Melatonin and brain barriers: The protection conferred by melatonin to the blood-brain barrier and blood-cerebrospinal fluid barrier.
Antioxidant
Blood-brain barrier
Blood-cerebrospinal fluid barrier
Melatonin, Anti- inflammatory
Journal
Frontiers in neuroendocrinology
ISSN: 1095-6808
Titre abrégé: Front Neuroendocrinol
Pays: United States
ID NLM: 7513292
Informations de publication
Date de publication:
10 Oct 2024
10 Oct 2024
Historique:
received:
02
05
2024
revised:
29
07
2024
accepted:
05
10
2024
medline:
13
10
2024
pubmed:
13
10
2024
entrez:
12
10
2024
Statut:
aheadofprint
Résumé
The blood-brain barrier and the blood-cerebrospinal fluid barrier separate the blood from brain tissue and cerebrospinal fluid. These brain barriers are important to maintain homeostasis and complex functions by protecting the brain from xenobiotics and harmful endogenous compounds. The disruption of brain barriers is a characteristic of neurologic diseases. Melatonin is a lipophilic hormone that is mainly produced by the pineal gland. The blood-brain barrier and the blood-cerebrospinal fluid barriers are melatonin-binding sites. Among the several melatonin actions, the most characteristic one is the regulation of sleep-wake cycles, melatonin has anti-inflammatory and antioxidant properties. Since brain barriers disruption can arise from inflammation and oxidative stress, knowing the influence of melatonin on the integrity of brain barriers is extremely important. Therefore, the objective of this review is to gather and discuss the available literature about the regulation of brain barriers by melatonin.
Identifiants
pubmed: 39395545
pii: S0091-3022(24)00038-4
doi: 10.1016/j.yfrne.2024.101158
pii:
doi:
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
101158Informations de copyright
Copyright © 2024 The Author(s). Published by Elsevier Inc. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.