Aims: To investigate the mechanism of Fuzheng Huayu decoction (FZHY) on hepatic stellate cells (HSCs) activation relating to TGF-1 signal transduction pathway. Methods: HSCs were isolated from normal rats by in situ pronase/collagenase perfusion followed by density gradient centrifugation. At day 4 after isolation, cells were stimulated with 100pM TGF-1 for 24h, then incubated with 10% FZHY pharmacological serum or 10 M T R -I inhibitor (SB-431542) for 24h. Protein expression of -SMA, Smad3 was assayed by immunofluorescent stain; Total protein expression of -SMA, T R -I, Smad2/3 and nuclear expression of Smad3 was analyzed by Western blotting. Results: FZHY pharmacological serum significantly decreased expression of -SMA, T R -I, and inhibited Smad3 nuclear expression and translocation in TGF-1 stimulated HSCs. Conclusions: Fuzheng Huayu decoction can prevent HSCs activation through TGF-1 signaling transduction pathway in HSCs, which may be the important molecular pharmacological mechanism of Fuzheng Huayu decoction action against liver fibrosis. Background: Fatty liver disease has become a health problem related to metabolic syndrome worldwide although its molecular pathogenesis has remained further studied and it is unclear whether advanced fibrosis induced by steatohepatitis will regress when diet is controlled. Aim of this study is 1) to study the involvement of endoplasmic reticulum stress (ER stress) in the occurrence of seatohepatitis and 2) to obtain the evidence of resolution of fibrosis by changing the diet. Methods: Non-alcoholic steatohepatitis with advanced fibrosis was produced in rats by giving methionine-choline-deficient diet (MCDD) for 10 weeks. Methionine-choline-control diet (MCCD) instead of MCDD was given for the last 2 weeks in an experimental group. Fibrosis and inflammation was determined by several tissue stainings. Gene expression related to fibrosis and inflammation was determined by immunoblotting and real-time PCR. Expression of caspase-12, caspase-7, and glucose-regulated protein 78 was evaluated to clarify the presence of ER stress Aim against liver fibrosis relating to hypoxia and angiogenesis regulation. Methods: The rats were divided into normal, model, SA-B and Perin control group. Rats in SA-B and Perindopril group were administrated with SA-B and Perindopril respectively. Liver fibrosis was induced by ip dimethylnitrosamine (DMN) for 4w. Fibrosis degree was observed by Sirius red staining. Col-I protein expression was analyzed by Western blot; Col-I , VCAM-1, ICAM-1, HIF-1 and vWF expression in liver tissue was checked by immunohistochemistry; gelatinase activities in liver tissue were detected by gelatin zymography and in situ flourescent zymography.