GLT1参与大鼠脑缺血预处理诱导的脑缺血耐受.doc

GLT1参与大鼠脑缺血预处理诱导的脑缺血耐受
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作者:耿进霞潘培森李领香
【摘要】目的应用谷氨酸转运体GLT1抑制剂二氢卡因酸盐(DHK)验证GLT1在脑缺血耐受诱导中的作用。方法采用四血管闭塞法(4VO)制作大鼠全脑缺血模型。脑组织切片硫堇染色法观察海马CA1区锥体神经元迟发性死亡(DND)程度。结果预先给予3 min脑缺血预处理(CIP)可显著对抗8 min 缺血打击引起的DND;与CIP+脑缺血打击(IS)组相比,DHK+CIP+IS组出现明显的DND。结论GLT1参与了CIP诱导的脑缺血耐受。
【关键词】脑缺血预处理 DHK 大鼠
【Abstract】ObjectiveThe role of glutamate transporter subtype GLT1 in the acquisition of brain ischemic tolerance was investigated by administering dihydrokainate (DHK), a selective inhibitor of GLT1. MethodsGlobal cerebral ischemic model was made by Four
vessel occlusion. The brain of the rats was sectioned and stained with thionin to show the degree of delayed neuronal death (DND) in the CA1 hippocampus. ResultsCerebral ischemic preconditioning(CIP) for 3 minutes effectively protected pyramidal neurons in the CA1 hippocampus against DND normally induced by ischemic insult for 8 minutes. DND was significantly obvious in DHK + CIP + brain ischemic insult(IS) pared with CIP + IS group. ConclusionGLT1 participates in brain ischemic tolerance induced by CIP.

【Key words】Cerebral ischemic preconditioning; Dihydrokainate; Rat

脑缺血预处理(cerebral ischemic preconditioning,CIP)[1]对后续的缺血性打击产生保护作用,这一现象被称为脑缺血耐受(brain ischemic tolerance,BIT)。脑缺血时细胞外液中谷氨酸等兴奋性氨基酸浓度异常增高,从而产生兴奋性神经毒性,谷氨酸转运体(glutamate transporter,GLT)可调控脑内细胞外液谷氨酸浓度,其中星形胶质细胞GLT1的作用尤为重要[2]。本试验旨在观察