Abstract |
Gastrodin (Gas) has exhibited protective activity in neurological disorders. Here, we investigated the neuroprotective effect and potential mechanisms of Gas against cognitive impairment via regulating gut microbiota. APPswe/PSEN1dE9 transgenic (APP/PS1) mice were treated intragastrically with Gas for 4 weeks, and then cognitive deficits, deposits of amyloid-β (Aβ) and phosphorylation of tau were analyzed. The expression levels of insulin-like growth factor-1 (IGF-1) pathway-related proteins, such as cAMP response element-binding protein (CREB), were detected. Meanwhile, gut microbiota composition was evaluated. Our results showed that Gas treatment significantly improved cognitive deficits and Aβ deposition in APP/PS1 mice. Moreover, Gas treatment increased the level of Bcl-2 and decreased level of Bax and ultimately inhibited neuronal apoptosis. Gas treatment markedly increased the expression levels of IGF-1 and CREB in APP/PS1 mice. Moreover, Gas treatment improved abnormal composition and structure of gut microbiota in APP/PS1 mice. These findings revealed that Gas actively participated in regulating the IGF-1 pathway to inhibit neuronal apoptosis via the gut-brain axis and that it can be considered a new therapeutic strategy against Alzheimer's disease.
|
Authors | Yuhe Zhang, Yan Chen, Shushu Yuan, Qingxia Yu, Jianjiong Fu, Luyun Chen, Jiaming Liu, Yuping He |
Journal | Experimental brain research
(Exp Brain Res)
Vol. 241
Issue 6
Pg. 1661-1673
(Jun 2023)
ISSN: 1432-1106 [Electronic] Germany |
PMID | 37199774
(Publication Type: Journal Article)
|
Copyright | © 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature. |
Chemical References |
- Insulin-Like Growth Factor I
- gastrodin
- Amyloid beta-Peptides
|
Topics |
- Mice
- Animals
- Insulin-Like Growth Factor I
- Brain-Gut Axis
- Mice, Transgenic
- Alzheimer Disease
(drug therapy)
- Amyloid beta-Peptides
- Cognitive Dysfunction
(etiology)
- Disease Models, Animal
|