Parthenolide inhibits the initiation of experimental autoimmune neuritis

- Parthenolide inhibited TNF-α and IL-17 production and lymphocyte proliferation in vitro.
- Parthenolide inhibited the initiation of experimental autoimmune neuritis (EAN) in early phase.
- Parthenolide inhibited the production of TNF-α, IFN-γ, IL-1β and IL-17, and decreased Th1 and Th17 cells at early time point of EAN.
- Parthenolide impeded the recovery of EAN in late phase.
- The anti-inflammatory effect of parthenolide vanished at late time point of EAN, which was accompanied with inhibited apoptosis of inflammatory cells.

A growing body of evidence suggests the anti-inflammatory and antitumor effects of parthenolide (PAR). Here we show that PAR treatment inhibits the initiation of experimental autoimmune neuritis (EAN), suppresses the production of TNF-α, IFN-γ, IL-1β and IL-17, and decreases Th1 and Th17 cells at early time point. However, such anti-inflammatory effect vanishes later and PAR impedes the recovery of EAN in late phase, which is accompanied with inhibited apoptosis of inflammatory cells. Our results indicate that PAR plays dual roles in EAN and it is not proper to be applied in autoimmune diseases of nervous system.

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