2026-04-29T02:37:28Zhttps://repisalud.isciii.es/rest/oai/request

oai:repisalud.isciii.es:20.500.12105/181792024-11-28T15:31:32Zcom_20.500.12105_15322com_20.500.12105_2051col_20.500.12105_16927

00925njm 22002777a 4500 dc Gil, Antonio author Martín-Montañez, Elisa author Valverde, Nadia author Lara, Estrella author Boraldi, Federica author Claros, Silvia author Romero-Zerbo, Silvana-Yanina author Fernández, Oscar author Pavia, Jose author Garcia-Fernandez, Maria author 2020-12-29 Imbalance in the oxidative status in neurons, along with mitochondrial damage, are common characteristics in some neurodegenerative diseases. The maintenance in energy production is crucial to face and recover from oxidative damage, and the preservation of different sources of energy production is essential to preserve neuronal function. Fingolimod phosphate is a drug with neuroprotective and antioxidant actions, used in the treatment of multiple sclerosis. This work was performed in a model of oxidative damage on neuronal cell cultures exposed to menadione in the presence or absence of fingolimod phosphate. We studied the mitochondrial function, antioxidant enzymes, protein nitrosylation, and several pathways related with glucose metabolism and glycolytic and pentose phosphate in neuronal cells cultures. Our results showed that menadione produces a decrease in mitochondrial function, an imbalance in antioxidant enzymes, and an increase in nitrosylated proteins with a decrease in glycolysis and glucose-6-phosphate dehydrogenase. All these effects were counteracted when fingolimod phosphate was present in the incubation media. These effects were mediated, at least in part, by the interaction of this drug with its specific S1P receptors. These actions would make this drug a potential tool in the treatment of neurodegenerative processes, either to slow progression or alleviate symptoms. http://hdl.handle.net/10668/4508 http://hdl.handle.net/20.500.12105/18179 33383658 10.3390/cells10010034 2073-4409 Cells Sphingosine-1-phosphate receptor analogue Fingolimod phosphate Neuroprotection Mitochondrial damage Glycolytic pathway Pentose phosphate pathway Redox homeostasis Receptores de esfingosina-1-fosfato Neuroprotección Mitocondrias Glucólisis Vía de la pentosa-fosfato Oxidación-reducción Homeostasis Neuronal Metabolism and Neuroprotection: Neuroprotective Effect of Fingolimod on Menadione-Induced Mitochondrial Damage