AIM: To study the effects of interleukin-10 (IL-10)on the expression of a-smooth muscle actin (α-SMA),nuclear factor-κB(NF-κB) and Fas/Fas ligand (FasL) in hepatic stellate cells of experimental rats with hepatic fibrosis. METHODS: Sixty clean SD rats were randomly divided into control group (group N), liver fibrotic group (group C) and IL-10 treatment group (group I). Control group a week. Fibrotic group was injected intraperitoneally a week. IL-10 treatment group was given IL-10 at a from the third week. Hepatic stellate cells (HSCs) were isolated from these rats at the seventh and eleventh weeks during the course of liver fibrosis, respectively.The expression of α-SMA and NF-κB in HSCs was measured by S-P immunohistochemistry. The expression of Fas and FasL mRNA was measured by RT-PCR.Furthermore, liver tissues were harvested from three groups at the same time.RESULTS: The CCl4- induced experimental rat hepatic fibrosis model was established successfully. The purity of extracted hepatic stellate cells was about 95% and the yield of hepatic stellate cells was 1.2-2.3x106/g liver tissue averagely. The positive expression of α-SMA and NF-κB was 36.5% and 28.5% respectively in group N.The positive levels of α-SMA and NF-κB were increased significantly in group C compared to group N (P<0.01).The positive signals decreased significantly (P<0.05) in group I. In the 11th week, the HSCs of group I became round with visible pyknotic nuclei. The expression of NF-κB in group C was significantly increased in a timedependentmanner (P<0.01), but there was no difference and FasL in group C was significantly increased in a timedependent manner compared to that in control group.After treated with IL-10, the expression level of Fas and FasL was higher in group I than in group C.CONCLUSION: The positive expression of α-SMA and NF-κB in hepatic stellate cells is decreased by ectogenic IL-10 in liver fibrosis induced by CCl4. The expression of Fas and FasL is increased in the course of liver fibrosis,and is further increased by IL-10. IL-10 could inhibit the activation of HSCs and cause apoptosis of activated HSCs.