Abstract
Background: The reported statistics suggest that alcoholic liver disease is on the rise. Furthermore, medications used to treat the disease have unpleasant effects, and this necessitates the need to continuously investigate hepatoprotective agents. This study investigates animal models of alcoholic liver disease used to evaluate hepatoprotective activity. Content: A good number of published articles evaluating hepatoprotective activity were summarized. The studies used three ethanol-induced liver injury models: the acute ethanol-induced liver injury model, the chronic ethanol-induced liver injury model, and Lieber– DeCarli model. Summary: Wistar rats were primarily used in the ethanol-induced liver injury model. High levels of alanine transaminase (ALT) and aspartate transaminase (AST) and histopathological alterations were found in all animal models (acute ethanol-induced liver injury, chronic ethanol-induced liver injury, and Lieber–DeCarli models). Severe steatosis was shown in both chronic ethanol-induced liver injury and Lieber–DeCarli models. However, fibrosis was undetected in all models.
Highlights
Alcohol drinking has been a part of social activities in most countries [1]
The chronic ethanol-induced liver injury model is associated with a long period of excessive ethanol consumption
Chronic ethanol consumption can promote the formation of hepatic steatosis—the early symptom of alcoholic liver disease
Summary
The reported statistics suggest that alcoholic liver disease is on the rise. This study investigates animal models of alcoholic liver disease used to evaluate hepatoprotective activity. Content: A good number of published articles evaluating hepatoprotective activity were summarized. The studies used three ethanol-induced liver injury models: the acute ethanol-induced liver injury model, the chronic ethanol-induced liver injury model, and Lieber– DeCarli model. Summary: Wistar rats were primarily used in the ethanol-induced liver injury model. High levels of alanine transaminase (ALT) and aspartate transaminase (AST) and histopathological alterations were found in all animal models (acute ethanol-induced liver injury, chronic ethanol-induced liver injury, and Lieber–DeCarli models). Severe steatosis was shown in both chronic ethanol-induced liver injury and Lieber–DeCarli models.
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