羟丁酸钠对大鼠原代培养皮层神经元缺氧复氧损伤的保护作用与GABAA受体的关系

目的 :探讨羟丁酸钠 (SO)对大鼠皮层神经元缺氧复氧损伤的保护作用与GABAA 受体的关系。方法 :采用原代培养大鼠皮层神经元建立缺氧复氧损伤模型 ,观察细胞的形态学 ,测定其LDH漏出率、MDA含量、SOD、GPx活力。结果 :缺氧复氧可引起神经元损伤 ,LDH漏出率增加 ,MDA含量升高 (P <0 .0 1) ,SOD、GPx活力降低 (P <0 .0 1)。SO能显著减少损伤神经元的LDH漏出率及MDA的生成 (P <0 .0 1) ,升高SOD、GPx(P <0 .0 1)的活力 ,这种作用可被GABAA 受体阻断剂seurinine减弱 (P <0 .0 1)。结论 :SO对缺氧复氧神经元损伤的保护作用可能与其激动GABAA 受体有关。

Relationship between the protective effect of sodium oxybate on neuronal damage induced by hypoxia-reoxygenation and GABAA receptor in primary cultured rat cortical neurons

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< 0.01 ), and increased SOD and GPx activities (P< 0.01 ). The effect could be abated by seurinine (P< 0.01 ). CONCLUSION: The protective effect of sodium oxybate on neuronal damage induced by hypoxia reoxygenation is related to excited GABA A receptor.