Please use this identifier to cite or link to this item: http://cmuir.cmu.ac.th/jspui/handle/6653943832/68206
Title: 5,6,7,4’-tetramethoxyflavanone protects against neuronal degeneration induced by dexamethasone by attenuating amyloidogenesis in mice
Authors: Kanet Pakdeepak
Ratchanaporn Chokchaisiri
Jiraporn Tocharus
Pranglada Jearjaroen
Chainarong Tocharus
Apichart Suksamrarn
Keywords: Agricultural and Biological Sciences
Biochemistry, Genetics and Molecular Biology
Pharmacology, Toxicology and Pharmaceutics
Issue Date: 1-Jan-2020
Abstract: © 2020, Leibniz Research Centre for Working Environment and Human Factors. All rights reserved. Long-term exposure to high glucocorticoid levels induces memory impairment and neurodegeneration in Alzheimer’s disease (AD) by increasing the expression of amyloid β and tau hyperphosphorylation (pTau). Previous studies showed beneficial effects of flavonoids in neurodegenerative models. 5,6,7,4'-tetramethoxyflavanone (TMF) is one of the active ingredients in Chromolaena odorata (L.), which R. M. King and H. Rob discovered in Thailand. This study focused on the effects of TMF on dexamethasone (DEX)-induced neurodegeneration, amyloidogenesis, pTau expression, neuron synaptic function, and cognitive impairment and the potential mechanisms involved. Mice were intraperitoneally administered DEX for 28 days before being treated with TMF for 30 days. The mice were randomly divided into six groups (twelve mice per group): control; TMF administration (40 mg/kg); pioglitazone administration (20 mg/kg); DEX administration (60 mg/kg); DEX administration plus TMF; and DEX administration plus pioglitazone. Behavioral tests showed that TMF significantly attenuated the memory impairment triggered by DEX. Consistently, TMF reduced DEX-induced amyloid beta production by reducing the expression of beta-site APP cleaving enzyme 1 (BACE1) and presenilin 1 (PS1), whereas it increased the gene expression of a disintegrin and metalloprotease 10 (ADAM10). TMF treatment also decreased pTau expression, inhibited phosphonuclear factor-kappa B (pNF-kB) and inhibited glycogen synthase kinase 3 (GSK-3) activity by increasing GSK3 phosphorylation (pGSK3). In addition, TMF also improved synaptic function by increasing the expression of synaptophysin (Syn) and postsynaptic density protein 95 (PSD95) while decreasing acetylcholine esterase activity. Conclusively, TMF provided neuroprotection against DEX-induced neurodegeneration. These findings suggest that TMF might have potential as a therapeutic drug for AD.
URI: https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85078559113&origin=inward
http://cmuir.cmu.ac.th/jspui/handle/6653943832/68206
ISSN: 16112156
Appears in Collections:CMUL: Journal Articles

Files in This Item:
There are no files associated with this item.


Items in CMUIR are protected by copyright, with all rights reserved, unless otherwise indicated.