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AIM: To investigate the relationship between the protective effect of sodium oxybate on neuronal damage induced by hypoxia reoxygenation and GABA A receptor in primary cultured rat cortical neurons. METHODS: The primary cultured rat cortical neurons were used to make the hypoxia reoxygenation damage model. The morphology of cell was observed. The lactate dehydrogenase (LDH) effluxed into the media as an indicator of neuronal injury was detected after 6 h of the reoxygenation injuries. The malonyldialdehyde (MDA) contents, superoxide dismutase (SOD) and glutathione peroxidase (GPX) activities were determined at the same time. RESULTS: The hypoxia reoxygenation caused neuronal swelling and widespread neuronal degeneration, increased LDH efflux and MDA contents, and decreased SOD and GPX activities. Sodium oxybate assuaged neuron damage, decreased LDH efflux and MDA contents (P
RESUMO
AIMTo study the protective effect of sodium oxybate (SO) against focal cerebral ischemia-reperfusion injury in rats, and the relationship between the effects of SO and ?-aminobutyric acid (GABA). METHODSThe reversible middle cerebral artery occlusion (MCAO)model in rats was established to investigate the role of SO. The scores of neurological deficits was detected by Longa EZ method in MCAO rats. The extracellular levels of glutamate (Glu) and GABA in CSF were measured by high performance liquid chromatography-fluorometer (HPLC-FR) method, and the weight of cerebral infraction was detected. RESULTSThe scores of neurological deficits and the weight of cerebral infraction markedly decreased by SO while the ratio of GABA/Glu obviously increased administered SO in MCAO rats. CONCLUSIONSSO could prevent MCAO rats from ischemia-reperfusion injury, the protective effect is related to SO keeping dynamic balance of excition-inhibition, and persisting inhibition-depended effect.