Protective effect of 4 ',5-dihydroxy-3 ',6,7-trimethoxyflavone from Artemisia asiatica against A beta-indueed oxidative stress in PC12 cells

Amyloid beta protein (A beta)-induced free radical-mediated neurotoxicity i s a leading hypothesis as a cause of Alzheimer's disease (AD). A beta incre ased free radical production and lipid peroxidation in PC12 nerve cells, le ading to apoptosis and cell death. The effect of 4',5-dihydroxy-3',6,7-trim ethoxyflavone from Artemisia asiatica on A beta induced neurotoxicity was i nvestigated using PC12 cells. Pretreatment with isolated 4',5-dihydroxy-3', 6,7-trimethoxyflavone and vitamin E prevented the A beta -induced reactive oxygen species (ROS). The 4',5-dihydroxy-3,6,7-trimethoxyflavone resulted i n concentration-dependant decreased A beta toxicity assessed by 3-(4,5-dime thylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. However, tre atment with these antioxidants inhibited the A beta -induced neurotoxic eff ect. Therefore, these results indicate that micromolecular A beta -induced oxidative cell stress is reduced by 4',5-dihydroxy-3',6,7-trimethoxyflavone from Artemisia asiatica.