Shikonin ameliorates Experimental Autoimmune Encephalomyelitis (EAE) via Immuno-modulatory, anti-apototic, and anti-oxidative activity

Abstract

Background Multiple sclerosis is a common auto-immuno-inflammatory diseases of the central nervous system in adults. There are several underlying mechanisms for pathogenesis of the disease, including inflammation, oligodendrocyte apoptosis, and oxidative stress. Methods We have investigated the mechanism of Shikonin action in C57BL/6 experimental autoimmune encephalomyelitis (EAE) model of multiple sclerosis. Results Our results revealed that EAE induction significantly increased the extent of demyelination in the corpus callosum tissues of the animals, while treatment of the mice with Shikonin, significantly decreased the extent of demyelination. Real-time PCR based analyzing the brain samples from the EAE mice, revealed a significant enhancement in the expression level of TNF-α , IFN-γ and Bax genes as well as a reduction in the expression level of TGF-β and Bcl2. Shikonin treatment significantly reduced the expression level of TNF-α , IFN-γ and Bax. On the other hand, the expression levels of TGF-β and Bcl2 as well as the Glutathione peroxidase-1 (GPX-1) enzyme were significantly increased following Shikonin treatment. Conclusion This study emphasizes the immune-modulatory, anti-apoptotic, and anti-oxitive effects of Shikonin, which may have an important healing influence on the severity of EAE.