The prophylactic effects and the mechanisms of curcumin on liver fibrosis are unclear. Liver fibrosis was induced in 72 Sprague-Dawley rats by intraperitoneal injection of carbon tetrachloride. Rats were divided into control, liver fibrosis, high, middle and low dose curcumin (200, 100, and 50mg.kg-1, respectively) and colchicine (0.1mg. kg-1) groups. After 8 weeks of treatment, hepatic stellate cells activity was examined by immuohistochemistry staining and apoptosis was detected by terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL). The liver fibrosis score in the high, middle and low dose curcumin group (5.79±1.80, 8.58±3.34 and 9.58±3.32, respectively) and the colchicine group (4.91±1.28) was significantly lower than in the fibrosis group (20.40±3.38, P<0.01). The ratio of activated hepatic stellate cells in the three curcumin (0.97±0.69, 2.06±0.58, and 3.49±1.03, respectively) and the colchicine group (0.78±0.31) was significantly lower than in the fibrosis group (6.08±1.13, P<0.05). The apoptosis index in the three curcumin groups (0.57±0.21, 0.37±0.22 and 0.34±0.21, respectively) was higher than in the fibrosis (0.09±0.09, P<0.05) or the colchicine group (0.16±0.19, P<0.05). In conclusion, curcumin prevents carbon tetrachloride-induced liver fibrosis in rats. The prevention of liver fibrosis may be due to the inhibition of the activity, and the induction of apoptosis of hepatic stellate cells.