Non-Excitatory Amino Acids, Melatonin, and Free Radicals: Examining the Role in Stroke and Aging
Por:
Carretero, VJ, Ramos, E, Segura-Chama, P, Hernández, A, Baraibar, AM, Alvarez-Merz, I, Muñoz, FL, Egea, J, Solís, JM, Romero, A, Hernández-Guijo, JM
Publicada:
1 oct 2023
Resumen:
The aim of this review is to explore the relationship between melatonin, free radicals, and non-excitatory amino acids, and their role in stroke and aging. Melatonin has garnered significant attention in recent years due to its diverse physiological functions and potential therapeutic benefits by reducing oxidative stress, inflammation, and apoptosis. Melatonin has been found to mitigate ischemic brain damage caused by stroke. By scavenging free radicals and reducing oxidative damage, melatonin may help slow down the aging process and protect against age-related cognitive decline. Additionally, non-excitatory amino acids have been shown to possess neuroprotective properties, including antioxidant and anti-inflammatory in stroke and aging-related conditions. They can attenuate oxidative stress, modulate calcium homeostasis, and inhibit apoptosis, thereby safeguarding neurons against damage induced by stroke and aging processes. The intracellular accumulation of certain non-excitatory amino acids could promote harmful effects during hypoxia-ischemia episodes and thus, the blockade of the amino acid transporters involved in the process could be an alternative therapeutic strategy to reduce ischemic damage. On the other hand, the accumulation of free radicals, specifically mitochondrial reactive oxygen and nitrogen species, accelerates cellular senescence and contributes to age-related decline. Recent research suggests a complex interplay between melatonin, free radicals, and non-excitatory amino acids in stroke and aging. The neuroprotective actions of melatonin and non-excitatory amino acids converge on multiple pathways, including the regulation of calcium homeostasis, modulation of apoptosis, and reduction of inflammation. These mechanisms collectively contribute to the preservation of neuronal integrity and functions, making them promising targets for therapeutic interventions in stroke and age-related disorders.
Filiaciones:
Carretero, VJ:
Univ Autonoma Madrid, Teofilo Hernando Inst, Fac Med, Dept Pharmacol & Therapeut, Ave Arzobispo Morcillo 4, Madrid 28029, Spain
Ramos, E:
Univ Complutense Madrid, Fac Vet Med, Dept Pharmacol & Toxicol, Madrid 28040, Spain
Segura-Chama, P:
Inst Nacl Psiquiatria Ramon de la Fuente Muniz, Mexico CONAHCYT, Calzada Mexico Xochimilco 101, Mexico City 14370, Mexico
Hernández, A:
Univ Nacl Autonoma Mexico, Inst Neurobiol, Santiago De Queretaro 76230, Queretaro, Mexico
Baraibar, AM:
Univ Pais Vasco UPV EHU, Achucarro Basque Ctr Neurosci, Dept Neurociencias, Barrio Sarriena S-N, Leioa 48940, Spain
Alvarez-Merz, I:
Univ Autonoma Madrid, Teofilo Hernando Inst, Fac Med, Dept Pharmacol & Therapeut, Ave Arzobispo Morcillo 4, Madrid 28029, Spain
Muñoz, FL:
Univ Camilo Jose Cela, Fac Hlth Sci, C Castillo Alarcon 49, Madrid 28692, Spain
Hosp 12 Octubre, Neuropsychopharmacol Unit, Res Inst I 12, Avda Cordoba S-N, Madrid 28041, Spain
Egea, J:
Hosp Univ Princesa, Hosp Univ Santa Cristina, Hlth Res Inst, Mol Neuroinflammat & Neuronal Plast Res Lab, Madrid 28006, Spain
Solís, JM:
Hosp Ramon & Cajal, Neurobiol Res Serv, Carretera Colmenar Viejo,Km 9, Madrid 28029, Spain
Romero, A:
Univ Complutense Madrid, Fac Vet Med, Dept Pharmacol & Toxicol, Madrid 28040, Spain
Hernández-Guijo, JM:
Univ Autonoma Madrid, Teofilo Hernando Inst, Fac Med, Dept Pharmacol & Therapeut, Ave Arzobispo Morcillo 4, Madrid 28029, Spain
Hosp Ramon & Cajal, Ramon y Cajal Inst Hlth Res IRYCIS, Carretera Colmenar Viejo,Km 9, Madrid 28029, Spain
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