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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 and lipopolysaccharide in acute liver failure in rats. Methods Male SD rats of 8 weeks old were used to establish acute hepatic failure model by intraperitoneal injection of D-galactosamine (D-GalN, 1250mg / kg) and lipopolysaccharide (LPS, 200μg / kg) A variety of biochemical indicators of liver homogenates and pathological changes of liver tissue. Results Intraperitoneal injection of D-GalN at 1250mg / kg and LPS at 200μg / kg could induce acute lethal liver injury in rats, and the levels of TNF-α and IL-1β were significantly increased in rats. GSH , GR and SOD were decreased, while MDA, NO, T-NOS and iNOS were increased. Compared with normal rat liver homogenate protein isolates, , 6 peak decreased more obvious. Conclusion The rat model of acute hepatic failure can be prepared by intraperitoneal injection of D-GalN of 1250mg / kg and LPS of 200μg / kg, the pathogenesis of which may be related to D-GalN and LPS can promote a large number of inflammatory cytokines TNF-α, IL- , Promote the body’s excessive oxidation reaction and the production of oxidation products, resulting in the increase of some molecular weight range in liver tissue and the decrease of other molecular weight range.