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作 者:钟巨斌[1] 敖当[1] 郑小清[2] 王旭光[3] 揭新明[4]
机构地区:[1]广东医学院附属医院儿科 [2]广东湛江中心人民医院药剂科 [3]广东医学院附属医院中心实验室 [4]广东医学院分析中心,广东湛江524000
出 处:《广东医学院学报》2007年第4期378-380,共3页Journal of Guangdong Medical College
基 金:2004年度湛江市科技攻关项目(湛科[2004]88号)
摘 要:目的观察单唾液酸四己糖神经节苷脂(简称GM1)对豚鼠胆红素神经毒性的影响。方法在制作胆红素脑病动物模型基础上予GM1干预,观察对照组、模型组、干预组新生豚鼠(每组12只)干预后4、8h的脑组织ATP含量与含水量、脑组织超微结构。结果模型组与干预组脑组织ATP含量(4、8h)明显低于对照组(P<0.05),且干预组与模型组比较差异也有统计学意义(P<0.05);模型组脑组织含水量在干预后8h显著增高(P<0.05),GM1干预治疗可显著减轻胆红素毒性脑水肿(P<0.05);脑组织超微结构变化与之相符。结论沉积于脑组织胆红素可抑制神经元能量代谢,致脑细胞水肿;GM1可影响能量代谢变化,减轻脑水肿,对胆红素神经毒性具有治疗作用。Objective To observe the effect of GM1 on the neurotoxicity of bilirubin. Methods Thirty-six guinea pigs were randomly divided into control, model and treatment groups, and the bilirubin encephalopathic model was established only in the latter two groups, followed by intraperitoneal injection of normal saline and GM1 (10mg/kg), respectively. The brain ATP level, water content and ultrastructure were measured at 4 and 8 hours, Results The brain ATP production in guinea pigs decreased within 4 hours after exposure to bilirubin, especially in model group (P 〈 0.05 ). The water content in model group was superior to that in treatment and control groups at 8 hours (P 〈 0.05). The improvement of neuronal and mitochondrial swelling was seen in treatment group at 8 hours as compared with model group. Conclusion Bilirubin deposition in the brain could result in the brain edema via the inhibition of energy metabolism, GM1 is effective in the treatment of bilirubin encephalopathy by way of the improvement of energy metabolism and brain edema.
关 键 词:单唾液酸四己糖神经节苷脂 腺苷三磷酸 胆红素脑病
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