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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。
Objective To study the pathogenesis of cerebral energy failure after hypoxic-ischemic brain damage (HI) at the molecular level and to provide theoretical and practical evidence for the establishment of a safe and effective neonatal hypoxic-ischemic encephalopathy (HIE) regimen. Methods One hundred and ten newborn SD rats were randomly divided into three groups: HI group and normal group. The neonatal rats in each group were sacrificed at 2,2,48,72 and 7 days after HI, Lateral brain tissue, cortex and hippocampus. The expression of GLUT1 and GLUT3 in brain of neonatal rats at different time points was investigated by RT-PCR. The effects of HI on GLUT1 gene And GLUT3 gene expression. Results Under normal conditions, both GLUT1 and GLUT3 genes were increased with age, and the expression in the hippocampus was generally higher than that in the cortex. HI can cause GLUT gene expression was significantly increased, cortical parts of the expression was generally higher than the hippocampus. HI reached the peak at 24 hours, and then dropped to the 7th day after HI, which was significantly lower than that of the normal group. Conclusion The up-regulation of GLUT gene is of great significance for maintaining the energy supply of brain tissue and delaying the cascade reaction induced by energy failure.