AIM: To examine the protective effect of green tea extract (GT) on hepatic fi brosis in vitro and in vivo in dimethylnitrosamine (DMN)-induced rats.METHODS: HSC-T6, a rat hepatic stellate cell line, was used as an in vitro assay system. Cell proliferation, collagen content, and type 1 collagen expression were examined in activated HSC-T6 cells. Collagen was determined by estimating the hydroxyproline content. In rats with DMN-induced hepatic fi brosis, serum aspartate aminotransferase and alanine aminotransferase concentrations, liver hydroxyproline and lipid peroxides were determined. Pathologic changes were examined by hematoxylin & eosin staining.RESULTS: GT administration prevented the development of hepatic fibrosis in the rat model of DMN-induced liver fi brosis. These results were confi rmed both by liver histology and by quantitative measurement of hepatic hydroxyproline content, a marker of liver collagen deposition. Accordingly, inhibition of proliferation, reduced collagen deposition, and type 1 collagen expression were observed in activated HSC-T6 cells following GT treatment. These results imply that GT reduced the proliferation of activated HSC and down regulated the collagen content and expression of collagen type 1, thereby ameliorating hepatic fibrosis.CONCLUSION: This study demonstrates that greentea administration can effectively improve liver fibrosis caused by DMN, and may be used as a therapeutic option and preventive measure against hepatic f ibrosis. AIM: To examine the protective effect of green tea extract (GT) on hepatic fi brosis in vitro and in vivo in dimethylnitrosamine (DMN) -induced rats. METHODS: HSC-T6, a rat hepatic stellate cell line, was used as an in In vitro experiments were carried out on HSC-T6 cells. Collagen was determined by estimating the hydroxyproline content. In rats with DMN-induced hepatic fi brosis, serum aspartate aminotransferase and alanine aminotransferase concentrations Pathologic changes were examined by hematoxylin & eosin staining .RESULTS: GT administration prevented the development of hepatic fibrosis in the rat model of DMN-induced liver fi brosis. These results were confi rmed both by liver histology and by quantitative measurement of hepatic hydroxyproline content, a marker of liver collagen deposition These results imply that GT reduced the proliferation of activated HSC and down regulated the collagen content and expression of collagen type 1, thereby ameliorating hepatic fibrosis. CONCLUSION: This study demonstrates that greentea administration can effectively improve liver fibrosis caused by DMN, and may be used as a therapeutic option and preventive measure against hepatic f ibrosis.