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. 2012 Mar;14(3):164-70.
Epub 2012 Mar 1.

Thioacetamide-induced acute hepatic encephalopathy in rat: behavioral, biochemical and histological changes

M Farjam  1 , P Dehdab, F Abbassnia, D Mehrabani, N Tanideh, S Pakbaz, M H Imanieh
Affiliations

Thioacetamide-induced acute hepatic encephalopathy in rat: behavioral, biochemical and histological changes

M Farjam et al. Iran Red Crescent Med J. 2012 Mar.

Abstract

Background: As a serious neuropsychiatric disease, hepatic encephalopathy (HE) is a clinical condition with several types regarding chronicity and clinical diversity that can develop as a complication of both acute and chronic liver failure. This study evaluates changes in thioacetamide (TAA)-induced acute hepatic encephalopathy (AHE) in rat as an animal model.

Methods: Both genders of C57BL6, BALB/C mice and Sprague Dawley rats; (10 animals in each group) were compared for induction of AHE to clarify which animal and gender were appropriate. The animals (10 male rats in each group) were categorized in 4 groups according to the dose of the TAA administered (200, 300 and 400 mg/kg of TAA at 24 h intervals for 4 days). A control group was treated with solvent of TAA which was water (5 ml/kg/day). The behavioral, biochemical markers of hepatic failure and histological aspects of thioacetamide (TAA) induced AHE and the correlation between the clinical severity and liver failure biomarkers were evaluated.

Results: Rat was shown to be an animal model of choice for AHE while the optimum dosage of TAA to induce AHE was 300 mg/kg/day at 24 h intervals for 4 days. The behavioral score was partially correlated with the rising of some biomarkers and pathological findings.

Conclusion: Rat can be introduced as the animal of choice for AHE to study the pathophysiology, pharmacology and the survival rate of disease in liver transplant patients.

Keywords: Acute hepatic encephalopathy; Rat; Thioacetamide.

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Conflict of interest statement

Conflict of interest: None declared.

Figures

Fig. 1
Fig. 1
Control group receiving distilled water (x200, H and E).
Fig. 2
Fig. 2
Liver inflammation after administration of 200 mg/kg of TAA (x200, H and E).
Fig. 3
Fig. 3
Extensive inflammation, necrosis and fibrosis in liver after administration of 300 mg/kg of TAA (x200, H and E).
Fig. 4
Fig. 4
Extensive inflammation, necrosis and fibrosis in liver after administration of 300 mg/kg of TAA (x200, Masson Trichrome).
Fig. 5
Fig. 5
Inflammation, necrosis and fibrosis in liver after administration of 400 mg/kg of TAA (x400, H and E).
See this image and copyright information in PMC

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