Protective effect of 4',5-dihydroxy-3',6,7-trimethoxyflavone from Artemisia asiatica against Abeta-induced oxidative stress in PC12 cells.

H J Heo, H Y Cho, B Hong, H K Kim, E K Kim, B G Kim, D H Shin

Index: Amyloid 8(3) , 194-201, (2001)

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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.