Thesis (M.Sc.) - Cairo University - Faculty of Pharmacy - Department of Pharmacology and Toxicology

Inflammation and hepatic stellate cell (HSC) activation are the most crucial steps in the formation of hepatic fibrosis. Hepatocytes damaged by viral or bacterial infection, alcohol or toxic chemicals initiate an inflammatory response that activates collagen production by HSCs. Through this mechanism chronic administration of thioacetamide for 8 weeks at dose (100 mg/kg body weight) effectively induced liver injury and dysfunction and caused hepatic fibrosis. In this study, the effect of Betalactglobulin (Ý-LG), Lacprodan R alpha-10(LAC) and L-methionine were evaluated in TAA-induced hepatic fibrosis in rats. Method: Seventy two Sprague Dawley rats were divided into nine groups. Group 1 received saline only; all groups were injected with TAA two times / week, concurrently, Group3-4 received daily Ý-LG (100mg/kg and 200 mg/kg given orally), respectively.Group 5 received a combination of Ý-LG (50 mg/kg body weight) and l-methionine (40 mg/kg body weight).Groups 6,7 and 8were received the same as groups 3,4 and 5 except we use LAC instead of Ý-LG ,while group 9 was received L-methionine (40 mg/kg body weight) only. Results: TAA induced extensive liver damage that is evidenced by significant increase in serum levels of alanine amino transferase (ALT), Aspartate aminotransferase (AST), alkaline phosphatase (ALP) and total bilirubin(TB) .Moreover, TAA induced oxidative stress as indicated by significant increase in the hepatic lipid peroxidation (LPO)marker malondialdehyde (MDA) and nitric oxide content(NO) as well as significant decrease in antioxidant enzymes like hepatic reduced glutathione concentration (GSH) and superoxide dismutase (SOD) activities

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