Objective: To study the effects of interleukin-10 on the expression of fas and fasL in hepatic stellate cells in experimental rat hepatic fibrosis. Methods: Sixty clean SD rats were divided into control group (8 in group N), the model group (28 in group C) and the IL- 10 treated group (24 in group I) randomly. The rats were administered CCl4 with or without IL-10 treatment. Hepatic stellate cells (HSCs) were isolated from these rats at the beginning of the seventh and eleventh weeks during the course of liver fibrosis, respectively. Semi-quantitative RT-PCR and Western-blot were used to analyze mRNA and protein expressions of Fas and FasL from freshly isolated HSC. The liver tissues were harvested from three groups. Results: The CCl4- induced experimental rat hepatic fibrosis model was established successfully. The IL-10 could decrease the fibrotic degree of rat liver. The Fas and FasL mRNA can be measured in HSC of 3 groups. The mRNA of Fas and FasL in group C were significantly increased time-dependently compared to those of control group. In the 7th week, the expression level of Fas and FasL in group C was 0.66±0.02 and 0.45±0.33 respectively, and in the group I, the level was 0.74±0.02 and 0.52±0.05 respectively. In the 11th week, the level in group C was 0.72±0.02 and 0.62±0.04 respectively, and in the group I, the level was 0.73±0.04 and 0.83±0.04 respectively. The western-blot analysis showed that there was no FasL expression in group N, the expression of Fas and FasL in group C was significantly increased timedependently compared to those of control group. After being treated with IL-10, the expression level of Fas and FasL was higher than those of group C. In group C, the expression level of Fas and in the 11th week was 0.92±0.02and 0.99±0.02 respectively, and in group I, the level was 0.96±0.16 and 1.22±0.03 respectively. In group C, the level of FasL in the 7th week and in the 11th week was 1.24±0.03 and 1.33±0.03 respectively, and in group I, the level was 1.36±0.16 and 1.39±0.19 respectively. Conclusions: The expression of Fas and FasL increased in the course of the liver fibrosis, and would be furthered by IL- 10. The IL-10 could cause the apoptosis of activated HSC, and making antifibrogenic come into effect in these ways.