葡萄糖转运蛋白-1和-3在缺氧缺血性脑损伤新生大鼠脑内表达的变化及意义

目的：探讨缺氧缺血性脑损伤(H IBD)后脑内负责葡萄糖转运的两个重要蛋白质葡萄糖转运蛋白-1(GLUT-1)与葡萄糖转运蛋白-3(GLUT-3)表达的变化,揭示H IBD后脑内能量衰竭的发病机制。方法：将30只7日龄W istar大鼠随机分为正常对照组(n=5)、假手术对照组(n=5)和H IBD组(n=20)。H IBD组大鼠模型的制备参照R ice。方法结扎右侧颈总动脉后8%低氧暴露1 h。假手术对照组只分离右侧颈动脉,不予结扎和缺氧。缺氧缺血后1,3,5,10 d各处死5只H IBD大鼠,免疫组化方法检测大鼠脑内GLUT1及GLUT3表达,并与对照组和假手术组比较。结果：正常新生大鼠脑内微血管即可见GLUT1表达。H IBD后1 d,缺血侧半球GLUT1表达略有增加,3 d达高峰,至5 d时仍高于正常,10 d基本恢复正常水平。H IBD后1 d,GLUT3表达无明显变化,3 d时GLUT3表达已明显减少,5 d时进一步减少,10 d时仍显著低于对照组。GLUT3表达减少最显著的部位为海马CA1区。结论：H IBD后脑内GLUT1和GLUT3的表达异常可导致脑能量代谢途径改变,加重缺氧缺血后神经元的损伤及影响损伤神经元的修复。

Expression of glucose transporter proteins in the brain of neonatal rats with hypoxic-ischemic brain damage

Objective In order to study the mechanisms of cerebral energy failure after hypoxic-ischemic brain damage(HIBD),the effects of hypoxia-ischemia(HI) on glucose transporter proteins(GLUT1 and GLUT3) expression in the brain were investigated in neonatal rats.Methods Thirty seven-day-old Wistar rats were randomly assigned into Normal(n=5),Sham-operated(n=5) and HIBD model groups(n=20).The HIBD model was established by ligating the right common carotid artery combined with the hypoxia exposure(8% oxygen).The rats were sacrificed at 1,3,5 and 10 days after HIBD.The expressions of GLUT1 and GLUT3 in the brain were examined by immunohistochemistry.Results Microvascular GLUT1 was seen in the Normal group.GLUT1 immunoreactivity began to increase in ipsilateral hemisphere 1 day after HI,peaked on the 3rd day,and remained high on the 5th day.No significant changes in GLUT3 immunoreactivity were observed 1 day after HI.Three days after HI,there was a pronounced decrease in GLUT3 staining;and on the 5th day the decrease of GLUT3 staining was most significantly.The maximal decrease of GLUT3 staining was seen in the hippocampal CA1 region.Conclusions HI may result in an abnormal expression of glucose transporter proteins in the brain,which might aggravate the neuronal injury and interfere with its repair.