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目的探讨胆红素的神经毒性机制。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变化,检测海马区神经细胞Fas蛋白表达率及神经细胞凋亡率,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Fas蛋白表达率在实验组1(T1G,腹腔注射胆红素0.171μmol/g体重为(19.13±0.25)%,实验组2(T2G,腹腔注射胆红素0.342μmol/g体重)为(33.38±3.45)%,T1G神经细胞凋亡率为(6.13±0.37)%,T2G为(15.44±0.64)%,均较对照组差异有显著性(P<0.001),二者与脑组织胆红素浓度均呈显著正相关。结论胆红素通过Fas系统的参与,传递凋亡信号,介导胆红素神经毒性,导致神经细胞凋亡。
Objective To explore the neurotoxic mechanism of bilirubin. Methods Animal models of hyperbilirubinemia were established. The histological changes of neurons in the hippocampus were observed. The expression of Fas protein in hippocampal neurons and the rate of neuronal apoptosis were detected, and the correlation was also discussed. Results When hyperbilirubinemia was observed, histological changes of apoptotic neurons in hippocampus were observed. The expression of Fas protein in neurons was significantly higher in experimental group 1 (T1G, intraperitoneal injection of 0.171 μmol / g body weight bilirubin (19.13 ± 0.25) (33.38 ± 3.45)% in experimental group 2 (T2G), the rate of apoptotic cells in T1G was (6.13 ± 0.37)% and that in T2G was (15.44 ± 0.64)%, (P <0.001), both of which had a significant positive correlation with the concentration of bilirubin in brain tissue.Conclusion Bilirubin, through the participation of Fas system, transmits the signal of apoptosis and mediates the expression of bilirubin Toxicity, leading to nerve cell apoptosis.