The therapeutic effects of ginkgolides in Guillain-Barré syndrome and experimental autoimmune neuritis


      • Th17 cells and IFN-γ and IL-12p70 are involved in the pathogenesis and progression of GBS/EAN.
      • Administration of ginkgolides delayed the peak of disease and ameliorated the maximal scores of EAN in C57BL/6 mice might via down-regulating the proportions of Th17 cells in EAN spleens.
      • Ginkgolides suppressed inflammation response by decreasing pro-inflammatory cytokines IFN-γ and IL-12 in GBS patients.



      Guillain-Barré syndrome (GBS) is an acquired immune-mediated inflammatory peripheral neuropathy. The immune regulation of ginkgolides have been revealed in recent years. We herein investigate the potential therapeutic effects of ginkgolides both on GBS and its animal model, experimental autoimmune neuritis (EAN).


      EAN in C57BL/6 mice induced by subcutaneous injection with peripheral nerve myelin P0 protein peptide 180–199 (P0 peptide) were treated with ginkgolides at three different doses. GBS patients were randomly divided into two groups, the experimental group and the control group. The experimental group were treated with ginkgolides as soon as diagnosed.


      Our data indicated that ginkgolides administration daily ameliorated the score of EAN and delayed the peak of disease in EAN mice. Ginkgolides also down-regulated the proportions of T helper (Th) 17 cells in EAN spleens. Furthermore, we also found that administration of ginkgolides significantly decreased the levels of interferon (IFN)-γ and interleukin-12 (IL)-12 in GBS patients.


      Our results suggested that ginkgolides ameliorated the clinical score of EAN through down-regulating the proportions of Th 17 cells. Ginkgolides also suppressed inflammation response by decreasing pro-inflammatory cytokines IFN-γ and IL-12, suggesting ginkgolides had potential therapeutic effects on GBS patients and EAN in the future.



      GBS (Guillain-Barré syndrome), EAN (experimental autoimmune neuritis), GB (ginkgolide B), PAF (platelet-activating factor), MNCs (mononuclear cells), IFN (interferon), IL (interleukin), p.i (post-immunization), Th (T helper), Treg (regulatory T), IVIg (immunoglobulin), HFGS (functional grading scale), MRC (Medical Research Council), CBA (cytometric beads array), (macrophages), NF-κB (nuclear factor-κB), TLR (toll-like receptors), MyD88 (myeloid differentiation factor 88)
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