114E-28 |
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H. J. HEO1, S. J. Choi2, H. K. Kim3, and D. H. Shin*2. (1) Food Science & Technology, Cornell Univ., New York State Agricultural Experiment Station, 630 W. North St., Geneva, NY 14456-1371, (2) Graduate School of Biotechnology, Korea University, Anam-dong 5-1, SungBuk-gu, Seoul, 136-701, South Korea, (3) Department of Food and Biotechnology, Hanseo University, DaeGok-li 360, HaeMi-myeon, Seosan, ChungNam, 356-706, South Korea Amyloid b protein (Ab)-induced free radical-mediated neurotoxicity is known as a leading hypothesis for a cause of Alzheimer’s disease. Ab increased free radical production and lipid peroxidation in PC12 nerve cells, resulting in apoptosis and cell death. The protective effect of naringenin, a major flavanone constituent isolated from Citrus junos, against Ab-induced neurotoxicity was investigated using PC12 cells. Pretreatment with isolated naringenin and vitamin C prevented the generation of the Ab-induced reactive oxygen species. Naringenin resulted in the decrease of Ab toxicity in a manner of concentration-dependence, which was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. However, treatment with these antioxidants inhibited the Ab-induced neurotoxic effect. The anti-amnestic activity of naringenin in vivo was also evaluated using ICR mice with amnesia induced by scopolamine (1 mg/kg body weight). Naringenin, when administered to ICR mice at 4.5 mg/kg body weight, significantly ameliorated scopolamine-induced amnesia as measured in the passive avoidance test. Therefore, these results indicate that micro-molecular Ab-induced oxidative cell stress is reduced by naringenin and naringenin may be a useful chemopreventive agent against a neurodegenerative disease such as Alzheimer’s disease.
Session 114E, Nutraceuticals & Functional Foods: Bioactivity measurement and mechanism
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