| Abstrakt: |
Introduction: Multiple sclerosis (MS) is a disease of the central nervous system (CNS) that is characterized by demyelination, axonal injury, and neurological deterioration. Due to the role of oxidative stress and inflammation in MS, antioxidants and anti-inflammatory agents can be used in the prevention and treatment of this disease. Lutein is a carotenoid with reported antioxidant, anti-inflammatory, and neuroprotective properties. This study aimed to evaluate the ability of Lutein to improve Cuprizone-induced motor and histopathological changes in the prefrontal cortex of C57BL/6 male mice . Methods and Materials: C57Bl/6 mice were fed 0.2% Cuprizone mixed into rodent chow for 8 weeks. Lutein (50, 100 200 mg/kg/day) was administered by oral gavage during the last 3 weeks. Rotarod performance test, Narrow beam walking test, LFB and H&E staining, and immunohistochemistry (IHC) staining of Olig-2 were performed . Results: Treatment with Cuprizone induced weight loss during treatment compared to the control group, which was reversed by the administration of Lutein. Motor tests (Rotarod performance test and Narrow beam walking test) showed a decrease in coordination and balance in the group treated with Cuprizone. Treatment with Lutein during the last three weeks was able to improve these motor deficiencies. Histopathological examination also evidenced an increase in demyelination in the Cuprizone group, which was improved by Lutein administration. There was a remarkable increase in the fraction of Olig-2 positive cells in all Cuprizone-fed mice compared to the control. Furthermore, consuming Lutein has been shown to significantly increase Olig-2 levels, thereby enhancing the process of remyelination. Conclusion: These findings suggest that Lutein may have a neuroprotective effect by reducing demyelination and improving remyelination in the Cuprizone-induced demyelination model. [ABSTRACT FROM AUTHOR] |
