Lutein improves remyelination by reducing of neuroinflammation in C57BL/6 mouse models of multiple sclerosis.

Multiple sclerosis (MS) is an inflammatory neurodegenerative disorder characterized by demyelination. Lutein, a xanthophyll carotenoid, has well-known antioxidant and anti-inflammatory properties. In this experiment, we aimed to investigate the neuroprotective and remyelination potential of lutein in comparison with dimethyl fumarate (DMF) as a reference drug in post-cuprizone-intoxicated C57BL/6 mice. Lutein (50, 100, and 200 mg/kg/day; p.o.) and DMF (15 mg/kg/day, i.p.) were administered either alone or in combination for three weeks at the end of the six-week cuprizone (0.2 % w/w) feeding period. At the end of the study, behavioral tests, histopathological staining, immunohistochemistry (olig2), ELISA, and real-time PCR were performed to evaluate the target parameters. Lutein treatment significantly enhanced motor functions, reversed cuprizone-induced demyelination and increased serum TAC. In addition, treatment with lutein increased the number of Olig2+ cells in the corpus callosum, reduced the IL-1β and TNF-α and increased BDNF. Lutein administration significantly increased the expression levels of genes involved in myelin production (MBP, PLP, MOG, MAG, and OLIG-1) and notably reduced GFAP expression levels. In the present study, our results showed that lutein treatment could promote remyelination and neuroprotective effects by reducing neuroinflammation and upregulating the expression of the genes involved in myelin formation These findings suggest that lutein could serve as a potential adjuvant therapy for patients with multiple sclerosis. Further clinical trials are necessary to confirm its efficacy.