In vivo Experimental Models for hepatotoxin Induced Fibrosis – A Toxicological View
Liver fibrosis is common sequel of chronic liver injury regardless of any etiology. The experimental animal models of hepatic fibrosis remain hallmark for the evaluation of antifibrotic agents prior to clinical studies. Accumulating evidence indicates that carbon tetrachloride, N-nitrosodimethylamine, thioacetamide, ethanol and bile duct ligation models are commonly employed and these models have been extensively studied for their potency of inducing hepatic fibrosis and for the evaluation of various antifibrotic agents in experimental animals. However, none of these experimental models reproduces exactly human liver fibrosis, each model has its own limitation and disadvantages i.e., development of ascites, extra hepatic toxicity, mortality etc. The development, progression and resolution of hepatic fibrosis induced by these hepatotoxins in experimental animals varying on the routes of their administration, frequency (intermittent/chronic) of administration, dose, species, and strain. Nevertheless, over past three decades knowledge gained from these hepatotoxin induced fibrosis models has advanced our understanding of the pathophysiology, molecular mechanisms and wide spectrum of signaling pathways associated with hepatic fibrosis. This article reviews some of the most studied hepatic fibrosis experimental models.
Carbon Tetrachloride, Ethanol, Liver Fibrosis, Oxidative Stress, Thioacetamide.
Pharmacy and Pharmacology
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