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Animal model of biliary obstruction recanalization


Animal model of biliary obstruction recanalization

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Postoperative recovery from obstructive jaundice
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Postoperative recovery from obstructive jaundice

Introduction to Animal Models of Biliary Obstruction

This model is typically established by surgically ligating or transecting the common bile duct (BDL), thereby preventing normal biliary drainage into the intestine. This leads to progressive intrahepatic bile accumulation, resulting in cholestasis, hepatocellular injury, and an inflammatory response. As the model progresses, marked jaundice, hepatic fibrosis, bile duct hyperplasia, and abnormal liver function may develop, accompanied by elevated levels of ALT, AST, and bilirubin. With its high stability and excellent reproducibility, this model serves as a crucial in vivo platform for investigating the mechanisms underlying cholestatic liver injury and for evaluating anti‑fibrotic, hepatoprotective, and choleretic agents.

Service Advantages of the Aniphe BioLab Biliary Obstruction Animal Model Platform

The Aniphe BioLab animal model platform for bile duct obstruction (BDO/BDL) is centered on its ability to stably induce cholestasis and reproducibly generate hepatobiliary injury, providing a reliable in vivo model system for studying the pathogenesis of cholestatic liver diseases and for evaluating anti‑fibrotic and choleretic therapeutics.

 Comprehensive model coverage

The classical model framework is well-established.

It supports standard surgical models such as bile duct ligation (BDL), with standardized and stable technical procedures.

 Standardization of the modeling process

The degree of obstruction is controllable.

By manipulating the ligation site and surgical precision to regulate the degree of bile stasis, we can establish models corresponding to different stages of injury.

 Multidimensional Evaluation System

The model exhibits high reproducibility.

Standardized surgical techniques and perioperative management reduce intra‑procedural variability and enhance batch-to-batch consistency.

 Adapted for multi-cycle studies

Pathological features closely resemble clinical findings.

It can stably reproduce features such as cholestasis, hepatocellular injury, bile duct proliferation, and hepatic fibrosis.

 Standardization of Data Delivery

Biochemical markers are steadily increasing.

It can induce a marked elevation of bilirubin and ALT/AST, reflecting a typical cholestatic state.

 Standardization of Data Delivery

The multidimensional evaluation system has been refined.

Systematic assessment is achieved by integrating histopathological findings, collagen deposition, and liver function tests.

Modeling cycle

2–4 weeks

1  Laboratory animals

C57BL/6 mice, BALB/c mice, and SD rats

1  Positive drug

Ursodeoxycholic acid (UDCA), obeticholic acid (OCA), N-acetylcysteine (NAC), and others are commonly used to alleviate cholestasis, reduce oxidative stress, and promote hepatic functional recovery.

1  Application areas

It is primarily used in studies on hepatic repair mechanisms following the resolution of cholestasis, bile duct recanalization–induced injury, reversal of liver fibrosis, and biliary regeneration, while also being widely employed for in vivo pharmacological evaluation of hepatoprotective, anti‑inflammatory, anti‑fibrotic, and cholestasis‑related therapeutics.

Construction of an Animal Model of Biliary Obstruction

A cholestatic model was established by common bile duct ligation (BDL): the common bile duct was surgically isolated and ligated to sustain obstruction of bile flow for approximately 7 days, thereby inducing cholestasis, hepatocellular injury, and an inflammatory response. Subsequently, a second surgical procedure was performed to release the ligation or establish biliary drainage, restoring normal bile flow and mimicking the reperfusion and repair processes that occur after relief of clinical biliary obstruction.

The model can stably induce pathological changes such as hepatic repair, resolution of inflammation, and reversal of fibrosis following cholestasis, making it an important animal model for investigating the mechanisms of biliary re‑obstruction–induced injury and for evaluating hepatoprotective, anti‑inflammatory, and antifibrotic therapies.