复方861是抗肝纤维化的有效药物，可通过下调TGF-β1发挥抗肝纤维化作用。新近研究显示，核转录抑制因子SnoN是调节纤维化形成的重要因子，其表达异常直接影响肝纤维化进程，而TGF-β1和BMP-7介导的Smads信号能分别下调和上调SnoN表达，但二者交互作用尚不清楚。本项目利用大鼠胆管梗阻肝纤维化模型：1.观察复方861对纤维化肝组织SnoN基因和蛋白表达的影响；2.观察复方861对TGF-β1/Smad2/Smad3和BMP-7/Smad1/Smad5两条信号通路表达变化的影响，探讨其调控SnoN表达分子机制；3.利用BMP-7干预纤维化进程，观察SnoN、TGF-β1信号表达变化，明确两条信号通路调控SnoN表达的交互作用，并观察复方861对BMP-7调控SnoN表达的干预作用。本项目从细胞信号交互作用水平探讨肝纤维化发病机制及复方861干预作用，为中医药治疗纤维化提供实验依据。

Our previous studies had shown that herbal compound 861 (Cpd861)could up-regulate TGF-β1 to play the role of in treating hepatic fibrosis. It was reported recently that Smad transcriptional co-repressor SnoN acts as an antagonist that tightly controls the trans-activation of TGF-β1/Smad target,and the loss of SnoN is a critical,pathogenic event that may lead to hepatic fibrosis, TGF-β1 signal downregulation the expression,and BMP-7 signal have an opposite role.But,the cross-talk of the two signal in regulation of SnoN expression is remain unknow. In this study, we will use bile duct ligation(BDL) induced liver fibrosis rat model.1.Observation the influence of Cp861 on the protein and mRNA expression of SnoN in liver fibrosis.2.We will detected Cp861 on the expression of the two main signals that regulation SnoN expression TGF-β1/Smad2/Smad3, BMP-7/Smad1/Smad5/Smad8 , and discuss the molecular and mechanism of Cp861 regulation the expression of SnoN.3.By intervening liver fibrosis progression use BMP-7,detecting the expression of TGF-β1/Smad2/Smad3 signal molecules, SnoN pretein and mRNA.Finally,Cp861 will be used to intervention the regulation of BMP-7 on SnoN expression.This study will help to provide more experimental basis for the mechanism of Cpd861 removing blood stasis in treating hepatic fibrosis.