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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。
Objective To investigate the changes of GLUT-1 and GLUT-3, which are responsible for glucose transport in the brain following hypoxic-ischemic brain damage (HIBD), revealing that H Pathogenesis of brain energy failure after IBD. Methods Thirty 7-day-old Wistar rats were randomly divided into normal control group (n = 5), sham operation control group (n = 5) and HIBD group (n = 20). The rat model of HIBD group was prepared according to R ice. Methods The right common carotid artery was ligated with 8% hypoxia for 1 hour. Sham operation control group only isolated right carotid artery, not ligation and hypoxia. Five HIBD rats were killed at 1, 3, 5 and 10 days after hypoxia-ischemia. The expression of GLUT1 and GLUT3 in rat brain was detected by immunohistochemistry and compared with the control group and the sham operation group. Results The expression of GLUT1 was observed in the capillaries of normal neonatal rats. On the first day after HIBD, the expression of GLUT1 in the ischemic hemisphere increased slightly and peaked on the third day. It remained higher than normal on the 5th day and returned to its normal level on the 10th day. At 1 d after HIBD, the expression of GLUT3 had no significant change. At 3 d, the expression of GLUT3 was significantly decreased and further decreased at 5 d, but still significantly lower than that of the control group on the 10th day. The most significant site of GLUT3 expression was the hippocampal CA1 region. Conclusions The abnormal expression of GLUT1 and GLUT3 in the brain after HIBD can lead to the change of brain energy metabolism pathway, aggravating the damage of neurons after hypoxia and ischemia and affecting the repair of damaged neurons.