POSTER PRESENTATION ABSTRACTS
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Salons 10-12.
THURSDAY, 10:15-11:00 AM
Koo KA, Kim SH*, Lee MK, Jeong EJ, Kim YC.
Acteoside and its aglycones attenuate glutamate-induced
neurotoxicity in rat cortical cultures.
College of Pharmacy, Seoul National University
youngkim@snu.ac.kr *Presenting
author
In the course of our search for neuroprotective compounds
from natural products using glutamate-injured primary cultures of rat
cortical cells as a screening system, we found that the methanol extract
of the leaves of Callicarpa dichototma Rauaeuschel (Verbenaceae)
has significant neuroprotective activity (63.7% protection at 50 _g/ml,
p<0.01). By bioactivity-guided fractionation, we isolated acteoside,
a phenylethanoid glycoside, as an active constituent (72.2% protection
at 10 _M, p<0.01). To determine the essential structural moiety within
this phenylethanoid glycoside needed to exert neuroprotective activity,
acteoside was hydrolyzed with acid into its aglycones, caffeic acid
and 3_,4_-dihydroxyphenylethanoid. Caffeic acid and 3_,4_-dihydroxyphenylethanoid
also showed significant neuroprotective activities (55.0% and 58.3%
protection at 10 _M, respectively, p<0.01). Acteoside and its aglycones
inhibited glutamate-induced intracellular Ca2+ influx resulting in overproduction
of nitric oxide and reduced the formation of reactive oxygen species.
These compounds preserved the mitochondrial membrane potential and the
activities of antioxidative enzymes, such as superoxide dismutase, glutathione
reductase and glutathione peroxidase reduced by glutamate. It was followed
by the preservation of the level of glutathione and finally the inhibition
of membrane lipid peroxidation. In addition, they effectively scavenged
SNAP-released nitric oxide or DPPH radicals in our experimental systems.
At present, the enhancement of the antioxidative defense system by acteoside,
caffeic acid and 3_,4_-DHPE accompanied by the decrease of Ca2+ entry
results in the attenuation of glutamate-induced neurotoxicity. These
results offer acteoside, caffeic acid and 3_,4_-DHPE as useful therapeutic
candidates for the treatment of neurodegenerative disorders.
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