Many animal models are available to investigate the pathogenesis of pancreatitis, an inflammatory disorder of the pancreas. However, the secretagogue hyperstimulation model of pancreatitis is the most commonly used. Animals infused with high doses of cholecystokinin (CCK) exhibit hyperamylasemia, pancreatic edema, and acinar cell injury, which closely mimic pancreatitis in humans. Intra-acinar zymogen activation is an essential early event in the pathogenesis of secretagogue-induced pancreatitis. Early in the course of pancreatitis, lysosomal hydrolases colocalize with digestive zymogens and activate them. These activated zymogens then cause acinar cell injury and necrosis, a characteristic of pancreatitis. Besides being the site of initiation of injury in pancreatitis, acinar cells also synthesize and release cytokines and chemokines very early in the course of pancreatitis, which then attract and activate inflammatory cells and initiate the disease's systemic phase.

中文翻译：

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为什么胰腺过度刺激会导致胰腺炎？

许多动物模型可用于研究胰腺炎（胰腺炎性疾病）的发病机制。但是，胰腺炎的促分泌素过度刺激模型是最常用的。注入高剂量胆囊收缩素（CCK）的动物表现出高淀粉血症，胰腺水肿和腺泡细胞损伤，这与人类的胰腺炎极为相似。腺泡内酶原激活是促分泌素诱导的胰腺炎发病机理中必不可少的早期事件。在胰腺炎的早期，溶酶体水解酶与消化酶原共定位并激活它们。这些活化的酶原然后会引起腺泡细胞损伤和坏死，这是胰腺炎的特征。除了是胰腺炎损伤的起始部位，