Multiple sclerosis (MS) is an autoimmune disease of the central nervous system (CNS) that leads to an inflammatory demyelination and axonal damage. MS disease often displays a relapsing-remitting course of neurological manifestations that is mimicked by experimental autoimmune encephalomyelitis (EAE) in animal models. The aim of the present research was to test the therapeutic effect of small molecule G2013, a novel designed non-steroidal anti-inflammatory agent in EAE. All experiments were conducted on C57BL/6 male mice aged 10 weeks. To induce the EAE, we performed subcutaneously injection of myelin oligodendrocyte glycoprotein-35-55 (MOG35-55) in Complete Freund's Adjuvant (CFA) emulsion, and for treatment of EAE we used intraperitoneal (IP) injection of G2013. On day 21 post-immunization, for total antioxidant, nitric oxide (NO) and TNF-α assessment, blood samples were taken from the heart and mice were killed, and the brains and cerebellums were then removed for histological analysis. Our findings demonstrated that G2013 had beneficial effects on EAE by lower incidence, attenuation in the severity, and a delay in the onset of disease. Histological analysis showed that inflammation criteria including the number of inflammatory cells and plaques as well as demyelination in G2013 dosed mice were lower than control group. Moreover, the serum level of NO in G2013-treated mice was significantly less than control animals. These data indicate that G2013 therapy can attenuate the disease progression in experimental model of MS.

Our data showed the safety and efficacy of G2013 as a novel designed NSAID on various oxidative stress determinants.

Dasatinib with its potential therapeutic effects and immunomodulatory properties may be recommended, after additional necessary tests and trials, for the treatment of MS.

Hydroxycitric acid (HCA) is derived primarily from the Garcinia plant and is widely used for its anti-inflammatory effects. Multiple sclerosis can cause an inflammatory demyelination and axonal damage. In this study, to validate the hypothesis that HCA exhibits therapeutic effects on multiple sclerosis, we established female C57BL/6 mouse models of multiple sclerosis, i.e., experimental autoimmune encephalomyelitis, using Complete Freund's Adjuvant (CFA) emulsion containing myelin oligodendrocyte glycoprotein (35–55). Treatment with HCA at 2 g/kg/d for 3 weeks obviously improved the symptoms of nerve injury of experimental autoimmune encephalomyelitis mice, decreased serum interleulin-6, tumor necrosis factor alpha, nitric oxide, and malondialdehyde levels, and increased superoxide dismutase and glutathione reductase activities. These findings suggest that HCA exhibits neuroprotective effects on multiple sclerosis-caused nerve injury through ameliorating inflammation and oxidative stress.