Effects of Flavonoid Compounds on beta-amyloid-peptide-induced Neuronal Death in Cultured Mouse Cortical Neurons
- Author:
Seong Min CHOI
1
;
Byeong C KIM
;
Yeun Hee CHO
;
Kang Ho CHOI
;
Jane CHANG
;
Man Seok PARK
;
Myeong Kyu KIM
;
Ki Hyun CHO
;
Jong Keun KIM
Author Information
- Publication Type:Original Article
- Keywords: beta-Amyloid peptide; Alzheimer's disease; Flavonoids
- MeSH: Alzheimer Disease; Animals; Antioxidants; Apigenin; Ascorbic Acid; Catechin; Flavonoids; Luteolin; Mice; Neurons; Neuroprotective Agents; Oxidative Stress; Plant Cells; Quercetin
- From:Chonnam Medical Journal 2014;50(2):45-51
- CountryRepublic of Korea
- Language:English
- Abstract: Excessive accumulation of beta-amyloid peptide (Abeta) is one of the major mechanisms responsible for neuronal death in Alzheimer's disease. Flavonoids, primarily antioxidants, are a group of polyphenolic compounds synthesized in plant cells. The present study aimed to identify flavonoid compounds that could inhibit Abeta-induced neuronal death by examining the effects of various flavonoids on the neurotoxicity of Abeta fragment 25-35 (Abeta25-35) in mouse cortical cultures. Abeta25-35 induced concentration- and exposure-time-dependent neuronal death. Neuronal death induced by 20 microM Abeta25-35 was significantly inhibited by treatment with either Trolox or ascorbic acid. Among 10 flavonoid compounds tested [apigenin, baicalein, catechin, epicatechin, epigallocatechin gallate (EGCG), kaempferol, luteolin, myricetin, quercetin, and rutin], all except apigenin showed strong 1,1-diphenyl-2-pycrylhydrazyl (DPPH) scavenging activity under cell-free conditions. The flavonoid compounds except apigenin at a concentration of 30 microM also significantly inhibited neuronal death induced by 20 microM Abeta25-35 at the end of 24 hours of exposure. Epicatechin, EGCG, luteolin, and myricetin showed more potent and persistent neuroprotective action than did the other compounds. These results demonstrated that oxidative stress was involved in Abeta-induced neuronal death, and antioxidative flavonoid compounds, especially epicatechin, EGCG, luteolin, and myricetin, could inhibit neuronal death. These findings suggest that these four compounds may be developed as neuroprotective agents against Alzheimer's disease.
