Objectives : The aim of this study is to characterize the effect of Chungganhaeju-tang on $TGF-{eta}l$-induced hepatic fibrosis. Materials and Methods : mRNA and protein expression levels of $TGF-{eta}l$ in Chungganhaeju-tang treated HepG2 cells were compared to untreated cells using quantitative RT-PCR and ELISA assay, respectively. mRNA expression levels of the $TGF-{eta}l$ signaling pathway genes $(T{eta}R-I,;T{eta}R-II,;Smad2,;Smad3,;Smad4,;and;PAI-1)$ and fibrosis-associated genes (CTGF, fibronectin, and collagen type $l{alpha}$) were evaluated by quantitative RT-PCR. The effect of Chungganhaeju-tang on cell proliferation of T3891 human fibroblast was evaluated using $[^3H]Thymidine$ Incorporation Assay. Results : Inhibition of $TGF-{eta}l$ mRNA expression and protein production was observed with treatment of Chungganhaeju-tang and seen to be dose and time dependent. Whereas $TGF-{eta}l$-mediated induction of PAI-1 was suppressed with treatment of Chungganhaeju-tang, expression of the $TGF-{eta}l$ signaling pathway genes such as $T{eta}R-I$, $T{eta}R-II$, Smad2, Smad3, and Smad4 was not affected. With treatment of Chungganhaeju-tang, inhibition of $TGF-{eta}l$-induced cell proliferation of T3891 human fibroblast was observed, as well as abrogation of $TGF-{eta}l$-mediated transcriptional up-regulation of CTGF, fibronectin, and collagen type $I{alpha}$. Conclusion : This study strongly suggests that the liver cirrhosis-suppressive activity of Chungganhaeju-tang may be derived at least in part from its inhibitory effect on $TGF-{eta}l$ functions, such as blockade of $TGF-{eta}l$ stimulation of fibroblast cell proliferation and fibrosis-related gene expression as well as expression of $TGF-{eta}l$ itself.