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Amelioration of experimental autoimmune encephalomyelitis by curcumin treatment through inhibition of IL-17 production.

Abstract：

:Experimental autoimmune encephalomylitis (EAE), an animal mode of multiple sclerosis (MS), was previously considered that be mediated by Th1 cells. However, a number of recent studies provided strong evidence that T helper cells that produce IL-17 play a dominant role in the pathogenesis of EAE. Curcumin (1,7-Bis 94-hydroxy-3-methoxyphenyl)-1,6 heptadiene-3, 5-di-one) is a naturally occurring polyphenolic phytochemical isolated from the rhizome of the medicinal plant Curcuma longa. It has been strongly implicated as an anti-inflammatory agent, but the precise mechanisms of its action are largely unknown. In the present study, we have investigated the efficacy and mechanism of curcumin against EAE. The treatment of Lewis rats with curcumin significantly reduced the clinical severity of EAE, and had a dramatic reduction in the number of inflammatory cells infiltration in the spinal cord. The proliferation of the MBP-reaction lymphocyte also was reduced in a curcumin dose-dependent manner. Furthermore, the mRNA expression of the cytokine profiles was assessed by quantitative reverse-transcription polymerase chain reaction (qRT-PCR), revealing the dramatic decrease of IL-17, TGF-beta, IL-6, IL-21, STAT3, and RORgammat expression in curcumin-treated groups and STAT3-phosphorylation also was inhibited. These findings indicated that curcumin amelioration EAE was, to a large extent, due to inhibit differentiation and development of Th17 cells depends on down-regulating expression of IL-6, IL-21, RORgammat signaling and inhibition STAT3-phosphorylation, suggests it is useful in the treatment of MS and other Th17 cell-mediated inflammatory diseases.

journal_name

Int Immunopharmacol

journal_title

International immunopharmacology

authors

Xie L,Li XK,Funeshima-Fuji N,Kimura H,Matsumoto Y,Isaka Y,Takahara S

doi

10.1016/j.intimp.2009.01.025

subject

Has Abstract

pub_date

2009-05-01 00:00:00

pages

575-81

issue

5

eissn

1567-5769

issn

1878-1705

pii

S1567-5769(09)00033-2

journal_volume

9

pub_type

杂志文章

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