肝脏是一个具有独特免疫学特征的器官。Toll样受体（TLRs）能通过特异性地识别病原相关的分子模式，偶联信号传导，激活天然免疫和获得性免疫系统。最新研究表明，LPS/TLR4信号途径介导的免疫网络紊乱与肝衰竭有密切关系，从而为从免疫调控角度开展肝衰竭治疗学研究开辟了一条全新的思路。本课题组前期应用解毒化瘀Ⅱ方治疗肝衰竭，获得了降低病死率的满意疗效，并从炎症分子调控探讨了作用机制。但显然单一基因/蛋白的研究很难洞悉本病的免疫网络全貌及中药的药效靶点。蛋白质组学是一种强调将机体作为整体研究的方法学，与中医学整体观念及中药药效的多靶点性相切合。本项目以D-GalN+LPS复制肝衰竭大鼠模型，采用蛋白质芯片技术，动态观测各组大鼠血清、肝组织中LPS/TLR4信号途径免疫网络的蛋白质组学特征，并通过对肝衰竭免疫网络蛋白质谱解析，尝试从整体层面揭示肝衰竭的发病机制及解毒化瘀Ⅱ方的效用靶点。

Liver is an organ with unique immunological features. Toll-like receptors (TLRs) may activate the natural and acquired immune systems by recognizing pathogen-related molecules and coupling to signal transduction pathways. According to recent studies, hepatic failure is closely related to LPS/TLR4-mediated immune disorder. Our previous work showed that the use of the Jieduhuayu II preparation was associated with a reduced mortality rate in hepatic failure. The present study was designed to investigate the pathogenesis of liver failure and the potential target of the Jieduhuayu II preparation in rats with D-GalN+LPS-induced hepatic failure, by performing proteomic analysis of the LPS/TLR4 signaling pathway. So the cause of hepatic failure can be explained and the effective site of the Jieduhuayu II preparation be found.