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羟丁酸钠对大鼠局灶性脑缺血再灌注损伤的保护作用及与GABA的关系
引用本文:李梅,崔家勇,谷淑玲,姚兵,段世明.羟丁酸钠对大鼠局灶性脑缺血再灌注损伤的保护作用及与GABA的关系[J].中国药理学通报,2004,20(3):295-298.
作者姓名:李梅  崔家勇  谷淑玲  姚兵  段世明
作者单位:1. 徐州医学院药理学教研室,徐州,221002
2. 江苏省麻醉学重点实验室,徐州,221002
摘    要:目的 研究羟丁酸钠对大鼠局灶性脑缺血再灌注损伤的保护作用及该作用与γ 氨基丁酸 (GABA)的关系。方法 采用线栓法建立大鼠局灶性脑缺血再灌注损伤模型 ,观察损伤大鼠行为功能缺失并称量脑梗死区域组织重量。用高效液相 -荧光法测定大鼠脑脊液中氨基酸的含量并计算GABA/Glu的比值。结果 羟丁酸钠可明显降低缺血再灌注后大鼠行为学评分分值 ,减小脑梗死组织重量 ,增加GA BA/Glu的比值。结论 羟丁酸钠对大鼠局灶性脑缺血再灌注损伤有明显的保护作用 ,该作用与其提高抑制性氨基酸GABA的含量 ,维持脑内兴奋性氨基酸和抑制性氨基酸的动态平衡 ,产生抑制性保护作用有关

关 键 词:羟丁酸钠  局灶性脑缺血  神经功能缺失  脑梗死  γ-氨基丁酸  谷氨酸
文章编号:1001-1978(2004)03-0295-04
修稿时间:2003年12月11

Neuroprotective effect of sodium oxybate against focal cerebral ischemia-reperfusion injury and the relation to GABA in rats
LI Mei,CUI Jia-Yong,GU Shu-Ling,YAO Bing,DUAN Shi-Ming.Neuroprotective effect of sodium oxybate against focal cerebral ischemia-reperfusion injury and the relation to GABA in rats[J].Chinese Pharmacological Bulletin,2004,20(3):295-298.
Authors:LI Mei  CUI Jia-Yong  GU Shu-Ling  YAO Bing  DUAN Shi-Ming
Affiliation:LI Mei,CUI Jia-Yong,GU Shu-Ling,YAO Bing,DUAN Shi-Ming 1
Abstract: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 γ-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.
Keywords:sodium oxybate  focal cerebral ischemia  neurological deficits  cerebral infraction  γ-aminobutyric acid (GABA)  glutamate(Glu)
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