坏死是重症急性胰腺炎（SAP）中胰腺腺泡细胞的主要死亡方式，而程序性坏死作为一种可调控的坏死方式在SAP中发挥着重要的作用。研究发现通过调控程序性坏死通路中受体相互作用蛋白3（RIP3），可以减少腺泡细胞坏死，减轻SAP病情。“通里攻下”方剂大承气汤可通过抑制胰腺腺泡细胞坏死进而治疗SAP。本课题组前期研究发现，大承气汤能够抑制SAP发生过程中RIP3蛋白的上调，同时，在泛Caspase抑制剂zVAD条件下，同样能够下调RIP3的蛋白表达。据此我们认为大承气汤通过Caspase非依赖程序性坏死途径是治疗SAP的主要作用机制之一。基于这个假设，本课题旨在于以体内外SAP模型，RIP3基因突变、缺失细胞及动物为研究对象，阐明大承气汤通过抑制SAP程序性坏死过程中RIP3的分子机制。该研究成果对于揭示大承气汤抑制SAP程序性坏死的分子机制，明确大承气汤治疗SAP的重要靶点有着重要的意义。

Necrosis is the major type of pancreatic acinar cell death in severe acute pancreatitis (SAP). Programmed cell necrosis, necroptosis was plays an important role in SAP. Reportedly, RIP3 is a potential target for effectively regulating SAP. Purging prescription Dachengqi Decoction could ameliorate the severity of SAP by reducing acinar cell necrosis. However, the biological mechanism governing its action is remain unclear. Previously, we found that Dachengqi Decoction prevent SAP necroptosis though inhibiting the expression of RIP3 by a caspase 8 independent manner. Based on our previous study, we will perform the following two studies: Reveal the pharmacological effect of Dachengqi Decoction on RIP3 mediated necroptosis in SAP. (2) Clarify the mechanism of RIP3 on Dachengqi Decoction ameliorated the acinar cell necroptosis during SAP. This research will reveal the molecular mechanism of the Dachengqi Decoction inhibiting necroptosis in SAP.