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中国临床药理学与治疗学 ›› 2004, Vol. 9 ›› Issue (1): 83-86.

• 研究原著 • 上一篇    下一篇

神经节苷脂GM1 对缺血缺氧后谷氨酸及其转运体神经元的作用

胡志兵, 陆雪芬1, 郑德枢1   

  1. 广州市第十二人民医院神经内科, 广州 510620, 广东;
    1广州医学院神经科学研究所, 广州 510180, 广东
  • 收稿日期:2003-05-19 修回日期:2003-06-10 出版日期:2004-01-26 发布日期:2020-11-16
  • 通讯作者: 胡志兵,男, 硕士研究生, 副主任医师, 从事脑血管疾病的基础和临床研究。Tel:020-85591881-3706 E-mail: zhibinghu@hotmail.com
  • 基金资助:
    广东省医学科研基金资助项目(No.B2001101)

Expressions of glutamate and EAAC1 glutamate transporter in neonatal rat after hypoxia-ischemia and their changes after administrated ganglioside GM1

HU Zhi-Bing, LU Xue-Fen1, ZHENG De-Shu1   

  1. Department of Neurology, the No.12 Hospital of Guangzhou, Guangzhou 510620, Guangdong, China;
    1 Neuroscience Institute of Guangzhou Medical College, Guangzhou 510180, Guangdong, China
  • Received:2003-05-19 Revised:2003-06-10 Online:2004-01-26 Published:2020-11-16

摘要: 目的: 探讨神经节苷脂GM1 对新生大鼠缺氧缺血性脑病保护作用及其可能的机理。方法: 通过建立新生鼠缺氧缺血性脑病动物模型, 应用免疫组化方法, 观察缺血缺氧后不同时期脑组织中谷氨酸及其转运体阳性神经元的动态变化, 以及GM1 对其的影响。结果: 缺血缺氧后6 h 、1 、3 d 大脑皮层和纹状体中谷氨酸阳性神经元明显减少, 而谷氨酸转运体阳性神经元有所增加,GM1 组脑组织损伤明显减轻, 谷氨酸神经元及谷氨酸转运体神经元较单纯缺氧缺血组明显增多。结论: 神经节苷脂GM1 对谷氨酸神经元具有保护作用, 可能是通过部分提高谷氨酸转运体的表达而发挥作用。

关键词: 神经节苷脂GMI, 新生鼠, 缺氧缺血, 谷氨酸神经元, 谷氨酸转运体Ⅲ

Abstract: AIM: To study the neuroprotective effect and possible mechanism of ganglioside GM1 on neonatal rats with hypoxic-ischemic-encephalopathy (HIE).METHODS: A rat model of neonatal HIE was established, then the pathological changes and expressions of glutamate and EAAC1 glutamate transporter in the brain tissues were investigated in different periods after hypoxiaischemia (HI)and the subsequent changes of the above results after GM1 administrated were studied too.RESULTS: The damages of the brain by exposed to HIwere alleviated remarkably afterGM1 administrated.The levels of glutamate neuron expressions in the brain tissue decreased after HI but EAAC1 increased.GM1 could partly prevent glutamate neuron reduction induced by HI and increase EAAC1 expression.CONCLUSION: GM1 may have some protective effects on glutamate neuron in neonatal HIE, and the possible mechanism is related to the partial increasing of EAAC1 expression.

Key words: ganglioside GM1, newborn rats, hypoxia-ischemia, glutamate neuron, EAAC1 glutamate transporter

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