Neobavaisoflavone Ameliorates Memory Deficits and Brain Damage in Aβ_25-35-Induced Mice by Regulating SIRT1.

ABSTRACT:

Background

Alzheimer's disease (AD) is a common chronic neurodegenerative disease in older people, and there is no specific treatment that can stop or reverse its progression. Neobavaisoflavone (NBIF) is a flavonoid that has been shown to have neuroprotective effects, but its role in AD has not been revealed. The present study investigated the role and mechanism of NBIF on Aβ_25-35-induced brain injury.

Methods

In this experiment, the AD mouse model was established by injection of Aβ_25-35 peptides (200 μM, icv), and Donepezil (Don, 10 mg/kg/days), NBIF-L (15 mg/kg/days), and NBIF-H (30 mg/kg/days) were administered orally for 4 weeks. Learning memory, hippocampal pathological changes, pathological markers, apoptosis, oxidative stress, inflammation, immun

SUBMITTER: Hao F 

PROVIDER: S-EPMC11469773 | biostudies-literature | 2024 Oct

REPOSITORIES: biostudies-literature