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Alcoholic liver disease (ALD) animal model

Alcoholic liver disease (ALD) animal model

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Alcoholic liver disease/alcoholic liver injury
Psychiatric & neurological disease models

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Model Introduction

Model Introduction

Platform Service Advantages

Platform Service Advantages

Experimental results

Experimental results

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Alcoholic liver disease/alcoholic liver injury

Introduction to the ALI Animal Model

Alcoholic liver injury (ALI) refers to a condition characterized by hepatic metabolic damage caused by alcohol consumption. With the ongoing improvement in living standards, the incidence of alcoholic liver disease has been increasing year by year. In its early stages, the disease typically manifests as fatty liver; if left untreated, it may progress to more severe conditions such as hepatitis, hepatic fibrosis, and cirrhosis.

Advantages of Aniphe BioLab’s ALD Animal Model Platform Services

Aniphe Biolaboratory Animal Model Platform for Alcoholic Liver Injury (ALI) is centered on its ability to stably induce hepatic metabolic dysfunction and to reproducibly establish hepatic inflammation and steatosis, providing a reliable in vivo model system for studying the mechanisms of alcoholic liver disease and for evaluating hepatoprotective and anti-inflammatory therapeutics.

Comprehensive model coverage

The damage process is controllable.

By precisely modulating alcohol concentration, exposure duration, and nutrient ratios, liver injury models can be established at different stages.
Standardization of the modeling process

The model exhibits high reproducibility.

Standardize dietary and administration protocols to reduce inter‑individual variability and enhance the consistency of steatosis and inflammation.
Multidimensional Evaluation System

Pathological features closely resemble clinical findings.

It can stably reproduce typical features such as hepatic steatosis, hepatocellular injury, and inflammatory infiltration.
Adapted for multi-cycle studies

Metabolic mechanisms simulate reality.

It can reflect key processes such as ethanol metabolism dysregulation, enhanced oxidative stress, and hepatic dysfunction.
Standardization of Data Delivery

The multidimensional evaluation system has been refined.

Systematic assessment is achieved by integrating ALT/AST assays, histopathological analysis, and oxidative stress biomarkers.
Modeling cycle

2 weeks

1  Laboratory animals

C57 male mice

1  Positive drug

Polyene Phosphatidylcholine

1  Application areas

It is used for research on the mechanisms of alcoholic fatty liver, alcoholic hepatitis, and liver injury, as well as for in vivo efficacy evaluation of hepatoprotective, antioxidant, and anti-inflammatory drugs.

Experimental results

Construction of the ALI animal model

Animal models of alcoholic liver injury are typically established using a “chronic–acute combined” approach to mimic the progression of acute liver damage superimposed on chronic alcohol consumption.

During the chronic induction phase, animals are fed an alcohol‑containing liquid diet for 4–8 consecutive weeks, with the ethanol concentration gradually increased to maintain a stable long-term intake. This protocol induces hepatic steatosis, heightened oxidative stress, and progressive impairment of liver function. Subsequently, an acute ethanol gavage challenge is administered, delivering a single high dose to rapidly exacerbate hepatic metabolic dysregulation and inflammatory responses, thereby further aggravating liver injury.

This model consistently exhibits hallmark features such as elevated serum ALT and AST levels, hepatic steatosis, and upregulated inflammatory cytokines, making it a classic experimental platform for investigating the pathogenic mechanisms of alcoholic liver disease and evaluating hepatoprotective agents.

Liver coefficient and biochemical results

In the model group, the liver coefficient was significantly increased, and the levels of triglycerides (TG), alanine aminotransferase (ALT), and aspartate aminotransferase (AST) were markedly elevated. Hepatocytes in the model group exhibited large, red‑stained lipid droplets with widespread distribution, and obvious steatosis was observed. Furthermore, hepatocytes showed marked enlargement, disorganized arrangement, and the presence of irregular lipid vacuoles. These findings confirm that the alcoholic liver injury model was successfully established.

 

 

Oil Red O staining results

Oil Red O staining revealed that hepatocytes in the control group contained virtually no red lipid droplets, whereas the liver of the alcohol‑induced model group was densely populated with numerous red‑stained lipid droplets, with extensive lipid accumulation in hepatocytes, thereby confirming the successful establishment of the alcohol‑induced fatty liver model.

 

 

HE staining results

Hematoxylin–eosin staining revealed that the liver tissue in the control group maintained an intact architecture with no obvious lipid droplet vacuolization; in contrast, the model group exhibited hepatocytes densely packed with numerous lipid vacuoles and severe steatosis, indicating that the alcoholic fatty liver model was successfully established.

 

 

Summary of Experience

01 In this experiment, the feed was formulated into a liquid state; it is optimal to replace the feed daily. Any excess prepared feed should be stored at 4°C in a sealed container for no more than one week.

02 Alcohol affects food intake; if animals exhibit poor condition or mortality, the concentration is recommended to be maintained at 4% or lower.

03 To exacerbate fatty liver and hepatic injury, a single high-concentration alcohol gavage can be administered on the final day of model induction.