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Preclinical liver toxicity models: Advantages, limitations and recommendations
Devaraj Ezhilarasan1, Sivanesan Karthikeyan2, Mustapha Najimi3
1Department of Pharmacology, Hepatology and Molecular Medicine Lab, Saveetha Dental College and Hospitals, Saveetha Institute of Medical and Technical Sciences, Chennai, Tamil Nadu, India.
Toxicology
|December 5, 2024
Summary
Experimental animal models are vital for studying liver injury and testing treatments. Standardized protocols are needed to select appropriate models for reproducible research on hepatotoxicity and fibrosis.
Area of Science:
- * Investigates the use of experimental animal models in liver injury research.
- * Focuses on hepatotoxic agents and their role in inducing liver damage and fibrosis.
- * Addresses the challenges in modeling metabolic dysfunction-associated liver disease (MAFLD).
Background:
- * Hepatotoxic agents like acetaminophen, carbon tetrachloride (CCl4), dimethylnitrosamine (DMN), and thioacetamide (TAA) are metabolized by CYP2E1, causing liver injury.
- * Specific agents induce distinct patterns of acute liver injury, including necrosis and inflammation.
- * Chronic exposure to CCl4, TAA, and DMN promotes hepatic stellate cell activation and liver fibrosis.
Purpose of the Study:
- * To review common experimental animal models for inducing liver injuries.
- * To discuss the mechanisms and characteristics of chemically induced liver damage and fibrosis.
- * To highlight the need for standardized protocols in selecting animal models for preclinical studies.
Main Methods:
- * Review of literature on experimental animal models for liver injury.
- * Analysis of various hepatotoxic agents (acetaminophen, CCl4, DMN, TAA, etc.) and their effects.
- * Discussion of factors influencing liver injury patterns and severity in animal models.
Main Results:
- * Different chemical agents induce specific types and patterns of acute liver injury (e.g., centrilobular necrosis).
- * Chronic administration of CCl4, DMN, and TAA leads to liver fibrosis via hepatic stellate cell activation, with varying rates and toxicity.
- * Modeling MAFLD presents challenges due to its complex, multifactorial nature.
Conclusions:
- * Experimental animal models are essential tools for understanding liver pathophysiology and evaluating hepatoprotective agents.
- * The choice of hepatotoxic agent, dosage, and administration significantly influences the induced liver injury.
- * Standardized protocols and regulatory guidelines are crucial for consistent and reliable preclinical liver research.
