高迁移率族蛋白 B1（HMGB1）是脓毒症致死效应的最重要的晚期炎症介质。研究表明，NALP3炎性体活化是脓毒症过程中巨噬细胞主动释放HMGB1的关键调节因素。中医认为脓毒症基本病机是正虚毒损、络脉闭阻，扶正解毒通络是主要治则，参附黄配方是其有效方剂。前期研究发现参附黄配方可延长脓毒症大鼠生存时间伴随HMGB1水平的降低，并具有抑制NALP3炎性体底物IL-1β分泌的作用。以此为线索，本课题首先复制CLP大鼠脓毒症模型，观察参附黄配方对大鼠HMGB1及炎症介质释放、NALP3炎性体活化的影响，明确脓毒症过程中NALP3炎性体活化及HMGB1释放的变化规律及参附黄配方的干预作用；同时通过LPS诱导巨噬细胞模型结合表达谱芯片检测，观察参附黄配方对差异基因/P2X7R/NALP3/HMGB1通路的调节，阐明参附黄配方的作用靶点。综合分析扶正解毒通络法的作用基础，提升其科学内涵，指导临床用药。

High mobility group protein B1 (HMGB1) is one of most important late inflammatory mediators which lead to the lethal effect of severe sepsis. Recent researches demonstrated that activation of NALP3 inflammasome contributes to the proactive releasement of HMGB1 from macrophages in sepsis. In clinical, 'Strengthening healthy energy and detoxifying and dredging collaterals therapeutics’ is the principle of sepsis treatment and Shen Fu Huang(SFH) prescription is an effective prescription. Our previous data showed that Shenfuhaung Decoction notably prolonged the survival time of sepsis rat via inhibiting the secretion of HMGB1 as well as IL-1β produced by NALP3 inflammasome. Based on our findings, we try to further detect the regulatory effect of Shenfuhuang Decoction on expression of HMGB1 and NALP3 inflammasome activation using a CLP rat sepsis model, which illustrates the roles of NALP3 inflammasome and HMBG1 in sepsis and the intervention of Shenfuhuang Decoction. Furthermore, we try to investigate the regulatory effect of Shenfuhuang Decoction on P2X7R/NALP3/HMGB1 signaling pathway in LPS-stimulated RAW264.7 macrophages in vitro, which may better our understanding of potential targets of Shenfuahung Decoction. we will explore the possible therapeutic targets of SFH prescription from animal model, cells and molecular levels and provide scientific evidence for clinical treatment.