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作 者:朱海鹏[1] 高志良[2] 谢婵[2] 郑玉宝[2] 彭亮[2]
机构地区:[1]东莞市人民医院,东莞525018 [2]中山大学附属第三医院,广州510630
出 处:《热带医学杂志》2009年第7期725-728,共4页Journal of Tropical Medicine
基 金:973课题(No.2008ZX10002-007)
摘 要:目的研究D-半乳糖胺和脂多糖导致大鼠急性肝衰竭的发病机理。方法8周龄雄性SD大鼠,使用D-半乳糖胺(D-GalN,1250mg/kg)和脂多糖(LPS,200μg/kg)腹腔注射建立急性肝衰竭模型,并研究肝衰竭大鼠血清和肝匀浆的各种生化指标及肝组织的病理学改变。结果使用1250mg/kg的D-GalN和200μg/kg的LPS腹腔注射能够导致大鼠出现急性致死性的肝损伤,大鼠血清中TNF-α、IL-1β显著升高;大鼠肝组织中GSH、GR和SOD降低,MDA、NO、T-NOS和iNOS升高;与正常大鼠的肝匀浆蛋白分离图相比,肝衰竭大鼠肝匀浆蛋白的1峰升高较明显,5峰、6峰降低较明显。结论使用1250mg/kg的D-GalN和200μg/kg的LPS腹腔注射能够制备急性肝衰竭大鼠模型,其发病机理可能与D-GalN和LPS能够促进炎症细胞因子TNF-α、IL-1等大量的产生,促进机体过度的氧化反应及氧化产物的产生,导致肝组织中某些分子量范围内蛋白的增加及另外一些分子量范围内蛋白的减少有关。Objective To study the pathogenesis of D-galactosamine (D-GaIN)- and lipopolysaccharides (LPS)-induced fulminant hepatic failure. Methods Fulminant hepatic failure was induced in male Sprague-Dawley rats by intraperitoneal injection with D-GaIN (1 250 mg/kg) and LPS (200 μg/kg). Biochemical indexes in rat serum were measured and the pathological change of hepatic tissue was examined. Results D-GalN and LPS caused a lethal hepatic injury in rat. The levels of TNF-α and IL-1β in serum were increased. The levels of GSH, GR and SOD in the liver were decreased, while the levels of MDA, NO, T-NOS and iNOS were increased after the treatment. Conclusion D-GalN and LPS can cause fulminant hepatic failure. The increase in the production of inflammatory cytokines and free radicals may contribute to the pathological damage of the liver.
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