CGA ameliorates cognitive decline by regulating the PI3K/AKT signaling pathway and neurotransmitter systems in rats with multi-infarct dementia.
PI3K/AKT signaling pathway
astragalosides
energy charge
ginsenosides
multi-infarct dementia
Journal
Experimental and therapeutic medicine
ISSN: 1792-0981
Titre abrégé: Exp Ther Med
Pays: Greece
ID NLM: 101531947
Informations de publication
Date de publication:
Nov 2020
Nov 2020
Historique:
received:
05
06
2019
accepted:
13
02
2020
entrez:
23
9
2020
pubmed:
24
9
2020
medline:
24
9
2020
Statut:
ppublish
Résumé
Multi infarct dementia (MID) is a form of dementia that is preventable and treatable. However, at present, the drugs used in MID treatment were developed for Alzheimer's disease. While only a limited range of drugs is available, the incidence of MID is increasing year on year. The present study aimed to investigate the effect and underlying mechanisms of a combination of ginsenosides and astragalosides (CGA) on cognitive decline in rats with MID. A rat model of MID was established using micro-thromboembolism, and the behavioral changes in the rats were evaluated using the Morris water maze and open field tests at 60 days post-CGA intervention. The pathological morphology of the hippocampal CA1 area was observed using hematoxylin and eosin staining. The contents of ATP, ADP and AMP were determined using high-performance liquid chromatography. Mitochondrial swelling and changes in the membrane potential in the hippocampus were detected using flow cytometry, and the changes in insulin, glutamate and γ-aminobutyric acid (GABA) content were detected using ELISA. Additionally, the expression of PI3K and AKT proteins was detected using western blot analysis. In a rat model of MID, CGA shortened the escape latency, increased the frequency of platform crossing, improved the disordered vertebral cell arrangement and reduced the cell number in the hippocampal CA1 area. CGA also reduced the degree of mitochondrial swelling, increased the mitochondrial membrane potential, and elevated the energy load and ATP content in the brain of rats with MID. Furthermore, CGA increased the insulin content and upregulated the expression of PI3K and AKT in the brain of rats with MID. In addition, in the rat model of MID, CGA also enhanced the movement time and the frequency of standing, and decreased the concentration of glutamate and GABA in the brain tissue. Amelioration of the cognitive decline in rats with MID by CGA was associated with its regulatory effect on the PI3K/AKT signaling pathway and neurotransmitter systems.
Identifiants
pubmed: 32963600
doi: 10.3892/etm.2020.9198
pii: ETM-0-0-09198
pmc: PMC7490799
doi:
Types de publication
Journal Article
Langues
eng
Pagination
70Informations de copyright
Copyright: © Fu et al.
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