新生大鼠缺血缺氧后胶质性谷氨酸转运体的表达及GM1的干预研究

目的探讨新生大鼠缺血缺氧性脑损伤后胶质性谷氨酸转运体的表达及神经节苷脂（GM1）的干预作用。方法通过建立新生大鼠缺血缺氧性脑损伤动物模型，应用免疫组化方法，观察缺血缺氧后不同时期大脑皮质胶质性谷氨酸转运体EAATI、EAAT2的动态表达度GM1对其表达的影响。结果缺血缺氧后6hEAAT1的表达开始上升、第2d达高峰，第3d恢复到假手术组水平；EAAT2的表达在缺血缺氧后12h开始上升，第3d达高峰，第5d恢复到假手术组水平；GM1干预组脑组织损伤明显减轻，EAAT1和EAAT2的表达较单纯缺血缺氧组显著增加（P〈0．01），持续时间延长。结论缺血缺氧诱导胶质性谷氨酸转运体的表达，GM1提高胶质性谷氨酸转运体的表达可能是GM1脑保护作用的重要机制之一。

Expressions of Glial Glutamate Transporters in Neonatal Rat after Hypoxia-ischemia and Their Changes after Administration of GM1

Objective To study the expressions of glial glutamate transporters in neonatal rat after hypoxia-ischemia(HI)and their changes after administration of GM1.Methods A rat model of neonatal hypoxic-ischemic-encephalopathy (HIE) was established,then the pathological changes and expressions of excitatory amino acid transporter-1 (EAAT1) and excitatory amino acid transporter-2 (EAAT2) in the brain tissues were investigated in different periods after hypoxia-ischemia,and the subsequent changes of the above results after GM1 administration were studied too.Results The damage of the brain by exposed to HI was alleviated remarkably after GM1 administrated.The expression of EAAT1 in the brain tissue was beginning up-regulated after 6 hours from hypoxia-ischemia,reaching the top after 48hours,and recovering normality after 72hours.The expression of EAAT2 was beginning up-regulated after 12hours from HI,reaching the top after 72hours,and recovering normality after 120hours.GM1 could to an extent increase the expressions of EAAT1 and EAAT2.Conclusion Hypoxia-ischemia can induce expressions of EAAT1 and EAAT2 in neonatal rat brain.GM1 may have some protective effects on HIE neonatal rat,and the possible mechanism is related to the partial increasing expressions of EAAT1 and EAAT2.