ArticleJournal of ginseng research2026
Ginsenoside Rg1 ameliorates experimental autoimmune myasthenia gravis by regulating T cell subsets, inhibiting PI3K-AKT pathway and modulating gut microbiota and metabolites.
Article in Journal of ginseng research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Ginsenoside Rg1 (GRg1), a bioactive saponin derived from ginseng, exhibits diverse pharmacological properties, including anti-inflammatory, antioxidant, and neuroprotective effects. However, its role in myasthenia gravis (MG) remains unexplored. This study investigated the therapeutic potential of GRg1 in experimental autoimmune myasthenia gravis (EAMG). Methods: The EAMG model was established in Lewis rats using the AChR97-116 peptide. ELISA was employed to determine serum anti-AChR antibody levels in rats, while Flow cytometry or PCR was used to analyze T cell subsets. Gut microbiota composition was assessed via 16S rRNA sequencing, while non-targeted metabolomics identified metabolic changes. Network pharmacology and molecular docking were employed to predict GRg1's therapeutic targets in EAMG, followed by experimental validation using immunohistochemistry. Results: GRg1 administration significantly alleviated the clinical symptoms of EAMG rats, reduced serum anti-AChR antibody levels, and modulated T cell responses. KEGG analysis implicating the PI3K-AKT pathway. Molecular docking confirmed strong binding affinities between GRg1 and key PI3K-AKT proteins. Immunohistochemistry revealed GRg1-mediated inhibition of PI3K/AKT phosphorylation in splenic tissues. Additionally, GRg1 restored gut microbiota homeostasis. Metabolomic analysis further revealed significant differences in metabolites between EAMG and CFA rats, which were inhibited after GRg1 treatment. Conclusions: GRg1 ameliorates EAMG through immunomodulation, PI3K-AKT pathway inhibition, gut microbiota restoration, and metabolic reprogramming, highlighting its potential as a novel therapeutic agent for MG.
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