Silybin, a component of sylimarin, exerts anti-inflammatory and anti-fibrogenic effects on human hepatic stellate cells

Background/Aims Hepatic fibrogenesis, a consequence of chronic liver tissue damage, is characterized by activation of the hepatic stellate cells (HSC). Silybin has been shown to exert anti-fibrogenic effects in animal models. However, scant information is available on the fine cellular and molecular events responsible for this effect. The aim of this study was to assess the mechanisms regulating the anti-fibrogenic and anti-inflammatory activity of Silybin. Methods Experiments were performed on HSC isolated from human liver and activated by culture on plastic. Results Silybin was able to inhibit dose-dependently (25–50μM) growth factor-induced pro-fibrogenic actions of activated human HSC, including cell proliferation ( P P de novo synthesis of extracellular matrix components ( P P P + /H + exchanger, P Conclusion The results of the study provide molecular insights into the potential therapeutic action of Silybin in chronic liver disease. This action seems to be mostly related to a marked inhibition of the production of pro-inflammatory cytokines, a clear anti-oxidant effect and a reduction of the direct and indirect pro-fibrogenic potential of HSC.