The effects of festidinol treatment on the D-galactose and aluminum chloride-induced Alzheimer-like pathology in mouse brain.
Aluminum chloride
Alzheimer-like pathology
D-galactose
Festidinol
Inflammation
Oxidative stress
Journal
Phytomedicine : international journal of phytotherapy and phytopharmacology
ISSN: 1618-095X
Titre abrégé: Phytomedicine
Pays: Germany
ID NLM: 9438794
Informations de publication
Date de publication:
Apr 2022
Apr 2022
Historique:
received:
08
10
2021
revised:
19
12
2021
accepted:
02
01
2022
pubmed:
2
2
2022
medline:
2
2
2022
entrez:
1
2
2022
Statut:
ppublish
Résumé
Festidinol is a flavan-3-ol which has been shown to reduce advanced glycation end products (AGEs) and reactive oxygen species, both of which play a crucial role in the pathology of many neurodegenerative diseases. This study aimed to investigate the effects of festidinol on oxidative stress, amyloidogenesis, phosphorylated tau (pTau) expression, synaptic function, and cognitive impairment, and the potential mechanisms involved, in a mouse model with an Alzheimer-like pathology. D-galactose (150 mg/kg) and aluminum chloride (10 mg/kg) were injected intraperitoneally into 40 mice for 90 days to generate an AD mouse model with cognitive impairment. Festidinol (30 mg/kg) and donepezil (5 mg/kg) were then administered orally for 90 days after which behavior and molecular changes in the brain were measured. The aluminum accumulated and the expression of the cell senescence marker P16 increased after exposure to D-galactose and AlCl Festidinol can ameliorate learning and memory impairments by modulating amyloidogenesis, tau hyperphosphorylation, cholinergic activity, neuroinflammation, and oxidative stress, and by regulating the brain-derived neurotrophic factor signaling pathway.
Sections du résumé
BACKGROUND
BACKGROUND
Festidinol is a flavan-3-ol which has been shown to reduce advanced glycation end products (AGEs) and reactive oxygen species, both of which play a crucial role in the pathology of many neurodegenerative diseases.
PURPOSE
OBJECTIVE
This study aimed to investigate the effects of festidinol on oxidative stress, amyloidogenesis, phosphorylated tau (pTau) expression, synaptic function, and cognitive impairment, and the potential mechanisms involved, in a mouse model with an Alzheimer-like pathology.
METHODS
METHODS
D-galactose (150 mg/kg) and aluminum chloride (10 mg/kg) were injected intraperitoneally into 40 mice for 90 days to generate an AD mouse model with cognitive impairment. Festidinol (30 mg/kg) and donepezil (5 mg/kg) were then administered orally for 90 days after which behavior and molecular changes in the brain were measured.
RESULTS
RESULTS
The aluminum accumulated and the expression of the cell senescence marker P16 increased after exposure to D-galactose and AlCl
CONCLUSION
CONCLUSIONS
Festidinol can ameliorate learning and memory impairments by modulating amyloidogenesis, tau hyperphosphorylation, cholinergic activity, neuroinflammation, and oxidative stress, and by regulating the brain-derived neurotrophic factor signaling pathway.
Identifiants
pubmed: 35104759
pii: S0944-7113(22)00003-4
doi: 10.1016/j.phymed.2022.153925
pii:
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
153925Informations de copyright
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