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GABA_A受体的关系  

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

作　　者：谷淑玲[1] 李梅[1] 崔家勇[1] 姚兵[1] 戴体俊[2] 

机构地区：[1]徐州医学院药理教研室,徐州221002 [2]江苏省麻醉学重点实验室,徐州221002

出　　处：《中国临床药理学与治疗学》2002年第5期385-388,共4页Chinese Journal of Clinical Pharmacology and Therapeutics

基　　金：江苏省麻醉学重点实验室开放课题资助项目 (№K2 0 92 ) ;国家自然科学基金项目 (№ 3 9970 715 )

摘　　要：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。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.

关 键 词：羟丁酸钠 GABAA受体 缺氧复氧损伤 脑缺血 血脑屏障 

分 类 号：R743.31[医药卫生—神经病学与精神病学] R965[医药卫生—临床医学]