卢艳秋,娄季宇

• 1:郑州大学第二附属医院重症监护病房
• 2:郑州大学第二附属医院神经内科

摘要(Abstract)：

目的研究鼠脑缺血再灌注损伤后脑组织兴奋性氨基酸(EAA)的变化及托吡酯的影响,探讨托吡酯的神经保护作用机制。方法用线栓法制备SD大鼠大脑中动脉阻塞再灌注(MCAO)模型,托吡酯100mg/kg灌胃,1次/d,通过免疫组化染色变化观察不同组NMDAR1及GABA染色变化。结果单纯缺血再灌注组与假手术组相比大鼠脑缺血侧脑组织GABAa明显降低,托吡酯治疗组较单纯缺血组GABAa增高。托吡酯预防组GABAa含量较单纯缺血再灌注组明显增高。单纯缺血组与假手术组相比大鼠脑缺血侧脑组织NMDAR1明显降低,托吡酯治疗组较单纯缺血组NMDAR1受体量降低,托吡酯预防组NMDAR1受体量与单纯缺血再灌注组相比明显降低。结论托吡酯保护大鼠脑缺血的重要机制之一可能是通过抑制兴奋性氨基酸释放,提高抑制性氨基酸释放及改变其受体表达实现的。

关键词(KeyWords)： 局灶性脑缺血;托吡酯;NMDAR1;GABA

Abstract:

Keywords:

基金项目(Foundation):

作者(Author): 卢艳秋,娄季宇

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