sabiporide and Brain-Ischemia

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.

Topics: Animals; Brain Infarction; Brain Ischemia; Calcium; Cell Death; Cells, Cultured; Cerebral Cortex; Disease Models, Animal; Dose-Response Relationship, Drug; Drug Interactions; Extracellular Space; Glutamic Acid; Guanidines; Mice; N-Methylaspartate; Neurons; Reperfusion; Sodium-Hydrogen Exchangers; Tetrazolium Salts; Thiazoles