Protective Effects of Piceatannol against Beta-Amyloid-Induced Neuronal Cell Death

摘要

Beta-amyloid (Aβ) is a main component of senile plaques in Alzheimer's disease (AD) that induces neuronal cell death. Since reactive oxygen species (ROS) have been implicated in Aβ-induced neurotoxicity, considerable attention has recently been focused on identifying natu rally occurring antioxidative phenolic phytochemicals that are able to decrease ROS levels. Piceatannol (trans-3,4,3',5'-tetrahydroxystilbene), which has a structure homologous to resveratrol, is an anti-inflammatory and antiproliferative stilbene compound derived from plants. This article investigated the possible protective effects of piceatannol on Aβ-induced PC12 neuronal cell death, and found that piceatannol exerted much stronger protective effects than did resveratrol. Piceatannol treatment attenuated the intracellular accumulation of ROS induced by treatment of PC12 cells with Ap, inhibited Aβ-induced apoptotic features include ing internucleosomal DNA fragmentation, nucleus condensation, cleav age of poly(ADP-ribose) polymerase (PARP), and activation of caspase-3. These results suggest that piceatannol blocks Aβ-induced accumulation of ROS, thereby protecting PC12 cells from oxidative stress.