【摘要】 缺血缺氧性脑病是新生儿期以后造成伤残儿童的主要原因之一。近几年大量生物学研究证实 ,脑缺氧缺血后可激活一系列分子反应 ,目前已知脑缺氧缺血后可引起神经元内多种即刻早基因表达增强 ,诱发或阻止神经元死亡 ;同时也发现神经细胞受损过程有多种细胞因子、神经介质蛋白释放 ,可在早期反映脑操作程度。因此相关生物学研究结果对判断HIE程度与预后 ,以及干预治疗有着十分重要意义。更多还原

【Abstract】 hypoxic-ischemic encephalopathy (HIE) in neonatal period is one of the leading causes to make the children disabled. Recently, more and more biological researches proved that ischemia and hypoxia in brain could activate a series of molecular reactions. For present, HIE has been known to cause express or enhanced express of many kinds of immediate early genes in neuron, which can induce or inhibit the neuron death. Meanwhile, various kinds of cellular factors, neurohumors, and antioxidants have also be found to participate in the course of damage of the nerve cells. The release level of some specific neuroprotein from injuried nerve cells could reflect the degree of brain damage in early time. Therefore, relevant biological findings are not only meaningful to judge the degree and prognosis of HIE, but also important for intervention treatment of the disease.更多还原