Protective effects of a chalcone derivative against Aβ-induced oxidative stress and neuronal damage

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Authors: Mi-Jeong Kim ; Yoo-Hyun Lee ; Jieun Kwak ; Younghwa Na ; Ho-Geun Yoon

MeSH: Amyloid beta-Peptides/administration & dosage ; Amyloid beta-Peptides/toxicity* ; Animals ; Body Weight/drug effects ; Cell Death/drug effects ; Cell Survival/drug effects ; Chalcone/administration & dosage ; Chalcone/analogs & derivatives* ; Chalcone/chemistry ; Chalcone/pharmacology* ; Free Radical Scavengers/pharmacology ; Male ; Memory/drug effects ; Mice ; Mice, Inbred ICR ; Neurons/drug effects* ; Neurons/pathology* ; Neuroprotective Agents/pharmacology* ; Oxidative Stress/drug effects* ; PC12 Cells ; Peptide Fragments/administration & dosage ; Peptide Fragments/toxicity* ; Rats

Keywords: Alzheimer's disease ; Chalcone derivative ; Cognitive function ; Neuroprotective effect ; β-amyloid

Abstract: Amyloid Β-peptide (AΒ-peptide)-induced oxidative stress is thought to be a critical component of the pathophysiology of Alzheimer's disease (AD). New chalcone derivatives, the Chana series, were recently synthesized from the retrochalcones of licorice. In this study, we investigated the protective effects of the Chana series against neurodegenerative changes in vitro and in vivo. Among the Chana series, Chana 30 showed the highest free radical scavenging activity (90.7%) in the 1,1-diphenyl-2- picrylhydrazyl assay. Chana 30 also protected against AΒ-induced neural cell injury in vitro. Furthermore, Chana 30 reduced the learning and memory deficits of AΒ(1-42)-peptide injected mice. Taken together, these results suggest that Chana 30 may be a promising candidate as a potent therapeutic agent against neurodegenerative diseases.