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1

中国临床药理学与治疗学 ›› 2002, Vol. 7 ›› Issue (5): 385-388.

• 研究原著 • 下一篇

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¹

谷淑玲, 李梅, 崔家勇, 姚兵, 戴体俊²

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

收稿日期:2002-07-15 修回日期:2002-07-26 发布日期:2020-11-26
通讯作者: 谷淑玲, 女, 副教授, 硕士生导师, 主要从事心脑血管药理研究。Tel:0516-5748484 Fax:0516-5748429 E-mail:gushling@163.com
作者简介:戴体俊, 男, 教授, 硕士生导师, 中国数学药理学会理事, 主要从事麻醉药理学研究。
基金资助:
1 江苏省麻醉学重点实验室开放课题资助项目(№K2092); 国家自然科学基金项目(№39970715)

Relationship between the protective effect of sodium oxybate on neuronal damage induced by hypoxia-reoxygenation and GABAA receptor in primary cultured rat cortical neurons¹

GU Shu-Ling, LIMei, CUI Jia-Yong, YAO Bin, DAI Ti-Jun²

Department of Pharmacology, Xuzhou Medical College, Xuzhou 221002;
²Jiangsu Provincial Key Laboratory of Anesthesiology, Xuzhou 221002

Received:2002-07-15 Revised:2002-07-26 Published:2020-11-26

摘要/Abstract

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 <0.01), SOD、GPx 活力降低(P <0.01)。SO 能显著减少损伤神经元的LDH 漏出率及MDA 的生成(P <0.01), 升高SOD、GPx (P <0.01) 的活力, 这种作用可被GABAA 受体阻断剂seurinine 减弱(P <0.01)。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。

关键词: 羟丁酸钠, seurinine, GABAA 受体, 缺氧复氧损伤

Abstract: AIM: To investigate the relationship between the protective effect of sodium oxybate on neuronal damage induced by hypoxia-reoxygenation and GABAA 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 GABAA receptor.

Key words: sodium oxybate, seurinine, GABAA receptor, hypoxia-reoxygenation injury

中图分类号:

R965

谷淑玲, 李梅, 崔家勇, 姚兵, 戴体俊. 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¹[J]. 中国临床药理学与治疗学, 2002, 7(5): 385-388.

GU Shu-Ling, LIMei, CUI Jia-Yong, YAO Bin, DAI Ti-Jun. Relationship between the protective effect of sodium oxybate on neuronal damage induced by hypoxia-reoxygenation and GABAA receptor in primary cultured rat cortical neurons¹[J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2002, 7(5): 385-388.

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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¹

Relationship between the protective effect of sodium oxybate on neuronal damage induced by hypoxia-reoxygenation and GABAA receptor in primary cultured rat cortical neurons¹

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