Neuroprotective effects
of SUN11602 and basic fibroblast growth
factor (bFGF) against glutamate-induced toxicity (150 μM) in
primary cultures of rat cerebrocortical neurons. The open bars reveal
that the effectiveness of SUN11602 and bFGF is ascribed to unimpaired
protein synthesis, by which they can activate their neuroprotective
mechanisms. Their neuroprotective effects were abolished by treatment
with either actinomycin D (1 μg/mL, black bar) or cycloheximide
(1 μg/mL, gray bar), which can interfere with transcription
or translation, respectively. Actinomycin D or cycloheximide was first
added to the cultures, and, 2 h later, SUN11602 or bFGF was added.
After a 24 h incubation, neurons in the cultures were exposed to 150
μM glutamate for another 24 h, and cell viability was determined
by a (3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H tetrazolium bromide
(MTT) assay. ***p < 0.001 compared to glutamate
alone (means ± SEM, n = 6, Dunnett’s
multiple comparison test).