Neuroprotective effect of S-allyl cysteine on an experimental model of multiple sclerosis: Antioxidant effects. (March 2018)

• Record Type: Journal Article
• Authors: Escribano, B.M.; Agüera, E.; Aguilar-Luque, M.; Luque, E.; Feijóo, M.; LaTorre, M.; Giraldo, A.I.; Galván-Jurado, A.; Caballero-Villarraso, J.; García-Maceira, F.I.; Santamaría, A.; Túnez, I.
• Is Part Of: Journal of functional foods. Volume 42(2018)
• Page Start: 281
• Page End: 288
• Publication Date: 2018-03
• Subjects: S-allyl cysteine -- Cell damage -- Experimental autoimmune encephalomyelitis -- Multiple sclerosis -- Oxidative damage; AGE aged garlic extract -- CNS central nervous system -- EAE experimental autoimmune encephalomyelitis -- DMF dimethyl fumarate -- GSH reduced glutathione -- GSSG oxidized glutathione -- LPO lipid peroxidation products -- MOG mielyn oligodencrocyte glycoprotein -- MS multiple sclerosis -- RRMS relapsing-remitting multiple sclerosis -- NAC N-acetyl cysteine -- NOx total nitrites -- Nrf2 nuclear factor erythroid 2-related factor 2 -- RNS reactive nitrogen species -- ROS reactive oxygen species -- SAC S-allyl cysteine -- tG total glutathione; Functional foods -- Analysis -- Periodicals; Food -- Biotechnology -- Periodicals; Nutrition -- Periodicals; 613.2
• DOI: 10.1016/j.jff.2017.12.068
• Languages: English
• ISSNs: 1756-4646

Abstract

Highlights: Experimental autoimmune encephalomyelitis consistently induces motor impairment. S-allyl cysteine (SAC) improves motor impairment in this model. SAC attenuates oxidative stress in the central nervous system. SAC decreases cell damage in brain. Abstract: S-allyl cysteine (SAC), has shown itself to performance important activity as a neuroprotective agent. This action is prompted by antioxidative activity. The aim of this study was to evaluate the neuroprotective effect of SAC, the principal organosulfur compound of garlic, on experimental autoimmune encephalomyelitis (EAE) as a model of multiple sclerosis (MS). Young-adult Dark Agouti rats were used. The experimental model of EAE was carried out by means of mielyn oligodendrocyte glycoprotein (MOG). The effects of MOG were evaluated by changes in: clinical score, biomarkers of oxidative/nitrosative stress, antioxidants, mitochondrial viability and neurohistologic viability. Our results reveal that MOG causes oxidative/nitrosative damage in brain and spinal cord, a decrease in the glutathione redox system and cell loss, whereas SAC administration attenuates the effects of MOG. In addition, SAC was the most effective treatment used in this study. The data show the ability of SAC to modify the development of EAE.