Acute pancreatitis (AP) is a common disorder that presents complex etiology, pathogenesis, and clinical manifestations - ranging from mild disease, to sepsis, and even multisystem organ failure (MOF). Severe acute pancreatitis (SAP) causes damage to multiple organs that may result in necrosis – which can lead to fatality rates up 50%～60%. At present, there is no specific treatment to prevent pancreatic necrosis. Since the establishment of the first experimental acute pancreatitis (AP) animal model in 1856, several AP mouse and rat models have been developed - which have played an important role in acute pancreatitis research. The main methods of acute pancreatitis (AP) animal model generation are as follows:
1. Sodium Taurocholate Modeling
Methods: Retrograde injection of sodium taurocholate into the bile duct result in acute pancreatic hyperemia and hematoma in mice.
Detection Index: Acute hyperemia and edema of pancreas and saponification spots in abdominal cavity were observed.
Picture 1: Acute hyperemia and edema of pancreas in 5 min after injection
Picture 2: Saponification spots were observed in abdominal cavity within 24-48 hours after injection
Acute Pancreatitis Modeling Course
Inquire to have Cyagen’s Professional Surgical Disease Models team present practical modeling cases for you, such as:
1) Mouse Acute Pancreatitis Modeling Method
2) Mouse Acute Pancreatitis Model Evaluation Method
2. Caerulein (INN) Modeling
Method: Mouse were fasted but drink freely 12 hours before surgery. Intraperitoneal injection with 25μg/kg dose Caerulein (a.k.a. INN, ceruletide) leads to development of edematous acute pancreatitis (CIP) in 5 hours.
Features: Present edematous acute pancreatitis (CIP), the pancreatitis is comparatively mild
3. Retrograde Infusion of Bile Duct
Retrograde infusion of the bile duct involves ligating the pancreaticobiliary duct, inserting a cannula in the main pancreatic duct and injecting a substance (like sodium deoxycholate and autologous bile etc.) such as pancreatin. The injection of pancreatin arouses acute pancreatitis (AP) - if perfused with Prostaglandin E2 (PGE2), it will cause acute necrotizing pancreatitis (NP). Perfusion of low-volume glycodeoxycholic acid combined with intravenous caerulein through pancreatic duct results in an rat model of AP which presents well-distributed injury of moderate acinar necrosis, which is suitable for pancreatitis research.
4. Pancreatic ductal ligation
Acute pancreatitis (AP) may be induced by ligating the distal bile duct in duodenum or pancreatic duct. Ligating the ampullary region leads to edematous pancreatitis in 6 hours, while at 12 hours post-ligation, the pancreas presents bleeding, necrosis, and inflammatory cell infiltration. This modeling method avoids chemically induced nonspecific systemic effects and it is phenotypically similar to human bile reflux pancreatitis. An improved modeling method has been developed - cutting off the duodenum’s proximal end and ligating both ends with common bile duct - letting pancreatic juice flow into the closed loop, increasing internal pressure, causing reflux, and resulting in acute necrotizing pancreatitis. Edema pancreatitis occurred 4h after operation, and hemorrhage and necrosis occurred 9-12h. In addition, there is also the use of pancreatic duct ligation and pancreatic artery or vein blockade to produce acute pancreatitis.
Cyagen can provide you with a variety of drug evaluation models along with phenotype analysis services – delivering reliable and expedient data reporting for your project.
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