Propofol-induced hippocampal Neurotoxicity: A mitochondrial perspective.
Anesthesia
Apoptosis
Neurodegeneration
Protection
Journal
Brain research
ISSN: 1872-6240
Titre abrégé: Brain Res
Pays: Netherlands
ID NLM: 0045503
Informations de publication
Date de publication:
28 Feb 2024
28 Feb 2024
Historique:
received:
19
01
2024
revised:
25
02
2024
accepted:
27
02
2024
medline:
2
3
2024
pubmed:
2
3
2024
entrez:
1
3
2024
Statut:
aheadofprint
Résumé
Propofol is a frequently used anesthetic. It can induce neurodegeneration and inhibit neurogenesis in the hippocampus. This effect may be temporary. It can, however, become permanent in vulnerable populations, such as the elderly, who are more susceptible to Alzheimer's disease, and neonates and children, whose brains are still developing and require neurogenesis. Current clinical practice strategies have failed to provide an effective solution to this problem. In addition, the molecular mechanism of this toxicity is not fully understood. Recent advances in molecular research have revealed that apoptosis, in close association with mitochondria, is a crucial mechanism through which propofol contributes to hippocampal toxicity. Preventing the toxicity of propofol on the hippocampus has shown promise in in-vivo, in-vitro, and to a lesser extent human studies. This study seeks to provide a comprehensive literature review of the effects of propofol toxicity on the hippocampus via mitochondria and to suggest translational suggestions based on these molecular results.
Identifiants
pubmed: 38428475
pii: S0006-8993(24)00095-7
doi: 10.1016/j.brainres.2024.148841
pii:
doi:
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
148841Informations de copyright
Copyright © 2024. Published by Elsevier B.V.