Protective effects of piceatannol against beta-amyloid-induced neuronal cell death.

Abstract:

:Beta-amyloid (Abeta) 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 Abeta-induced neurotoxicity, considerable attention has recently been focused on identifying naturally 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 Abeta-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 Abeta, inhibited Abeta-induced apoptotic features including internucleosomal DNA fragmentation, nucleus condensation, cleavage of poly(ADP-ribose) polymerase (PARP), and activation of caspase-3. These results suggest that piceatannol blocks Abeta-induced accumulation of ROS, thereby protecting PC12 cells from oxidative stress.

journal_name

Ann N Y Acad Sci

authors

Kim HJ,Lee KW,Lee HJ

doi

10.1196/annals.1397.051

subject

Has Abstract

pub_date

2007-01-01 00:00:00

pages

473-82

eissn

0077-8923

issn

1749-6632

pii

1095/1/473

journal_volume

1095

pub_type

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