KMID : 0880520140500020045
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Chonnam Medical Journal 2014 Volume.50 No. 2 p.45 ~ p.51
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Effects of Flavonoid Compounds on ¥â-amyloid-peptide-induced Neuronal Death in Cultured Mouse Cortical Neurons
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Choi Seong-Min
Kim Byeong-Chae Cho Yeun-Hee Choi Kang-Ho Chang Jane Park Man-Seok Kim Myeong-Kyu Cho Ki-Hyun Kim Jong-Keun
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Abstract
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Excessive accumulation of ¥â-amyloid peptide (A¥â) 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 A¥â-induced neuronal death by examining the effects of various flavonoids on the neurotoxicity of A¥â fragment 25-35 (A¥â25-35) in mouse cortical cultures. A¥â25-35 induced concentration- and exposure-time-dependent neuronal death. Neuronal death induced by 20 ¥ìM A¥â25-35 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 ¥ìM also significantly inhibited neuronal death induced by 20 ¥ìM A¥â25-35 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 A¥â-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.
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KEYWORD
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¥â-Amyloid peptide, Alzheimer¡¯s disease, Flavonoids
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