#CMSC16 – MS Mice Show Reduced Disease Severity After Treatment with Vegetable Compound

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Mice with the MS-like disease experimental autoimmune encephalomyelitis, or EAE showed reduced severity and slower disease progression when treated with the compound D3T, present in vegetables.

Research from Indiana University School of Medicine showed that D3T – a compound that triggers copying of antioxidant genes and production of the antioxidant glutathione – delays disease development and lowers disease severity in experimental autoimmune encephalomyelitis (EAE) animal models.

The models mimicked multiple sclerosis (MS) in humans, advancing further exploration of D3T as an MS treatment.

The data was presented at a Disease Management, Imaging, and Therapeutics session of the Consortium of Multiple Sclerosis Centers (CMSC) 2016 Annual Meeting, June 1-4 in National Harbor, Md.

D3T belongs to a group of substances called dithiolethiones, which are present in vegetables that include cauliflower, cabbage, and broccoli. Because its anti-inflammatory properties are known to prevent cancer growth, it is a compound of great interest for potential MS treatment.

To determine whether D3T might affect disease mechanisms in MS, the research team triggered EAE in mice, and assessed the presence of symptoms when D3T was administered before or after the induction of EAE.

The study, “3H-1,2-Dithiole-3-Thione as a Novel Therapeutic Agent for the Treatment of Experimental Autoimmune Encephalomyelitis,” showed that when the mice received D3T after induction of EAE, they developed disease later in time than non treated mice. The treatment also greatly reduced the severity of the disease, and prevented progression and exacerbations.

The research team then explored how D3T might affect the course and severity of EAE, and found that the compound blocked the expression of molecules that work as co-stimulators of dendritic cells — key players of the immune system. The action contributes to the initiation of an immune response by presenting antigens perceived as foreign to other immune cells that learn to target such structure.

Treatment with D3T also prevented the release of inflammatory cytokines by dendritic cells, and blocked the specialization of T-cells to the disease-causing Th1 and Th17 types.

The team also found that D3T affected brain immune cells called microglia, preventing their activation and the expression of inflammatory cytokines by the cells. Instead, the treatment promoted phase 2 enzymes capable of detoxifying harmful compounds and reactive oxygen species.

Researchers suggest that further studies should explore the potential therapeutic value of D3T in MS.

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