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目的研究c-Jun氨基末端激酶(JNK)在D-半乳糖胺/脂多糖(D-GalN/LPS)引起的小鼠急性肝衰竭模型肝组织中的表达及其意义。方法 32只C57BL/6小鼠随机分成实验组与对照组,利用D-GalN/LPS构建急性肝衰竭模型,于给药后0h、2h、4h、6h取材,应用蛋白免疫印迹、免疫组织化学的方法对磷酸化的JNK(p-JNK)进行检测并作半定量分析,观察其在模型中的变化情况。结果实验组肝组织损害、肝细胞坏死逐渐加重,6h最重;p-JNK在给药后的实验组小鼠肝组织中持续高表达,高峰出现在给药后2h。结论给小鼠注射D-GalN/LPS后可以增加JNK的磷酸化水平,JNK信号通路可能在D-GalN/LPS引起的急性肝衰竭损伤中起至关重要的作用。
Objective To investigate the expression and significance of c-Jun N-terminal kinase (JNK) in liver of mice with acute hepatic failure induced by D-galactosamine / lipopolysaccharide (D-GalN / LPS) Methods 32 C57BL / 6 mice were randomly divided into experimental group and control group. The model of acute liver failure was established by D-GalN / LPS. The model rats were drawn at 0h, 2h, 4h and 6h after administration. Western blotting, immunohistochemistry Methods The phosphorylation of JNK (p-JNK) was detected and semi-quantitative analysis was performed to observe its changes in the model. Results The hepatic tissue necrosis and hepatocyte necrosis gradually aggravated in experimental group and reached the peak at 6 hours. The expression of p-JNK in the experimental group was consistently high, and the peak appeared at 2 hours after administration. Conclusions Mice injected with D-GalN / LPS can increase the phosphorylation of JNK, and JNK signaling pathway may play a crucial role in D-GalN / LPS-induced acute liver failure.