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Original Article

Low-level laser therapy ameliorates disease progression in a mouse model of multiple sclerosis

, , , , , , & show all
Pages 132-142 | Received 12 Jul 2015, Accepted 14 Nov 2015, Published online: 24 Dec 2015
 

Abstract

Multiple sclerosis (MS) is an autoimmune demyelinating inflammatory disease characterized by recurrent episodes of T cell-mediated immune attack on central nervous system (CNS) myelin, leading to axon damage and progressive disability. The existing therapies for MS are only partially effective and are associated with undesirable side effects. Low-level laser therapy (LLLT) has been clinically used to treat inflammation, and to induce tissue healing and repair processes. However, there are no reports about the effects and mechanisms of LLLT in experimental autoimmune encephalomyelitis (EAE), an established model of MS. Here, we report the effects and underlying mechanisms of action of LLLT (AlGaInP, 660 nm and GaAs, 904 nm) irradiated on the spinal cord during EAE development. EAE was induced in female C57BL/6 mice by immunization with MOG35–55 peptide emulsified in complete Freund’s adjuvant. Our results showed that LLLT consistently reduced the clinical score of EAE and delayed the disease onset, and also prevented weight loss induced by immunization. Furthermore, these beneficial effects of LLLT seem to be associated with the down-regulation of NO levels in the CNS, although the treatment with LLLT failed to inhibit lipid peroxidation and restore antioxidant defense during EAE. Finally, histological analysis showed that LLLT blocked neuroinflammation through a reduction of inflammatory cells in the CNS, especially lymphocytes, as well as preventing demyelination in the spinal cord after EAE induction. Together, our results suggest the use of LLLT as a therapeutic application during autoimmune neuroinflammatory responses, such as MS.

Acknowledgements

We are grateful to the website team (mindthegraph.com) for the technical support on the creation of .

Declaration of interest

There are no conflicts of interest.

This work was supported by grants from the Universidade Federal de Santa Catarina (PIBIC/CNPq – PIBIC-Af/CNPq – BIPI/UFSC), the Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq), the Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES), the Programa de Apoio aos Núcleos de Excelência (PRONEX) and the Fundação de Apoio a Pesquisa do Estado de Santa Catarina (FAPESC), all of Brazil. EDG is an undergraduate student and received grants from CNPq; PSS is a master student of the Program of Health Sciences receiving grants from CAPES.

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