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

Abstract

Amyloid βprotein (Aβ)-induced free radical-mediated neurotoxicity is a leading hypothesis as a cause of Alzheimer's disease (AD), A β increased free radical production and lipid per oxidation in PC12 nerve cells, leading to apoptosis and cell death. The effect of 4′,5-dihydroxy-3′, 6,7-trimethoxyflmone fom Artemisia asiatica on A β induced neurotoxicity was investigated using PC12 cells. Pretreatment with isolated 4′,5-dihydroxy-3′,6,7-trimethoxyflavone and vitamin Eprevented the Aβ-induced reactive oxygen species (ROS). The 4′,5-dihydroxy-3′,6,7-trimethoxyflavone resulted in concentration-dependant decreased Aβ toxicity assessed by 3–(4,5– dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. However, treatment with these antioxidants inhibited the Aβ-induced neurotoxic effect. Therefore, these results indicate that micromolecular Aβ-induced oxidative cell stress is reduced by 4′, 5– dihydroxy-3 ', 6,7-trimethoxyflavone from Artemisia asiatica.

Key Words:

• 4′,5-dihydroxy-3′,6
• 7-trimethoxyflavone
• Artemisia asiatica
• Amyloid-β protein
• Oxidative stress
• Alzheimer's disease