Acute pancreatitis (AP) is an inflammatory reaction of pancreatic tissue self-digestion, edema, hemorrhage, and even necrosis after the activation of pancreatic enzymes in the pancreas caused by a variety of etiologies. This study was aimed to explore the functions and mechanism of Wip1 in AP. Twenty male SD rats were randomly assigned into 2 groups (control group: saline treatment; AP group: cerulein treatment). And cerulein-treated AR42J cells were conducted as AP model in vitro. The levels of amylase were detected by using the Beckman biochemical analyzer. The levels of IFNβ and TNFα were analyzed by ELISA. The autophagosomes were observed by transmission electron microscopy. The Wip1-specific shRNAs were transfected to AR42J cells to silence the expression of Wip1. The levels of Wip1 were measured by qRT-PCR and Western blot. The levels of STING/TBK1/IRF3 and LC3 were measured by Western blot. The AP model was successfully constructed by cerulein administration. Wip1 was notably upregulated in AP models. Autophagy and STING pathway activation were involved in the development of AP. Wip1 inhibition counteracts the promotion effect on inflammatory response induced by cerulein in AR42J Cells. Wip1 inhibition inhibited the activity of the STING/TBK1/IRF3 and reduced LC3 levels in AP. This study preliminarily explored that Wip1 could regulate autophagy and participate in the development of AP through the STING/TBK1/IRF3 signaling pathway.

急性胰腺炎(acute pancreatitis,AP)是多种病因引起胰腺内胰酶激活后胰腺组织自身消化、水肿、出血甚至坏死的炎症反应。本研究旨在探讨Wip1在AP中的功能和机制。20只雄性SD大鼠随机分为2组（对照组：盐水处理；AP组：雨蛙素处理）。并将经雨蛙素处理的 AR42J 细胞作为体外AP 模型进行. 使用贝克曼生化分析仪检测淀粉酶水平。通过ELISA分析IFNβ和TNFα的水平。通过透射电子显微镜观察自噬体。将 Wip1 特异性 shRNA 转染到 AR42J 细胞中以沉默 Wip1 的表达。通过 qRT-PCR 和蛋白质印迹测量 Wip1 的水平。通过蛋白质印迹测量 STING/TBK1/IRF3 和 LC3 的水平。雨蛙素给药成功构建了AP模型。Wip1 在 AP 模型中显着上调。自噬和 STING 通路激活参与了 AP 的发展。Wip1 抑制抵消了雨蛙素在 AR42J 细胞中诱导的炎症反应的促进作用。Wip1 抑制抑制了 STING/TBK1/IRF3 的活性并降低了 AP 中的 LC3 水平。