Astaxanthin effectiveness in preventing multiple sclerosis in animal model

The aim of the present study was to reveal the effect of therapeutic and prophylactic potential of astaxanthin in experimental autoimmune encephalomyelitis (EAE) as an acceptable model for the study of multiple sclerosis (MS). Astaxanthin has powerful antioxidant activities as well as several essent...

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Veröffentlicht in:Bratislava Medical Journal 2018, Vol.119 (3), p.160-166
Hauptverfasser: Bidaran, S, Ahmadi, A R, Yaghmaei, P, Sanati, M H, Ebrahim-Habibi, A
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Sprache:eng
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Zusammenfassung:The aim of the present study was to reveal the effect of therapeutic and prophylactic potential of astaxanthin in experimental autoimmune encephalomyelitis (EAE) as an acceptable model for the study of multiple sclerosis (MS). Astaxanthin has powerful antioxidant activities as well as several essential biological functions while multiple sclerosis prevention is highly regarded by researchers. The astaxanthin potential in prevention of multiple sclerosis was examined in the chronic model of experimental autoimmune encephalomyelitis (EAE) by using female C57BL/6 mice induced with oligodendrocyte glycoprotein (MOG). Splenocytes were assessed to measure the levels of proinflammatory and anti-inflammatory cytokines, proliferation rate and FoxP3+Treg cell frequency. Immunohistochemical examinations were performed on spinal cord and brain tissue. Astaxanthin reduced splenocytes proliferation index and proinflammatory cytokine levels, and vice versa increased the anti-inflammatory cytokine levels. Immunohistochemical studies of the spinal cord and brain showed that the infiltration with inflammatory cells was highly confined in the central nervous system. Protective effects of astaxanthin were visible by assigning low score recording in clinical behavior and disease severity. Astaxanthin is a powerful tool for intervention in EAE on a model of multiple sclerosis, so it can be studied further to prevent and treat MS (Tab. 2, Fig. 3, Ref. 41).
ISSN:0006-9248
1336-0345
1336-0345
DOI:10.4149/BLL_2018_031