Abstract
The present study examines the effect of the cognition enhancer (1R)-1-benzo[b]thiophen-5-yl-2-[2-(diethylamino)ethoxy]ethan-1-ol hydrochloride (T-588) on neuronal injury induced by serum deprivation or amyloid-beta protein (A beta). T-588 protected partially against neuronal injury induced by serum deprivation or A beta in cultured cortical neurons. T-588 did not affect the phosphorylation of extracellular signal-regulated kinase (ERK) in cortical neurons and SH-SY5Y cells. These results suggest that T-588 has a protective effect in neuronal injury models and the effect is not mediated by an ERK signal pathway.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Amyloid beta-Peptides / toxicity*
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Animals
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Cell Line, Tumor
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Cells, Cultured
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Cerebral Cortex / drug effects
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Cerebral Cortex / metabolism
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Culture Media, Serum-Free / pharmacology
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Diethylamines / pharmacology*
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Humans
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Mitogen-Activated Protein Kinases / metabolism
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Neurons / drug effects*
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Neurons / metabolism
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Neuroprotective Agents / pharmacology*
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Peptide Fragments / toxicity*
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Rats
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Thiophenes / pharmacology*
Substances
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Amyloid beta-Peptides
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Culture Media, Serum-Free
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Diethylamines
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Neuroprotective Agents
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Peptide Fragments
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Thiophenes
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amyloid beta-protein (25-35)
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T 588
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Mitogen-Activated Protein Kinases