胰酶异常激活和炎症反应是SAP发生发展的关键，自噬与胰酶激活呈正比关系，炎症因子能激活胰腺腺泡细胞自噬。本课题组前期发现，Ang(1-7)抑制胰腺腺泡细胞炎症反应，激活自噬信号ClassI PI3K通路，但Ang(1-7)在SAP胰腺细胞自噬中的作用及其机制尚不清楚。故本项目研究：Ang(1-7)在SAP胰腺腺泡细胞自噬中的作用：动态观察Ang(1-7)干预体内外SAP模型对自噬相关蛋白表达的影响，电镜和吖啶橙染色观察自噬体形成情况。明确Ang(1-7)在SAP细胞自噬中的作用，为寻找SAP治疗新靶点提供实验依据。

Inflammation and the inappropriate activation of trypsinogen to trypsin within pancreatic acinar cells are key initiating event in pancreatitis. Autophagy has direct relationship with activation of trypsin, moreover, autophagy of pancreatic acinar cells can be activated by inflammatory cytokines. Our previous research indicated that Ang(1-7) suppressed the inflammation of pancreatic acinar cells and activated ClassI PI3K signal pathway of autophagy, however, the mechanisms responsible for Ang(1-7) in autophagy of pancreatic acinar cells have not been elucidated with certainty..In this study, we will first observe the dynamic expression of autophagy related proteins and the formation of autophagosome by electron microscope and acridine orange staining after using Ang(1-7) on SAP model in vivo and in vitro to confirm the role of Ang(1-7) in pancreatic acinar cell of SAP. Second, we will use Ang(1-7) on cerulein-treated over-expressed or down-expressed ClassI P13K or ClassIII PI3K AR42J or MPC-83 cells to clarify the molecular mechanism of Ang (1-7) in regulating autophagy of pancreatic acinar cell via PI3K pathways. Confirmating the role and mechanism of Ang (1-7) in autophagy can provide experimental and theoretical basis to find new targets for treatment of SAP.