Protective Activity of Taurine and Molecular Fibrogenesis in Iron Overloaded Hepatic Tissues

Background and Objective: Hepcidin as iron hormone regulator was shown to be responsible for the hemostatic balance of iron content in liver cells. It shows significant role in the prognosis of fibrosis in iron overloaded hepatic tissues. In excess iron treated models, Taurine (TAU) was shown to play a protective role against hepatic fibrosis. However, little is known about the effect of TAU on hepcidin expression and its correlation with collagen content in hepatic tissues. Thus, the current study evaluated the protective role of TAU and its effects on the regulation of hepcidin expression, oxidative stress and apoptosis in iron overload induced liver cell fibrosis in rat models. Methodology: Iron overloaded rats were administered TAU therapy (40 mg kg(-1)/day) in drinking water for 4 months. Histochemical and biochemical analysis were performed to estimate fibrosis score, iron content, hepcidin and 8-OHdG, TAC and bcl-2 as markers of oxidative stress and apoptosis respectively pre and post TAU therapy. Results: The data showed significant improvements in the levels of hepatic iron content, hepcidin, 8-OHdG, TAC and bcl-2 in both fibrotic (score: 2-3) and non-fibrotic (0-1) iron treated rats. Liver fibrosis scores correlated positively with the levels of hepatic iron, hepcidin and negatively with HPX content as marker of collagen, bcl-2 as a marker of liver cell apoptosis and TAC and 8-OHdG as oxidative stress markers. Conclusion: Present study showed that TAU therapy improves liver fibrosis via antioxidant and anti-apoptotic pathways as well as down regulation of hepcidin expression. This may prove the prophylactic role of TAU against early liver fibrosis. In addition, hepcidin was shown to be closely associated with liver fibrosis and cloud be used as a diagnostic marker in evaluating new therapeutic strategies against liver diseases.