Study of the Effects of Melatonin on Experimentally Induced Hepatic Fibrogenesis in Rats

Background: liver fibrosis is considered one of the most common consequences of liver damage caused by variety of liver diseases. Melatonin (n-acetyl-5-methoxy-tryptamine) is produced and secreted in circadian fashion mainly by the pineal gland. Aim: the aim of the present work was to study the effect of melatonin on hepatic fibrosis induced by thioacetamide (TAA) in rats. Materials and methods: this study was carried on 30 male waster rats, the animal were divided into 3 groups (each 10 rats). Control vehicle treated group, thioacetamide (TAA) group and thioacetamide -melatonin treated group. Blood and liver tissue were taken for estimation of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (alp), TNF-? and bilirubin in the serum. Caspase-3, hydroxyproline (HP), malondialdehyde (MDA). Ascorbic acid and glutathione (GSH) were determined in the liver tissue. Results: serum markers of liver damage were significantly elevated after TAA toxicity .melatonin administration nearly reversed these changes. Liver HP, MDA were increased in TAA but inhibited by melatonin. On the other hand there was significant reduction of the concentration of liver antioxidant GSH and ascorbic acid in TAA group compared with the control group. Melatonin significantly increased GSH and ascorbic acid. Biochemical changes were corroborated by histolopathological findings. Conclusion: liver fibrosis and liver damage caused by TAA were nearly reversed by melatonin treatment therefore, it can be concluded that melatonin could be considered antifibrotic therapy.