The anti-fibrotic effects of hot water extract of adventitious root culture of Panax ginseng (ARCP) and the possible mechanisms were investigated on $CCl_4-induced$ hepatotoxicity model mice. Fibrosis was induced by a mild treatment of $CCl_4$. Then silymarin as a positive control drug and ARCP or carrier alone as a negative control were treated. Serum GPT, GOT and ALP activity levels were lowered by 25, 21 and 11% for silymarin treated group and by 48, 39 and 14% for ARCP treated group compared to carrier treated alone. Hepatic collagen for ARCP treatment group was reduced by 18% and MDA contents decreased a little more. Pro-fibrotic gene ($TGF-{eta}1$, TIMP-1 and ${alpha}-SMA$) expression increased following the $CCl_4$ treatment, but both the silymarin and the ARCP treatments decreased the expressions of these genes by 20% to 50%. The antioxidant effect of ARCP was studied by DPPH free radical scavenging activity. In addition, a generation of reactive oxygen species (ROS) was also reduced in $H_2O_2-treated$ HepG2 cells upon the ARCP treatment. In summary, ARCP has antioxidant property, and can have some protection against oxidative stress; more importantly, ARCP can efficiently protect mice against $CCl_4-induced$ fibrosis.