【摘要】 目的　从分子水平研究脑缺氧缺血 (HI)损伤后脑内能量衰竭的发病机制 ,为今后建立安全有效的新生儿缺氧缺血性脑病 (HIE)治疗方案提供理论和实践依据。方法　SD新生大鼠 1 0 0只 ,分为HI组及正常组 ,各组新生大鼠分别于HI后 2、2 4、48、72h及 7d在无菌操作下断头取脑 ,分取右侧脑组织、皮质及海马组织 ,应用RT PCR方法 ,探讨各组各时段新生大鼠脑内葡萄糖转运蛋白 1 (GLUT1 )和葡萄糖转运蛋白 3(GLUT3)基因表达情况 ,以研究脑HI对GLUT1基因和GLUT3基因表达影响。结果　正常情况下GLUT1和GLUT3基因均随日龄增加而表达增高 ,海马部位表达普遍高于皮质部位。HI可致GLUT基因表达明显增高 ,皮质部位表达普遍高于海马部位。HI后 2 4h达高峰 ,至HI后 7d则显著低于正常组。结论　GLUT基因表达上调对于维持脑组织能量供给、延迟由能量衰竭引起的级联反应有重要意义。更多还原

【Abstract】 Objective To understand the mechanism of cerebral energy failure after hypoxia ischemia at the molecular level and to establish the protocol for the safe and effective treatment of hypoxic-ischemic encephalopathy(HIE).Methods One hundred neonatal rats were divided into normal control group and hypoxic-ischemic(HI) group. SD rats of both groups were decapitated at the time of 2 h,24 h,48 h,72 h and 7 d after HI.These tissues of cerebrum,cortex and hippocampus were taken out to explore the influence of HI on the expression of GLUT1 and GLUT3 genes with the method of RT-PCR.Results There was an enhancement in the expression of GLUT1 and GLUT3 genes with the increasing of day age. The expression was more intense in hippocampus than that in cortex. However, HI could significantly enhance the expression of GLUT genes. The expression was higher in cortex than that in hippocampus. The expression of two genes reached the peak at 24 h after HI, but was significantly lower than that in control group at 7 d after HI.Conclusion The increased expression of GLUT genes can maintain the energy supplement for the brain and delay a cascade reaction of cerebral energy failure.更多还原