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The chalcone derivative Chana 1 protects against amyloid β peptide-induced oxidative stress and cognitive impairment.

Authors
 Jieun Kwak  ;  Mi-Jeong Kim  ;  Kyung-Chul Choi  ;  Hyo-Kyung Choi  ;  Woojin Jun  ;  Hyun-Jin Park  ;  Yoo-Hyun Lee  ;  Ho-Geun Yoon 
Citation
 INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE, Vol.30(1) : 193-198, 2012 
Journal Title
 INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE 
ISSN
 1107-3756 
Issue Date
2012
MeSH
Alzheimer Disease/drug therapy* ; Amyloid beta-Peptides/metabolism* ; Animals ; Apoptosis/drug effects ; Cell Survival/drug effects ; Chalcone/analogs & derivatives* ; Chalcones/pharmacology* ; Chalcones/therapeutic use ; Chalcones/toxicity ; Cognition Disorders/drug therapy* ; Lethal Dose 50 ; Male ; Maze Learning ; Memory Disorders/drug therapy* ; Mice ; Mice, Inbred ICR ; Neuroprotective Agents/pharmacology ; Neuroprotective Agents/therapeutic use* ; Oxidative Stress/drug effects* ; Oximes/pharmacology* ; Oximes/therapeutic use ; Oximes/toxicity ; PC12 Cells ; Random Allocation ; Rats
Keywords
Alzheimer Disease/drug therapy* ; Amyloid beta-Peptides/metabolism* ; Animals ; Apoptosis/drug effects ; Cell Survival/drug effects ; Chalcone/analogs & derivatives* ; Chalcones/pharmacology* ; Chalcones/therapeutic use ; Chalcones/toxicity ; Cognition Disorders/drug therapy* ; Lethal Dose 50 ; Male ; Maze Learning ; Memory Disorders/drug therapy* ; Mice ; Mice, Inbred ICR ; Neuroprotective Agents/pharmacology ; Neuroprotective Agents/therapeutic use* ; Oxidative Stress/drug effects* ; Oximes/pharmacology* ; Oximes/therapeutic use ; Oximes/toxicity ; PC12 Cells ; Random Allocation ; Rats
Abstract
Alzheimer's disease (AD) is the most common neurodegenerative disease to cause dementia in the elderly. Amyloid β (Aβ)-peptide induced oxidative stress causes the initiation and progression of AD. Recently, new chalcone derivatives termed the Chana series were synthesized. Among them, Chana 1 showed high free radical scavenging activity (72.5%), as measured by a DPPH (1,1-diphenyl-2-picrylhydrazyl) assay. In this study, we investigated the effect of Chana 1 against Aβ-induced cytotoxicity and cognitive deficits. Additionally, we sought to estimate the lethal dose, 50% (LD50) of Chana 1 in mice using an acute oral toxicity test. We found that Chana 1 significantly protected against Aβ-induced neuronal cell death in PC12 cells. Oral administration of Chana 1 at a dose of 50 mg/kg body weight/day significantly improved Aβ-induced learning and memory impairment in mice, as measured in Y-maze and passive avoidance tests. In acute toxicity tests, the LD50 in mice was determined to be 520.44 mg/kg body weight. The data are valuable for future studies and suggest that Chana 1 has therapeutic potential for the management of neurodegenerative disease.
Full Text
http://www.spandidos-publications.com/ijmm/30/1/193
DOI
22552354
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Biochemistry and Molecular Biology (생화학-분자생물학교실) > 1. Journal Papers
Yonsei Authors
Kim, Mi Jeong(김미정) ORCID logo https://orcid.org/0000-0002-0758-7145
Yoon, Ho Geun(윤호근) ORCID logo https://orcid.org/0000-0003-2718-3372
Choi, Hyo Kyoung(최효경)
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/90494
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