THE EFFECT OF TROXEROTIN ON PRO-INFLAMMATORY CYTOKINES AND LYMPHOCYTE PROLIFERATION IN AN ANIMAL MODEL OF AUTOIMMUNE EXPERIMENTAL ENCEPHALOMYELITIS

Recent studies have demonstrated an important role for Th-17 lymphocytes and other cytokines in pathogenesis of multiple sclerosis. Although previous studies have demonstrated the anti-inflammatory potential of troxerutin,  the effects of troxerutin on multiple sclerosis have not been studied so far. The present study was carried out to investigate the therapeutic effects of troxerutin on experimental autoimmune encephalomyelitis (EAE) by reducing the production of pro-inflammatory cytokines IL-17, IL-1, TNF-α, and reducing nitric oxide levels and reducing immune cell proliferation.

EAE was induced by MOG35-55 peptide and complete Freundchr('39')s adjuvant in female C57BL/6 mice. The mice were placed in four therapeutic groups of 5. Treatment with troxerutin (135 mg/kg daily) was started in the treatment group when they developed a disability score. Signs of disease were recorded daily until the day 21 when mice were sacrificed. Then, Immune cells were tested to assess proliferation rate, cytokine, and nitric oxide by the 3-(4,5 dimethylthiozol-2-yl)-2,5- diphenyl-tetrazolium bromide (MTT) assay, enzyme-linked immunosorbent assay (ELISA), and Greiss, respectively.

The troxerutin significantly decreased the clinical signs of established EAE. Troxerutin significantly decreased the production of pro-inflammatory cytokines IL-17, IL-1 TNF-α and decreased levels of nitric oxide, while reduced the proliferation of immune cells (p<0.05).

Parallel with decreasing proliferation of Immune cells and cytokine production, troxerutin ameliorated established EAE.