Effects of (-)-epicatechin on neuroinflammation and hyperphosphorylation of tau in the hippocampus of aged mice.
Aging
/ drug effects
Amyloid beta-Peptides
/ metabolism
Animals
Anti-Inflammatory Agents
/ pharmacology
Catechin
/ pharmacology
Cytokines
/ metabolism
Glial Fibrillary Acidic Protein
/ metabolism
Hippocampus
/ metabolism
Inflammation
/ drug therapy
Male
Mice
Mice, Inbred C57BL
Oxidative Stress
/ drug effects
Phosphorylation
tau Proteins
/ metabolism
Journal
Food & function
ISSN: 2042-650X
Titre abrégé: Food Funct
Pays: England
ID NLM: 101549033
Informations de publication
Date de publication:
01 Dec 2020
01 Dec 2020
Historique:
pubmed:
18
11
2020
medline:
2
6
2021
entrez:
17
11
2020
Statut:
ppublish
Résumé
Evidence has implicated oxidative stress (OS) and inflammation as drivers of neurodegenerative pathologies. We previously reported on the beneficial effects of (-)-epicatechin (Epi) treatment on aging-induced OS and its capacity to restore modulators of mitochondrial biogenesis in the prefrontal cortex of 26-month-old male mice. In the present study using the same mouse model of aging, we examined the capacity of Epi to mitigate hippocampus OS, inflammation, hyperphosphorylation of tau protein, soluble β-amyloid protein levels, cell survival, memory, anxiety-like behavior levels and systemic inflammation. Mice were subjected to 4 weeks of Epi treatment (1 mg kg
Identifiants
pubmed: 33201160
doi: 10.1039/d0fo02438d
pmc: PMC7746633
mid: NIHMS1650067
doi:
Substances chimiques
Amyloid beta-Peptides
0
Anti-Inflammatory Agents
0
Cytokines
0
Glial Fibrillary Acidic Protein
0
tau Proteins
0
Catechin
8R1V1STN48
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
10351-10361Subventions
Organisme : NIDDK NIH HHS
ID : R01 DK098717
Pays : United States
Organisme : NIA NIH HHS
ID : R21 AG047326
Pays : United States
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