Abstract
Myasthenia gravis (MG) is an autoimmune disease characterized by fatigable muscle weakness. Ursolic acid (UA) is a pentacyclic triterpenoid with anti-inflammatory and immunomodulatory properties, especially inhibiting IL-17. We found that UA ameliorated the symptoms of experimental autoimmune myasthenia gravis (EAMG), a rat model of MG. Although both the low and high doses of UA shifted Th17 to Th2 cytokines, other mechanisms were dose dependent. The low dose enhanced Fas-mediated apoptosis, whereas the high dose up-regulated Treg cells and reduced the concentrations of IgG2b antibodies. These findings suggest a new strategy to treat EAMG and even human MG.
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