ACLF病理过程中过强的免疫反应加重肝细胞炎症及坏死，诱发死亡等不良预后。体外细胞实验发现在外源性PGE2刺激下，CD4+CD25+Treg细胞通过过表达APE1/Ref-1，使抑炎因子IL-10、TGF-β分泌下降，加重炎症。但APE1/Ref-1在ACLF免疫反应过程中的作用尚有待阐明。解毒化瘀Ⅱ方能上调IL-10，抑制炎症，有免疫调控作用。据此我们认为：解毒化瘀Ⅱ方可能通过CD4+CD25+Treg低表达APE1/Ref-1而上调IL-10、TGF-β表达，缓解肝细胞炎症及坏死。本项目拟通过构建ACLF大鼠模型，采用Western Blot、miRNA芯片等实验技术，揭示APE1/Ref-1在调控ACLF大鼠CD4+CD25+Treg细胞免疫过程中的作用及具体路径，明确解毒化瘀Ⅱ方对ACLF大鼠APE1/Ref-1表达的影响及免疫调控靶点，为寻求ACLF免疫调控治疗靶点提供科学依据。

ACLF pathology stimulates a strong immune response in the process of aggravating liver inflammation and necrosis, inducing adverse outcomes such as death. Found under exogenous PGE2 may stimulate the cells in vitro experiment, CD4+CD25+Treg cells through the expression of APE1/Ref-1, the suppression of inflammatory factor IL-10, TGF-beta secretion decline, accentuate inflammation. But in ACLF APE1/Ref-1 the role of immune response process remains to be elucidated. Detoxification blood Ⅱ can increase IL-10, inhibit inflammation and immune regulation function. Accordingly we think: blood detoxification Ⅱ may by CD4+CD25+Treg low expression of APE1/Ref-1 and IL-10, TGF-beta expression, relieve inflammation and liver cell necrosis. This project proposed by constructing ACLF rats model, using Western Blot, micrornas chips, such as experimental technology, reveal APE1/Ref-1 in regulating ACLF rat CD4+CD25+Treg cells in the process of immune function and specific path, clear blood detoxification on the Ⅱ party ACLF rats APE1/Ref1 expression and the influence of immune regulation target, which will provide a scientific basis for seeking ACLF immune regulation of therapeutic targets.