[Protective effects and mechanisms of OSR on primary cultured hippocampus neurons subjected to anoxic injury in neonatal rat].

OBJECTIVE: To investigate the protective effects of oxysophoridine (OSR) on primary cultured hippocampus neurons subjected to anoxia injury in neonatal rats and its mechanism. METHOD: The model of anoxia injury of hippocampus neurons in neonatal rats were primarily cultured in vitro by physical oxygen deficiency using glucose-free culture fluid. The survival rate of neurons, the leaking rate of lactate dehydrogenase (LDH), the intracellular contents of malondialdehyde (MDA) and nitric oxide (NO), the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-PX) and nitric oxide synthase (NOS) were measured. The intracellular free calcium concentration ([Ca2+]i) in hippocampus neurons were detected with Ca(2+)-sensitive dual wavelength fluorescence spectrophotometer. RESULT: Neuron death occurred in the anoxia injury model group with increase of LDH leaking rate, the contents of NO, MDA, intracellular [Ca2+] and the elevated activity of NOS while decreased activities of SOD and GSH-PX. The hippocampus neurons subjected to anoxia injury were alleviated in OSR (0.625, 5, 10 microg x L(-1)) group. CONCLUSION: OSR has significant protective effects on hippocampus neurons subjected to anoxic injury. The mechanism of its protective effect may relate to its reduction of calcium overload and against oxidation injury.