Involvement of JAK/STAT signaling in the effect of cornel iridoid glycoside on experimental autoimmune encephalomyelitis amelioration in rats

- We found that CIG has anti-inflammatory effect in MBP-EAE.
- CIG alleviated neuroinflammation and promoted myelination.
- JAK/STAT signaling pathway may be involved in the effect of CIG.
- CIG maybe a potential therapeutic agent for MS.

In the present study, we investigated the therapeutic benefit of cornel iridoid glycoside (CIG), the main component extracted from Cornus officinalis, in experimental autoimmune encephalomyelitis (EAE) rats. CIG was intragastrically administered daily after EAE initiation for 20 days and reduced disease severity, incidence, disease onset and ongoing paralysis. Histopathological staining showed that CIG could reduce T cell entry to the central nervous system and microglia activation, increased brain-derived neurotrophic factor (BDNF) expression and mature oligodendrocytes, and decreased oligodendrocyte progenitor cells (OPCs). Also, CIG treatment inhibited brain JAK/STAT1/3 and reduced proinflammatory cytokines. CIG might be a novel potential therapeutic agent for multiple sclerosis (MS).