Liver Disease Models
We provide a comprehensive portfolio of preclinical liver disease animal models to support drug discovery and translational research. Our offerings cover alcoholic liver disease (ALD), non-alcoholic steatohepatitis / metabolic dysfunction-associated steatotic liver disease (NAFLD/MASLD), liver fibrosis, acute liver injury, and chronic liver disease, enabling flexible model selection based on disease stage and mechanism of action.
To support robust and reproducible studies, we also offer integrated endpoint analyses, including histopathology, serum biochemistry, fibrosis markers, and molecular profiling.
Liver Disease Overview
Liver disease spans a wide range of disorders from early metabolic dysfunction to late-stage fibrosis, cirrhosis and Hepatocellular carcinoma (HCC). NAFLD/MASLD is now the most common form of chronic liver disease, affecting nearly 1 in 3 adults worldwide.
While early stages of disease are typically asymptomatic, over time the disease can progress to include steatosis, inflammation and fibrosis. Without intervention, liver disease can ultimately progress to cirrhosis or liver failure. Obesity, type 2 diabetes and metabolic syndrome have been closely linked to increased risk of liver disease and highlights the need for robust preclinical models.
Fig. 1. Core Pathogenesis of Liver Disease.
Creative Bioarray's Liver Disease Models
| Model | Type | Key Feature | Research Application | Drug Application |
| Lieber-DeCarli Liquid Diet Model | Diet-induced ALD model | Chronic ethanol-containing liquid diet that mimics long-term alcohol consumption and induces steatosis and mild inflammation | Early-stage ALD and fatty liver research | Metabolic regulators, anti-steatosis compounds |
| EtOH + HFD / LPS Models | Multi-hit combined model | Ethanol exposure combined with high-fat diet or LPS to mimic "second-hit" mechanism in ALD progression | ALD progression and inflammatory mechanisms | Anti-inflammatory, metabolic, and gut-liver axis-targeted therapies |
| Model | Type | Key Feature | Research Application | Drug Application |
| HFD Model | Diet-induced metabolic model | High-fat diet leading to obesity, insulin resistance, and hepatic steatosis | Early NAFLD research | Metabolic and anti-steatosis drugs |
| STZ + HFD Model | Multi-hit combined model | STZ + high-fat diet leading to diabetes-associated NASH with steatosis, inflammation, and fibrosis progression. | NASH progression, fibrosis, and HCC development research | Anti-steatotic, anti-inflammatory, and anti-fibrotic agents |
| MCD Diet Model | Nutrient-deficient diet model | Methionine and choline deficiency causing rapid NASH and fibrosis without obesity | NASH mechanism studies | Anti-inflammatory and anti-fibrotic agents |
| CDAA Diet Model | Amino acid-defined diet model | Gradual development of steatosis and fibrosis with better reproducibility | Progressive NASH research | Anti-fibrotic therapies |
| GAN Diet Model | Advanced diet-induced model | High-fat, high-fructose, and cholesterol diet mimicking human NASH progression | Translational NASH studies | Multi-target NASH drugs |
| ob/ob Mouse Model | Genetic obesity model | Leptin-deficient mice with severe obesity and insulin resistance | Metabolic dysfunction studies | Anti-diabetic and metabolic drugs |
| Model | Type | Key Feature | Research Application | Drug Application |
| CCl₄-Induced Fibrosis Model | Chemical-induced fibrosis model | Repeated carbon tetrachloride exposure causing hepatocyte injury, inflammation, and progressive extracellular matrix deposition | Classic liver fibrosis research and drug screening | Anti-fibrotic and antioxidant compounds |
| TAA-Induced Fibrosis Model | Chemical toxicity model | Thioacetamide-induced chronic hepatotoxicity leading to stable and reproducible fibrosis formation | Fibrosis progression studies | Anti-fibrotic and hepatoprotective agents |
| BDL Model | Surgical cholestasis model | Bile duct ligation causing bile accumulation, cholestatic injury, and rapid fibrosis development | Cholestatic liver disease studies | Anti-cholestatic and anti-fibrotic therapies |
| Genetic Fibrosis Models | Genetic model system | Gene knockout or mutation affecting liver metabolism or bile transport pathways | Mechanistic fibrosis research | Target-based therapeutic validation |
| Model | Type | Key Feature | Research Application | Drug Application |
| CCl₄ Chronic Model | Chemical-induced chronic injury model | Long-term carbon tetrachloride exposure leading to sustained inflammation and fibrosis progression | Chronic liver disease and fibrosis studies | Anti-fibrotic and antioxidant drugs |
| BDL Chronic Model | Surgical cholestatic injury model | Persistent bile duct obstruction causing chronic cholestasis and fibrosis | Cholestatic liver disease research | Anti-cholestatic and anti-fibrotic therapies |
| ALD / ASH Models | Alcohol-induced chronic disease model | Long-term ethanol exposure leading to steatosis, inflammation, and steatohepatitis | Alcohol-related chronic liver disease | Metabolic and anti-inflammatory drugs |
| NAFLD / MASLD Models | Diet-induced metabolic disease model | High-fat or nutrient-deficient diets inducing fatty liver, inflammation, and fibrosis | Metabolic-associated chronic liver disease | Anti-NASH and metabolic drugs |
| Model | Type | Key Feature | Research Application | Drug Application |
| APAP Overdose Model | Drug-induced acute injury model | Acetaminophen overdose causing oxidative stress and massive hepatocyte necrosis | Drug-induced liver injury (DILI) studies | Hepatoprotective and detoxification agents |
| CCl₄ Acute Model | Chemical injury model | Single high-dose exposure causing rapid hepatocyte damage and inflammation | Acute liver toxicity research | Antioxidants and protective compounds |
| TAA Acute Model | Chemical toxicity model | Acute thioacetamide exposure leading to severe liver injury and enzyme elevation | Hepatotoxicity evaluation | Liver-protective drugs |
| LPS / D-GalN Model | Immune-mediated injury model | Endotoxin-driven inflammatory liver failure via immune overactivation | Acute immune liver injury | Anti-inflammatory and immunomodulatory agents |
| ConA Model | T-cell mediated hepatitis model | Concanavalin A-induced immune activation causing autoimmune-like hepatitis | Immune liver disease research | Immunosuppressive therapies |
Available Endpoint
We provide comprehensive endpoint analysis to support efficacy evaluation and mechanistic studies, including:
Histopathological Analysis
- Hematoxylin & Eosin (H&E) staining for general liver morphology
- Oil Red O staining for hepatic lipid accumulation (steatosis)
- Sirius Red / Masson's Trichrome staining for collagen deposition and fibrosis
- NAFLD activity score (NAS) evaluation
- Fibrosis staging and histological grading
Serum Biochemical Analysis
- Alanine aminotransferase (ALT)
- Aspartate aminotransferase (AST)
- Alkaline phosphatase (ALP)
- Total bilirubin (TBIL)
- Lipid profile (TG, TC, LDL, HDL)
Fibrosis and Extracellular Matrix Markers
- α-Smooth muscle actin (α-SMA)
- Collagen type I (COL1A1 / COL1A2)
- Transforming growth factor-β (TGF-β)
- Hydroxyproline content
- Tissue inhibitor of metalloproteinases (TIMP)
Molecular Biology Analysis
- qPCR gene expression profiling
- Western blot protein quantification
- RNA sequencing (transcriptome analysis)
- Inflammatory cytokines (TNF-α, IL-6, IL-1β)
Inflammation & Oxidative Stress Markers
- Myeloperoxidase (MPO) activity
- Reactive oxygen species (ROS) levels
- NF-κB pathway activation
- Glutathione (GSH) and oxidative stress balance
Metabolic Function Assessment
- Glucose tolerance test (GTT)
- Insulin tolerance test (ITT)
- Body weight and liver index
- Hepatic triglyceride content
Need Help Choosing a Liver Disease Model?
Selecting the right preclinical liver disease model is essential for accurate study design and reliable drug evaluation.
Our experts can help you match your compound with the most suitable model based on disease stage and mechanism of action.
FAQ
What is the most frequently utilized model for NAFLD or MASH studies?
Typically, the high-fat diet (HFD) model is used to model metabolic dysfunction and obesity. For NASH progression and liver fibrosis studies, the MCD diet model and GAN diet model are among the most frequently utilized models. The choice depends on whether the focus is early metabolic changes or advanced disease stages.
Which model of liver fibrosis is most commonly used for preclinical studies?
Carbon tetrachloride (CCl₄) is by far the most common liver fibrosis model used due to its high reproducibility and robust induction of fibrosis. Other commonly used models include TAA model and bile duct ligation (BDL) model. These models are selected to target different underlying pathological causes of liver fibrosis.
What are the differences between models of acute versus chronic liver injury?
Models of acute liver injury (ALI), such as APAP or LPS-induced hepatotoxicity, are used to model rapid onset hepatocyte death and acute inflammation. Models of chronic liver injury, like CCl₄ or BDL models, are used to model progressive liver injury that leads to fibrosis and cirrhosis.
What endpoints are available for liver disease animal models?
We offer a variety of endpoint analysis for our liver disease models. From histology and serum biochemistry to molecular biology assays and fibrosis scoring, we will work with you to provide the highest quality and most reproducible data for your preclinical studies.