Objective:To investigate the inhibitory effects of mesenchymal stem cells (MSC) on hepatic fibrosis and activation degree of hepatic stellate cells (HSC) after transplantation. Methods: Ficoll-Hypaque density gradient centrifugation and adherent culture were performed to separate and purify bone marrow mesenchymal stem cells (BM-MSCs) from 4 months old SD rats. Liver fibrosis model of SD rats was induced by long-term intraperitoneal injection of low-dose of CCl4 for 8 weeks. A total of 18 rats were performed to make model, since 4 weeks after the modeling process, 9 of them were taken out to receive treatment of 6×106 MSCs for 4 weeks by tail vein injection, the remains were injected the same volume of saline without MSCs. The normal control group containing 9 rats were only given the same volume of saline injection for 4 weeks. ALT, AST, TBIL,and ALB levels of serum were determined by automatic biochemical analyzer every week from the start to the end of research in a total of 8. The localization and expression of alpha-smooth muscle actin (α-SMA), transforming growth factor beta 1 (TGF-β1), and collagen type Ⅰ (COL-Ⅰ) in liver tissues were analyzed by the immunohistochemical method. Density gradient centrifugation after situ perfusion and 326 nm of ultraviolet excitation together with α-SMA immunofluorescence staining were performed to isolate and identify HSC, respectively. The mRNA and protein expression levels of α-SMA and TGF-β1 in HSC were detected by qRT-PCR and Western blot, respectively. All above experiments were done at the end of the experiment at 8 weeks. Results: Compared with the model group, ALT, AST,and TBIL levels of serum; fibrosis and inflammation degree; α-SMA, TGF-β1,and COLⅠ expression levels in liver; the mRNA and protein expression levels of α-SMA and TGF-β1 in HSC were significantly reduced in the treatment group after MSCs transplantation. Conclusion: Liver fibrosis degree and liver function of SD rat were significantly reduced and improved after BM-MSC transplantation, respectively, which may be related to its inhibition of the activation level of HSC.