Multiple sclerosis (MS) is a chronic auto-inflammatory disease of the central nervous system (CNS) and hard to heal. This study aimed to investigate the effect of melatonin on mice with experimental autoimmune encephalomyelitis (EAE), a widely used MS model, and its potential mechanism underlying the action of MT on anti-oxidative stress. Female C57BL/6 mice were injected with MOG35-55 peptide to set up the EAE model, and for detection of the effect of melatonin (10 mg/kg i.p.) on the development and progression of EAE. Combining immunohistochemistry, biochemical technology and western blot approaches, the potential molecular mechanism of melatonin on EAE was evaluated as the levels of oxidative stress and the expression of Nrf2/ARE signal pathway. Our experiments showed a change of oxidative stress and Nrf2/ARE pathway expression in different groups, demonstrating that oxidative stress is associated with the pathophysiology of EAE. The administration of melatonin exerts neuroprotective effects against EAE, notably in suppressing the progression of EAE and pathological changes (lymphocytic infiltration). Furthermore, the effect of melatonin was probably related to decrease of the levels of oxidative stress, by activation of the Nrf2/ARE pathway and increased levels of anti-oxidant enzymes HO-1 and NQO1 expression. So, melatonin may be a promising reagent for intervention for multiple sclerosis in the future, and even for other autoimmune diseases.
Keywords: Experimental allergic encephalomyelitis; Melatonin; Multiple sclerosis; Nrf2; Oxidative stress.