摘要
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 molecular mechanism of bilirubin on hippocampus. Methods Setting up the historical hyperbilirubinemia model, the historical changes of neurons were observed and the neuronal apoptosis was evaluated with flow cytometry and TUNEL method The expression of Fas protein was investigated. The relationship between Fas protein and apoptoris was explored. Results In hyperbilimbinemia rats, there were apoptosis tissue changes of neurons in the hippocampus, the expression of Fas protein in experimental 1 （TtG intra peritoreal （IP） inject bilirubin 0. 171μmol/g body weight）and 2（T2G IP inject bilirubin 0.342μmol/g body weight） were （19.13±0.25）% and （33.38 ± 3.54）%, the rates of neuronal apoptosis in TIG and T2G were （6.13 ± 0.37）% and （ 15.44 ± 0.64） %, These were higher than those of control group （ P 〈 0.01 ）, Fas protein and apoptosis had correlation there positive correction with the level of brain bilirubin. Conclusions The bilirubin neurotoxicity is mediated by Fas protein, which induces neuronal apoptosis.
出处
《新生儿科杂志》
2005年第4期160-163,共4页
The Journal of Neonatology
