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Curcumin ameliorates rat experimental autoimmune neuritis
Author(s) -
Han Fuyu,
Luo Bangwei,
Shi Rongchen,
Han Changhao,
Zhang Zhonghao,
Xiong Jian,
Jiang Man,
Zhang Zhiren
Publication year - 2014
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.23357
Subject(s) - curcumin , neuritis , medicine , immunology , concanavalin a , autoimmune disease , curcuma , inflammation , spleen , proinflammatory cytokine , pharmacology , experimental autoimmune encephalomyelitis , tumor necrosis factor alpha , in vitro , biology , traditional medicine , antibody , biochemistry , psychiatry
Experimental autoimmune neuritis (EAN) is a helper T cell‐mediated autoimmune demyelinating inflammatory disease of the peripheral nervous system that serves as an animal model for human Guillain‐Barre syndrome. Curcumin, a naturally occurring polyphenolic phytochemical isolated from the medicinal plant Curcuma longa , has anti‐inflammatory activities. Here we investigated the therapeutic effects and potential mechanisms of curcumin in EAN rats. Exogenous curcumin treatment (100 mg/kg/day) significantly delayed the onset of EAN neurological signs, ameliorated EAN neurological severity, and reduced body weight loss of EAN rats. In EAN sciatic nerves, curcumin treatment suppressed the inflammatory cell accumulation and the expression of interferon (IFN)‐γ, tumor necrosis factor‐α, interleukin (IL)‐1β, and IL‐17. Furthermore, curcumin treatment significantly decreased the percentage of CD4 + T helper cells in EAN spleen and suppressed concanavalin A‐induced lymphocyte proliferation in vitro. In addition, curcumin altered helper T cell differentiation by decreasing IFN‐γ + CD4 + Th1 cells in EAN lymph node and spleen. In summary, our data demonstrate that curcumin could effectively suppress EAN by attenuating inflammation, indicating that curcumin might be a candidate for treatment of autoimmune neuropathies. © 2014 Wiley Periodicals, Inc.