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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 11 time in
Web of Science
Cited 13 time in Scopus
- Authors
- Issue Date
- 2007-06-30
- Publisher
- Wiley-Blackwell
- Citation
- J Neurosci Res. 2007 Aug 15;85(11):2500-11.
- Keywords
- Amyloid beta-Protein/toxicity ; Animals ; Apoptosis/drug effects ; Blotting, Western ; Caspase 3/drug effects ; Cognition/drug effects ; Coumaric Acids/*pharmacology ; Cytochromes c/drug effects ; Dementia/chemically induced/*drug therapy ; Disease Models, Animal ; Enzyme Activation/drug effects ; In Situ Nick-End Labeling ; Muscarinic Antagonists/toxicity ; Neuroprotective Agents/chemistry/*pharmacology ; Pyrones/*pharmacology ; Rats ; Rats, Wistar ; Reactive Oxygen Species/metabolism ; Scopolamine/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
https://hdl.handle.net/10371/24377
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