Abstract
We investigated the effects of an Na(+)/H(+) exchanger inhibitor, sabiporide, on excitotoxicity in cultured neuronal cells and in vivo. Sabiporide attenuated glutamate- or NMDA (N-methyl-d-aspartic acid)-induced neuronal cell death. Sabiporide also reduced glutamate or NMDA-induced increase in [Ca(2+)](i). In in vivo brain ischemia model, sabiporide produced protective effects, decreasing the infarct size and edema volume. Our results suggest that sabiporide elicits neuroprotective effect both in vitro and in vivo.
Publication types
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Comparative Study
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Brain Infarction / etiology
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Brain Infarction / pathology
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Brain Infarction / prevention & control
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Brain Ischemia / chemically induced
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Brain Ischemia / drug therapy
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Brain Ischemia / pathology*
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Calcium / metabolism
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Cell Death / drug effects
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Cells, Cultured
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Cerebral Cortex / pathology
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Disease Models, Animal
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Dose-Response Relationship, Drug
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Drug Interactions
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Extracellular Space / drug effects
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Glutamic Acid / adverse effects
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Guanidines / pharmacology*
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Guanidines / therapeutic use
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Mice
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N-Methylaspartate / adverse effects
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Neurons / drug effects*
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Neurons / pathology
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Reperfusion / methods
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Sodium-Hydrogen Exchangers / antagonists & inhibitors*
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Tetrazolium Salts
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Thiazoles
Substances
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Guanidines
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Sodium-Hydrogen Exchangers
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Tetrazolium Salts
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Thiazoles
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Glutamic Acid
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N-Methylaspartate
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thiazolyl blue
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Calcium
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sabiporide