重症急性胰腺炎（SAP）和中蛇毒者，有全身炎症反应综合征（SIRS）、组织坏死这两个相似的病理过程，两者均与分泌型磷脂酶A2（sPLA2）有关。为什么中蛇毒者会出现这么严重的后果，而蛇自身不出现中蛇毒的病理过程呢？原因是蛇血清中含磷脂酶A2抑制剂（PLI）。我们前期工作，从蛇血清中分离出多种新型PLI，并证实它们能抑制人源性sPLA2。而在SAP中，sPLA2可能通过炎症途径影响SIRS；并可能影响细胞的自噬功能，最终导致胰腺坏死。所以抑制sPLA2的活性有可能治疗SAP。本研究拟从江西常见蛇种血清中筛选出新型PLI。经过测序，找出新型PLI 抑制sPLA2的关键“基序”。以此设计合成小分子模拟肽，将其用于SAP大鼠；同时构建新型PLI的表达体系，并转染AR42J腺泡细胞，从体内和体外实验观察新型PLI抑制sPLA2的能力及其影响炎症通路、自噬与坏死的关系，为治疗SAP提供新的方法。

In patients of severe acute pancreatitis (SAP) and snake venom, two similar pathological process, systemic inflammatory response syndrome (SIRS) and tissue necrosis, both are related to secretory phospholipase A2 (sPLA2). Why does the patient of the snake venom show such serious consequences, but the snake itself never shows the pathological process? The reason is that the snake serum contains phospholipase A2 inhibitor (PLI) , New PLI were isolated from snake serum and proved that they can inhibit anthropogenic sPLA2 in our previous research. In the SAP,sPLA2 may affect SIRS through inflammatory pathways, and may affect cell autophagy function , eventually leading to pancreatic necrosis . Therefore, it is possible to Inhibit the activity of sPLA2 treatment SAP. This study plan to screen the new PLI from common snake serum in jiangxi. New PLI inhibiting sPLA2 key "motif” were found out after sequencing. We use them Design and synthesis of small molecule mimetic peptide , which was used for SAP rats ; meanwhile,building new PLI expression system , transfecting AR42J acinar cells , learning the new PLI suppress sPLA2 function in vitro and in vivo experimental, and impact the relation of inflammatory pathways,autophagy and necrosis , to provide a new method for the treatment of SAP .