Lu sur : https://www.ncbi.nlm.nih.gov/pubmed/31437793
Attention cela concerne une expérimentation animale
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Int Immunopharmacol. 2019 Oct;75:105822. doi: 10.1016/j.intimp.2019.105822. Epub 2019 Aug 19.
Metformin attenuates autoimmune disease of the neuromotor system in animal models of myasthenia gravis.
Cui Y1, Chang L1, Wang C2, Han X1, Mu L1, Hao Y1, Liu C1, Zhao J1, Zhang T1, Zhang H3, Zhang Y1, Liu Y1, Zhao W1, Wang J1, Liu X1, Sun B1, Wang G1, Kong Q4, Han J5, Li H6.
Metformin, the most widely used medicine for type 2 diabetes, displays anti-inflammatory functions via activating AMP-activated protein kinase (AMPK).
Circulating autoantibodies and disequilibrium of helper T cells and regulatory T cells are pathological hallmarks of myasthenia gravis (MG).
Rectify the imbalance of different T cell populations has become an important therapeutic strategy to treat MG.
In this study, we assessed the effect of metformin on the development of autoimmunity using an experimental autoimmune myasthenia gravis (EAMG) rat model. We first provided evidence that oral administration of metformin attenuated the onset of EAMG.
This effect was accompanied by a substantial decrease of circulating auto-antibody levels with no effect on blood glucose level.
While metformin treatment in vitro showed little effect on inducible Treg, metformin strongly inhibited Th17 cell differentiation through the increase of reactive oxygen species and AMPK.
Furthermore, an attenuation of antigen-induced IgG2b antibody production by two different doses of metformin was also observed in the AChR-specific recall response. In conclusion, the above results indicate that metformin may have therapeutic value for the clinical treatment of MG.
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