Development of Hepatotoxicity Model in Rats and its Application in Evaluation of Hepatoprotective Activity of Cell Wall Contents of Probiotics

The objective of present work is Development of Hepatotoxicity model in rats and to evaluate hepatoprotective activity of cell wall contents of probiotics. Animals were divided in four groups. The groups were normal saline group, diseased control group, standard drug treated group and 4th group was CCl4 +Cell wall contents of probiotics. In diseased control group chronic liver injury was induced by administration of Carbontetrachloride (CCl4) via intraperitoneal route (1 ml/kg) for seventy days. For standard drug treated group 1 ml Silymarin suspension (Orally) and CCl4 was given for seventy days. In fourth group cell wall contents (1 x 10 12 CFU/ml/animal) and CCl4 was given for seventy days. During disease induction and treatment period blood samples were collected and serum was separated which was used to analyse various parameters like Alanine aminotransferase (ALT), Aspartate aminotransferase, (AST), Alkaline phosphate (ALP), direct bilirubin, total protein and albumin levels to asses liver function. Along with these cholesterol, Glucose and Malondialdehyde were also measured. Liver fibrosis and cirrhosis was quantified by histopathological studies of small portion of the excised liver. Serum AST, ALT, ALP, and direct bilirubin were found to be significantly higher in CCl4 intoxicated rats. Total protein and albumin was decreased. Manondialdehyde was found to be significantly higher in CCl4 intoxicated rats which was main end product of Lipid Peroxidation. Whereas in cell wall contents probiotics and silymarin treated group improve the liver functions in CCl4 toxicated rats. We conclude that protein oxidation may play a role in the pathogenesis of CCl4 induced liver injury and that the accumulation of oxidised proteins may be an early indication of CCl4 induced liver damage. Silymarin and cell wall contents of probiotics were effective in liver injury by inhibiting protein oxidation.