کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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5834099 | 1122646 | 2012 | 6 صفحه PDF | دانلود رایگان |

The present study investigated the effects of the anthraquinone derivative (O,Oâ²-bis-(3â²-iodopropyl)-1,4-dihidroxyanthraquinone - DIPDHAQ), mitoxantrone analog, in an experimental autoimmune encephalomyelitis (EAE) model. The results showed that DIPDHAQ treatment improved the clinical signs of the disease (n = 10; vehicle: 3.8 ± 0.3; DIPDHAQ: 1.4 ± 0.9). The improvement was associated with a decrease of inflammatory cells, demyelination, IL-17, IFN-γ, IL-12p40, IL-6, TGF-β, CCL5 and CCL20 levels in the spinal cord. DIPDHAQ presented a low cytotoxicity when in vitro assays were performed. Therefore, the findings suggest a major role for DIPDHAQ in multiple sclerosis, disease characterized as an autoimmune inflammatory disorder against myelin proteins of the brain and spinal cord. The attenuation of inflammation and consequently improvement of clinical signs, involving a decrease of pro-inflammatory cytokines and the low cytotoxicity of DIPDHAQ, suggest that this compound could be used as an alternative treatment for autoimmune diseases in the central nervous system.
HighlightsâºEAE is a murine autoimmune disease used to study multiple sclerosis. âºThe use of a mitoxantrone analog (DIPDHAQ) in the treatment of EAE was investigated. âºDIPDHAQ treatment caused reduction of the EAE clinical signs. âºDIPDHAQ reduces infiltrated cells and demyelination in the spinal cords. âºDIPDHAQ reduces CCL5, CCL20, IL-6, IL-17, IL-12 and IFN-γ in the spinal cords.
Journal: International Immunopharmacology - Volume 14, Issue 2, October 2012, Pages 127-132