摘要
目的分析MHV-3诱导小鼠暴发性肝衰竭机制研究及夏枯草总三萜的改善作用,为肝衰竭的临床治疗和新药研发提供参考。方法将清洁级昆明小鼠随机分为对照组、模型组、夏枯草总三萜组和PD98059组。腹腔注射MHV-3建立小鼠暴发性肝衰竭模型,药物治疗组分别给予对应药物治疗。分析注射MHV-3后各组小鼠血清炎性因子水平及肝脏组织中MEK/ERK通路相关蛋白表达水平。结果模型组小鼠血清白细胞介素(IL)-2、IL-6及IL-10水平明显升高(P<0.05),且ERK信号通路蛋白Ras、Raf、MEK、ERK1/2表达明显升高(P<0.05),与对照组比较差异均具有显著性(P<0.05)。PD98059组和夏枯草总三萜组小鼠上述炎性因子和ERK通路蛋白的异常表达得到明显恢复(P<0.05)。结论夏枯草总三萜通过抑制过度激活的MEK/ERK信号通路和炎性反应减轻小鼠暴发性肝衰竭。
Objective To study the mechanism of MHV-3 induced fulminant hepatic failure in mice and the improvement of total triterpenoid of prunella vulgaris L,to provide a reference for the clinical treatment of liver failure and new drug research and development.Method Male Kunming mice were randomly divided into control group,model group,total triterpenoid of prunella vulgaris L group and PD98059 group.The fulminant hepatic failure mice were duplicated by injection of MHV-3.The other groups mice were received responding drug administration.Analysed of serum levels of inflammatory factors and MEK/ERK pathway related protein expression in liver tissue of mice after injection of MHV-3.Result Model group serum levels of interleukin（IL）-2,IL-6 and IL-10 levels were significantly higher（P〈0.05）,and ERK signaling pathway protein Ras,Raf,MEK,ERK1/2 expression were significantly increased（P〈0.05）,compared with control group differences were statistically significant（P〈0.05）.The abnormal expression of inflammatory cytokines and ERK pathway of mice in PD98059 and total triterpenoid of prunella vulgaris L group were significantly restored（P〈0.05）.Conclusion Total triterpenoid of prunella vulgaris L can inhibit excessive activation of MEK/ERK signaling pathway and inflammatory reaction to improve mice fulminant hepatic failure.
出处
《中国医学前沿杂志（电子版）》
2015年第10期133-136,共4页
Chinese Journal of the Frontiers of Medical Science(Electronic Version)
关键词
暴发性肝衰竭
炎性因子
ERK信号通路
Fulminant hepatic failure
Inflammatory factor
ERK signaling pathway
