脑缺氧缺血对GLUT1和GLUT3合成的影响  

Effect of cerebral hypoxic ischemia on the synthesis of glucose transporter 1 and 3 in neonatal rats

作　　者：杨友[1] 陈惠金[1] 钱龙华[1] 蒋明华[1] 

机构地区：[1]上海第二医科大学附属新华医院,上海200092

出　　处：《中国神经科学杂志》2004年第1期51-55,64,共6页

基　　金：国家自然科学基金资助项目 (3 0 0 70 789)

摘　　要：目的　 探讨脑缺氧缺血 (HI)对葡萄糖转运蛋白 1(glucosetransporter 1,GLUT1)和葡萄糖转运蛋白 3(glucosetransporter 3,GLUT3)合成的影响。方法　 在成功建立了缺氧缺血新生大鼠模型的基础上 ,应用免疫组化方法检测缺氧缺血新生大鼠脑内海马和皮质部位GLUT1和GLUT3的合成情况。结果　 正常情况下 ,海马和皮质部位GLUT1和GLUT3的合成量随日龄增加而增高。海马部位的合成量高于皮质部位 ;缺氧缺血可引起GLUT1和GLUT3的合成增加 ,HI后 2 4h时达到高峰 ,其后呈下降趋势 ,尤其是GLUT3在HI后 7d降至极低水平。皮质部位的合成量高于海马部位。 结论　HI可调控脑内GLUT1和GLUT3水平 ,使其在HI后短期内合成增高 ,以增加脑内葡萄糖的转运 ,适应无氧酵解增加的需要。Objective To explore the effect of cerebral hypoxic-ischemia(HI) on the synthesis of glucose transporter( GLUT)1 and 3. Methods Based on the successful preparation of hypoxic-ischemic neonatal rat model, immunohistochemical method was applied to detect the synthesis of GLUT1 and GLUT3 in cerebral hippocampus and cortex in neonatal rats with HI. Results There was a linear enhancement in the synthesis of GLUT1 and GLUT3 with the increase of day age. The synthesis was predominant in hippocampus comparing to that in cortex in normal group. However, HI could significantly enhance the synthesis of GLUT1 and GLUT3 in the early time after HI. The synthesis reached peak at 24 h after HI, and then declined, especially GLUT3 went down to a very low level at day 7 after HI. It was noticed that the synthesis was more in cortex than that in hippocampus in HI group. Conclusion It is suggested that the increased synthesis of GLUT1 and GLUT3 induced by HI could accelerate the utilization of glucose in the brain and adapt to the requirement of anaerobic glycolysis.

关 键 词：脑缺氧缺血 GLUT1 GLUT3 葡萄糖转运蛋白1 葡萄糖转运蛋白3 新生大鼠 

分 类 号：R741[医药卫生—神经病学与精神病学]