Objective To determine whether adipose stem cells (ADSC)-derived exosomes can alleviate liver fibrosis and to explore the mechanism underlying this effect. Methods Primary adipose stem cells were subcultured to the third to sixth generation in exosome-free medium, and the supernatant was collected periodically. The collected supernatant samples were then pooled, and the exosomes were separated by ultracentrifugation. A liver fibrosis model was established by intraperitoneal injecting 40 male SD rats weighing about 200 g with olive oil + carbon tetrachloride; a control group (10 rats) was injected with olive oil only. After 10 weeks, 10 rats randomly selected from the experimental group were sacrificed to confirm that the liver fibrosis had developed as expected, and the remaining 30 rats were randomly divided into ADSC, Exosome, and Model groups. After 2 weeks of treatment, serums levels of AST and ALT in serum were measured, liver tissues from each group were stained with HE and Sirius red, the expression of alpha smooth muscle actin (α-sma) was detected by immunohistochemistry, and the expression levels of transforming growth factor beta 1 ( TGF-β1) and the apoptosis-related proteins Bax, BcL-2, and Caspase 3 were detected by western blotting. Results (1) Serum ALT and AST levels were significantly lower in the ADSC and Exosome groups compared with the Model group (P <0. 05); (2) HE and Sirius red staining showed large areas of hepatocyte apoptosis and significant connective tissue proliferation in the Model group, with little hepatocyte apoptosis or connective tissue proliferation seen in the ADSC and Exosome groups. (3) The total area of α-sma expression was significantly lower in the ADSC (P <0. 05) and Exosome (P <0. 01) groups compared with the Model group; (4) TGF-β1, Bax, and Caspase 3 expression levels were significantly higher in the model group than in the ADSC and Exosome groups (P <0. 05). Conversely, BcL-2 expression was significantly higher in the ADSC and Exosome groups ( P < 0. 05) compared with the Model group. Conclusions ADSCs and their derived exosomes can alleviate liver fibrosis by reducing hepatocyte apoptosis and inhibiting hepatic stellate cell activation.