ReferenceID 739

Safflower leaf ameliorates cognitive impairment through moderating excessive astrocyte activation in APP/PS1 mice

Food Funct

In addition to beta-amyloid (Abeta) plaques and neurofibrillary tangles, Alzheimer's disease (AD) is typically triggered or accompanied by abnormal inflammation, oxidative stress and astrocyte activation. Safflower (Cart

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Reference Id
739
Evidence Id
17329
Core Evidence Id
17329
Source Reference Id
1460
Herb2 Reference Id
HBREF002257
Subject Paper Key
HERB002276_34730571
Pubmed Id
34730571
Doi
10.1039/d1fo01755a
Paper Title
Safflower leaf ameliorates cognitive impairment through moderating excessive astrocyte activation in APP/PS1 mice
Paper Abstract
In addition to beta-amyloid (Abeta) plaques and neurofibrillary tangles, Alzheimer's disease (AD) is typically triggered or accompanied by abnormal inflammation, oxidative stress and astrocyte activation. Safflower (Carthamus tinctorius L.) leaf, featuring functional ingredients, is a commonly consumed leafy vegetable. Whether and how dietary safflower leaf powder (SLP) ameliorates cognitive function in an AD mouse model has remained minimally explored. Therefore, we orally administered SLP to APP/PS1 transgenic mice to explore the neuroprotective effects of SLP in preventing AD progression. We found that SLP markedly improved cognitive impairment in APP/PS1 mice, as indicated by the water maze test. We further demonstrated that SLP treatment ameliorated inflammation, oxidative stress and excessive astrocyte activation. Further investigation indicated that SLP decreased the Abeta burden in APP/PS1 mice by mediating excessive astrocyte activation. Our study suggests that safflower leaf is possibly a promising, cognitively beneficial food for preventing and alleviating AD-related dementia.
Journal
Food Funct
Publish Year
2021
Experiment Subject
mouse
Experiment Type
Animal Experiment
Phenotype Related
Ad-related Dementia; Neurofibrillary Tangles; Alzheimer's Disease
Paper Title Cn
Paper Title En
Safflower leaf ameliorates cognitive impairment through moderating excessive astrocyte activation in APP/PS1 mice
Bilingual Status
semi_complete