大鼠高胆红素血症与海马神经细胞凋亡关系的实验研究

目的探讨高胆红素血症新生大鼠海马区Fas蛋白、N-甲基-D-天冬氨酸(NMDA)受体的表达、神经细胞凋亡率及其相关性，以进一步阐明胆红素的神经毒性机制。方法通过制作高胆红素血症动物模型，采用免疫组化法、TUNEL法及流式细胞术检测大鼠海马区Fas蛋白、NMDA受体的表达率及神经细胞的凋亡率，并探讨其问相关性。结果高胆红素血症时，海马区神经组织，Fas蛋白、NMDA受体表达率及神经细胞凋亡率明显增高，且与脑组织胆红素浓度呈正相关。结论高胆红素血症时，胆红索可通过NMDA受体过度活化和Fas系统的参与，传递凋亡信号，介导胆红素神经毒性的发生，导致神经细胞凋亡。

Relationship between hyperbilirubinemia and nerve cell apoptosis in rat hippocampus

Objective To explore the molecular mechanism of bilirubin in the hippocampus of the newborn rats with hyperbilirubinemia. Methods Hyperbilirubinemia model was established. The expression levels of Fas protein and N methyl D aspartate (NMDA) receptor and the apoptosis rate of nerve cells in rat hippocampus were detected with immunochemistry, TUNEL method and cytometry. Results Histological changes of nerve cells were found in hippocampal area of rats with hyperbilirubinemia. Significantly increased expression levels of Fas protein and NMDA receptor and apoptosis rate of nerve cells were positively correlated with the bilirubin level in rat brain tissues. Conclusion The bilirubin neurotoxicity is mediated by the excessive activation of NMDA receptor and participation of Fas system, which induces the apoptosis of nerve cells.