Science, and Cochrane CENTRAL through October 2025. Standardized mean differences (SMD) with 95% confidence intervals (CI) were calculated using random-effects models. Primary outcomes were disease severity and central nervous system (CNS) histopathology in animal models, and fatigue scores in clinical trials.Results Ten preclinical and two clinical studies met inclusion criteria. In animal models, P. ginseng significantly reduced peak clinical scores (SMD: −2.18; 95% CI: −3.25 to −1.12; P = 0.002), CNS inflammation (SMD: −1.81; 95% CI: −2.71 to −0.91; P = 0.005), and demyelination (SMD: −2.12; 95% CI: −3.06 to −1.19; P = 0.002). It decreased T helper 17 (Th17) cell infiltration (SMD: −1.95; P = 0.01) and interferon-gamma (IFN-γ) mRNA expression (SMD: −3.07; P = 0.005) while preserving myelin basic protein (SMD: 2.77; P = 0.045). However, a pooled analysis of two randomized trials (n = 110) found no significant effect on fatigue (SMD: 1.02; 95% CI: −3.18 to 5.22; P = 0.20).Conclusion P. ginseng demonstrates robust neuroprotective and immunomodulatory effects strictly within preclinical models. However, the available human evidence remains preliminary, underpowered, and clinically inconclusive. Current clinical data do not confirm significant benefits for MS-related fatigue, highlighting a translational gap. Large, well-designed trials using standardized preparations are needed to clarify its therapeutic potential.