녹아웃(KO) 마우스 | Cyagen Korea

급성 췌장염 마우스 모델


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급성 췌장염(acute pancreatitis, AP)은 사망률이 높고, 병인, 발병 메커니즘 및 임상 증상이 복잡하다. 현재 췌장 괴사의 발생과 발전을 막을 수 있는 효과적인 치료 방법이 없고, 한번 발병하면 다기관 손상을 유발할 수 있으며, 그 사망률은 50~60%이다. 1856년 첫 AP 동물 모델이 제작된 이래 동물 모델은 AP 연구에서 중요한 역할을 해 왔습니다. 췌장염 동물 모델의 제작 방법에는 주로 다음과 같다.

 

1. Sodium Taurocholate Modeling

Methods: Retrograde injection of sodium taurocholate into the bile duct resulted 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
Cyagen Professional Surgical Disease Models Team Will Elaborately Present Practical Modeling Case for You:
1) Mouse Acute Pancreatitis Modeling Method
2) Mouse Acute Pancreatitis Model Evaluate Method

 

2. Ceruletide (INN) Modeling

Method: Mouse were fasted but drink freely 12 hours before surgery. Intraperitoneal injection with 25μg/kg dose Ceruletide (a.k.a. INN, caerulein) 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 - if perfused with PGE2, it will cause acute necrotizing pancreatitis. Schmidt’s team perfused low-volume glycodeoxycholic acid combined with intravenous caerulein through pancreatic duct to create rat acute pancreatitis model which present well-distributed injury of moderate acinar necrosis, which is suitable for pancreatitis research.

 

4. Pancreatic ductal ligation

Acute pancreatitis may be induced by ligating the distal bile duct in duodenum or pancreatic duct. Lerch’s team ligated in the ampullary region and edematous pancreatitis appeared in 6 hours, while at 12 hours post-ligation the pancreas presented bleeding, necrosis, inflammatory cell infiltration. The advantage of this modeling is includes avoidance of the drug-induced nonspecific systemic effects and it is similar to human bile reflux pancreatitis. Runzi’s team improved the modeling method - cutting off the duodenum’s proximal end and ligate both ends with common bile duct, lettijg pancreatic juice to flow into the closed loop - as its internal pressure increases, reflux occurs, 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.

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