Curcumin prevents liver fibrosis by inducing apoptosis and suppressing activation of hepatic stellate cells

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.