BACKGROUND: Hepatic fibrosis, a common response to chronic liver injury, is characterized by increased produc tion of extracellular matrix components, whose major par is produced by hepatic stellate cells (HSCs). Taurine is a sulfur containing beta-amino acid rich in human body, and our previous experiments showed that it can inhibit the de position of the extracellular matrix in the damaged liver. This work was to investigate the effects of taurine on prolife ration and apoptosis of HSC and its possible mechanism. METHODS: Cell proliferation was detected by the thiazole blue (MTT) colorimetric assay. Cell apoptosis and cell cy cle were assessed via flow cytometry. The morphology o apoptotic cells was observed by phase-contrast fluorescen micrography after orange acridine staining, and the cAMP content was measured by radioimmunoassay. The expres sion of c-jun and c-fos was determined by the combination of immunocytochemistry and image analysis software. RESULTS: Taurine dose-dependently inhibited the prolife ration of HSCs at the concentration of 5-50 mmol/L, resul ting in more cells in the G0/G1 phase and fewer in the S phase. Taurine markedly increased the synthesis of cAMP and suppressed the gene expression of c-jun and c-fos (P < 0.01) in addition to the inhibition of the proliferative effec of platelet-derived growth factor BB on HSC. However taurine had no effect on induction of cell apoptosis. CONCLUSIONS: Taurine can significantly inhibit the proli feration of HSC, causing a G0/G1-phase arrest. This effec on HSC proliferation is associated with the enhancement o the synthesis of cAMP and inhibition of the gene expression of c-jun and c-fos. However it can not induce the apopto sis of HSC. BACKGROUND: Hepatic fibrosis, a common response to chronic liver injury, is characterized by increased produc tion of extracellular matrix components, whose major par is produced by hepatic stellate cells (HSCs). Taurine is a sulfur containing beta-amino acid rich in human body , and our previous experiments showed that it can inhibit the deposition of the extracellular matrix in the damaged liver. This work was to investigate the effects of taurine on prolife ration and apoptosis of HSC and its possible mechanism. METHODS: Cell proliferation was detected by The thiazole blue (MTT) colorimetric assay. Cell apoptosis and cell cy cle were assessed via radio cytometry. The morphology o apoptotic cells was observed by phase-contrast fluorescen micrography after orange acridine staining, and the cAMP content was measured by radioimmunoassay. The expres sion of c-jun and c-fos was determined by the combination of immunocytochemistry and image analysis software. RESULTS: Taurine dose-dependent ly inhibited the proliferation of HSCs at the concentration of 5-50 mmol / L, resul ting in more cells in the G0 / G1 phase and fewer in the S phase. Taurine markedly increased the synthesis of cAMP and suppressed the gene expression of c -jun and c-fos (P <0.01) in addition to the inhibition of the proliferative effector of platelet-derived growth factor BB on HSC. However taurine had no effect on induction of cell apoptosis. CONCLUSIONS: Taurine can significantly inhibit the proli feration of HSC, causing a G0 / G1-phase arrest. This effector on HSC proliferation is associated with the enhancement o the synthesis of cAMP and inhibition of the gene expression of c-jun and c-fos. However it can not induce the apopto sis of HSC.