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Protective Effects of Piceatannol against Beta‐Amyloid–Induced Neuronal Cell Death
Author(s) -
KIM HYO JIN,
LEE KI WON,
LEE HYONG JOO
Publication year - 2007
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1397.051
Subject(s) - piceatannol , chemistry , reactive oxygen species , programmed cell death , poly adp ribose polymerase , neurotoxicity , apoptosis , resveratrol , oxidative stress , microbiology and biotechnology , amyloid beta , senile plaques , intracellular , dna damage , pharmacology , biochemistry , alzheimer's disease , biology , toxicity , polymerase , enzyme , medicine , dna , peptide , disease , organic chemistry , pathology
: 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 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 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 Aβ, inhibited Aβ‐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 Aβ‐induced accumulation of ROS, thereby protecting PC12 cells from oxidative stress.