| Literature DB >> 11676296 |
H J Heo1, H Y Cho, B Hong, H K Kim, E K Kim, B G Kim, D H Shin.
Abstract
Amyloid beta protein (Abeta)-induced free radical-mediated neurotoxicity is a leading hypothesis as a cause of Alzheimer's disease (AD). Abeta increased free radical production and lipid peroxidation in PC12 nerve cells, leading to apoptosis and cell death. The effect of 4',5-dihydroxy-3',6,7-trimethoxyflavone from Artemisia asiatica on Abeta induced neurotoxicity was investigated using PC12 cells. Pretreatment with isolated 4',5-dihydroxy-3',6,7-trimethoxyflavone and vitamin E prevented the Abeta-induced reactive oxygen species (ROS). The 4',5-dihydroxy-3',6,7-trimethoxyflavone resulted in concentration-dependant decreased Abeta toxicity assessed by 3-(4, 5- dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. However, treatment with these antioxidants inhibited the Abeta-induced neurotoxic effect. Therefore, these results indicate that micromolecular Abeta-induced oxidative cell stress is reduced by 4,5-dihydroxy-3',6,7-trimethoxyflavone from Artemisia asiatica.Entities:
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Year: 2001 PMID： 11676296 DOI： 10.3109/13506120109007362
Source DB: PubMed Journal: Amyloid ISSN： 1350-6129 Impact factor: 7.141