Inhibition of β-amyloid peptide-induced neurotoxicity by kaempferol 3-O-(6″-acetyl)-β-glucopyranoside from butterbur (Petasites japonicus) leaves in B103 cells

One of predominant hallmarks in Alzheimer's disease (AD) is extracellular senile plaques containing β-amyloid peptide (Aβ). Aβ is known to be directly responsible for the free radical production and lipid peroxidation, leading to apoptosis and cellular death. In this study, we investigated the possible protective effect of kaempferol 3-O-(6″-acetyl)-β- glucopyranoside (KAG) isolated from butterbur (Petasites japonicus) leaves against Aβ-induced neurotoxicity. Exposure of mouse neuroblastoma B103 cells to Aβ(25-35) at the concentration of 50 μM significantly reduced cellular viability and increased both oxidative stress and apoptotic rate. However, pretreatment of B103 cell with isolated KAG at 10 μM significantly inhibited AP-induced apoptotic cellular damage and reactive oxygen species (ROS) generation. Pretreatment of KAG also completely inhibited caspase-3 activity to the basal level at the concentration of 10 μM. This study therefore demonstrated that Aβ induced cellular death might be prevented by KAG from butterbur leaves by the suppression of ROS and the subsequent recovery of apoptotic cell death.