Introduction to AP Animal Models

The animal model of acute pancreatitis (AP) is a classic experimental system used to mimic acute pancreatic inflammatory injury and the systemic inflammatory response syndrome. It is commonly established through methods such as retrograde injection into the biliopancreatic duct, pharmacological induction, or dietary/metabolic interventions, including models based on repeated injections of high-dose caerulein, L‑arginine–induced models, and models involving retrograde infusion of bile salts or sodium taurocholate into the pancreatic duct.

Once established, the model can induce pancreatic acinar cell injury, aberrant activation of pancreatic enzymes, and autolysis of pancreatic tissue, leading to marked pathological changes such as pancreatic edema, hemorrhage, and necrosis, accompanied by inflammatory cell infiltration and significant elevations in pro-inflammatory cytokines like TNF‑α and IL‑6. In some severe cases, systemic inflammatory responses and multiorgan dysfunction may also occur, making this model an essential tool for investigating the pathogenesis of acute pancreatitis and for evaluating anti‑inflammatory and pancreatic‑protective therapeutics.

Advantages of Aniphe BioLab’s AP Animal Model Platform Services

Aniphe Biolaboratory acute pancreatitis (AP) animal model platform is centered on its ability to stably induce pancreatic inflammation and reliably reproduce pancreatic injury, providing a robust in vivo model system for studying the mechanisms of pancreatitis and for evaluating anti-inflammatory and pancreatic‑protective therapeutics.

	Multiple modeling approaches are well-established. It supports classic models such as caerulein‑induced, L‑arginine‑induced, and retrograde intraductal injection of bile salts/sodium taurocholate.
	The extent of the injury is controllable. By precisely controlling the dose, administration frequency, and induction pathway, mild, moderate, and severe pancreatitis models can be established.
	The model exhibits high reproducibility. Standardized induction protocols reduce inter‑individual variability and enhance the consistency of inflammatory severity and pathological findings.
	Pathological features closely resemble clinical findings. It can reliably reproduce the typical features of pancreatic edema, hemorrhage, necrosis, and acinar cell injury.
	Inflammatory response is stable. It can induce a significant increase in inflammatory cytokines such as TNF-α and IL-6, as well as local and systemic inflammatory responses.
	The multi-dimensional evaluation system has been refined. Systematic assessment is achieved by integrating serum enzymatic markers (such as amylase and lipase), histopathological findings, and inflammatory biomarkers.

Modeling cycle	About one week
Laboratory animals	C57BL/6 mice and SD rats
Positive drug	Octreotide (a somatostatin analog), gabexate (a protease inhibitor), ulinastatin, and others; dexamethasone was used as an anti-inflammatory control, while edaravone was employed to assess antioxidant stress.
Application areas	Pathogenesis of pancreatitis (autodigestion by pancreatic enzymes, inflammatory cascade, and microcirculatory dysfunction); screening for biomarkers predictive of disease severity; evaluation of anti-inflammatory and pancreatic‑protective agents; research on intervention strategies for SIRS and MODS.

Construction of AP animal models

In the caerulein‑induced intraperitoneal injection model, animals are subjected to repeated intraperitoneal injections of caerulein at intervals while fasting. This sustained stimulation of pancreatic acinar cell secretion leads to excessive activation of pancreatic enzymes and edema of the pancreatic stroma, thereby establishing acute edematous pancreatitis. In contrast, the retrograde injection of sodium taurocholate into the biliopancreatic duct model involves surgically exposing the common bile and pancreatic ducts, followed by retrograde infusion of a defined concentration of sodium taurocholate. This directly damages pancreatic acinar cells and triggers premature activation of pancreatic enzymes, rapidly inducing hemorrhagic necrosis of the pancreas and a robust inflammatory response.

These two methods are respectively suitable for studying mild-to-moderate and severe acute pancreatitis, and constitute classic in vivo models commonly used in pharmacological efficacy evaluation and mechanistic studies.