摘要
目的:从分子水平探讨胆红素对神经细胞的毒性机理,为新生儿胆红素脑病的防治提供新的途径。方法:制作高胆红素血症动物模型,观察海马区神经细胞的组织学改变,检测脑组织胆红素浓度及海马区神经细胞凋亡率,并探讨其间相关性。结果:高胆红素血症时,海马区神经细胞出现凋亡的组织学改变,神经细胞凋亡率明显增高,与脑组织胆红素浓度呈正相关。结论:胆红素通过诱导海马区神经细胞凋亡介导其神经毒性的产生。
Objective: To explore the toxicity mechanism of bilirubin that effects nerve cells from the molecular level of bilirubin, To provide a new way of prevention and treat ment of the neonatal bilirubin encephalopathy. Methods: To make hyperbilirubinemia animal model. To observe the histological changes of nerve cells in hippocampus region , To detecte the bilirubin concentration in the brain tissue and the apoptosis rate of nerve cells in hippocampus region and explore thief relativity. Results:The nerve cells in hippocampus region appeared the histological changes of apoptosis in the state of hyperbilirubinemia; and the apoptosis rate of nerve ceils was significantly increased. There was positive relationship with the bilirubin concentration of brain tissue. Conclusion: Bilirubin neurotoxicity can be formed by inducing the apoptosis of nerve cells in hippocampus region.
出处
《现代临床医学》
2008年第1期24-26,共3页
Journal of Modern Clinical Medicine
关键词
胆红素
海马
神经细胞
凋亡
bilirubin
hippocampus
nerve cells
apoptosis