Objective：To study the regulatory effects of antifibrotic cytokines, interleukin 10 (IL-10), hepatocyte growth factor (HGF), and interferon-gamma (IFN-γ) on activity of transforming growth factor-β1(TGF-β1 ) gene promoter, so as to assess the antifibrotic mechanism of cytokines. Methods: Sequence -1328-+812 of TGF-β1 gene, which contains the -509 C>T polymorphism, was selected as putative promoter. The recombinant constructions containing -1328-+812 of TGF-β1 gene and CAT reporter gene (phTGF2.14T, phTGF2.14C) were constructed and transfected into HepG2 cells with liposomal transfection method, then the transfected HepG2 cells were treated with IL-10（4 ng/ml）, HGF（10 ng/ml） or IFN-γ（20 ng/ml）. Reporter gene activity was analyzed by ELISA. Results: Reporter gene activity in cells transfected with phTGF2.14C was significantly higher than those transfected with phTGF2.14T (P＜0.01). IFN-γ significantly inhibited the reporter gene activity in HepG2 cells transfected with phTGF2.14C or phTGF2.14T(P＜0.05); HGF significantly increased the reporter gene activity in cells transfected with phTGF2.14C (P＜0.05). IL-10 had no effects on the activities of cells transfected with phTGF2.14C or phTGF2.14T.Conclusion: C allele at -509 can increase the promoter activity of TGF-β1 gene in HepG2 cells. The antifibrotic effect of IFN-γ might be related to its inhibitory effect on the putative promoter activity of TGF-β1 gene; the antifibrotic effects of HGF and IL-10 may not be through regulation of TGF-beta1 gene transcription.