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A novel compound, maltolyl p-coumarate, attenuates cognitive deficits and shows neuroprotective effects in vitro and in vivo dementia models

Cited 10 time in Web of Science Cited 11 time in Scopus
Authors
Shin, Ki Young; Lee, Geon Ho; Park, Cheol Hyoung; Kim, Hee Jin; Park, Soo-Hyun; Kim, Seonghan; Kim, Hye-Sun; Lee, Kwan-Sun; Won, Beom Young; Lee, Hyung Gun; Choi, Jin-Ho; Suh, Yoo-Hun
Issue Date
2007-06-30
Publisher
Wiley-Blackwell
Citation
J Neurosci Res. 2007 Aug 15;85(11):2500-11.
Keywords
Amyloid beta-Protein/toxicityAnimalsApoptosis/drug effectsBlotting, WesternCaspase 3/drug effectsCognition/drug effectsCoumaric Acids/*pharmacologyCytochromes c/drug effectsDementia/chemically induced/*drug therapyDisease Models, AnimalEnzyme Activation/drug effectsIn Situ Nick-End LabelingMuscarinic Antagonists/toxicityNeuroprotective Agents/chemistry/*pharmacologyPyrones/*pharmacologyRatsRats, WistarReactive Oxygen Species/metabolismScopolamine/toxicity
Abstract
To develop a novel and effective drug that could enhance cognitive function and neuroprotection, we newly synthesized maltolyl p-coumarate by the esterification of maltol and p-coumaric acid. In the present study, we investigated whether maltolyl p-coumarate could improve cognitive decline in scopolamine-injected rats and in amyloid beta peptide(1-42)-infused rats. Maltolyl p-coumarate was found to attenuate cognitive deficits in both rat models using passive avoidance test and to reduce apoptotic cell death observed in the hippocampus of the amyloid beta peptide(1-42)-infused rats. We also examined the neuroprotective effects of maltolyl p-coumarate in vitro using SH-SY5Y cells. Cells were pretreated with maltolyl p-coumarate, before exposed to amyloid beta peptide(1-42), glutamate or H2O2. We found that maltolyl p-coumarate significantly decreased apoptotic cell death and reduced reactive oxygen species, cytochrome c release, and caspase 3 activation. Taking these in vitro and in vivo results together, our study suggests that maltolyl p-coumarate is a potentially effective candidate against Alzheimer's disease that is characterized by wide spread neuronal death and progressive decline of cognitive function.
ISSN
0360-4012 (Print)
Language
English
URI
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=17600377

http://hdl.handle.net/10371/24377
DOI
https://doi.org/10.1002/jnr.21397
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College of Medicine/School of Medicine (의과대학/대학원)Pharmacology (약리학전공)Journal Papers (저널논문_약리학전공)
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