Development of an experimental hepatic encephalopathy in a rabbit model: Biochemical and immunohistochemical study

Abstract

This study was designed to estimate the biochemical, histochemical, and immunohistochemical aspects of hepatic encephalopathy (HE) induced experimentally by using Thioacetamide (TAA). Twenty-four male rabbits were separated into four main groups (6 each), the Control group (group I) and Group II; rabbits were injected with TAA dissolved in distal water at 200 mg/kg B.W. twice weekly for eight weeks. Group III was given silymarin orally dissolved in saline 200mg/kg B.W. daily for eight weeks. Group IV animals received TAA and Silymarin 200 mg/kg B.W. for eight weeks. The results revealed animals treated with TAA indicated a significant decrease in the level of TSP and a significant increase in the levels of TSB, ALP, ALT, and AST. Histopathological examination of each liver and brain indicates necrosis of the hepatocytes, Cholangitis, biliary duct epithelium hyperplasia and preductular fibrosis, and collagen fiber deposition in the portal triad. Necrosis of the neurons, Purkinjean, and molecular cells with a decrease in granular cells and thickening of meninges. The histochemical examination of the liver revealed the presence of fibrosis in the portal area and the peri-lobular septa and the presence portal to portal bridging fibrosis. The immunohistochemical stain of the liver section revealed a positive reaction for collagen type IV, especially in/and around the portal tried as well as in the septa between the lobules. In conclusion, in the rabbit's model, hepatotoxicity to the early stages of the pathogenesis of hepatoencephalopathy.