In this study, significantly suppressed HSCs activation and less collagen accumulation in hAMC transplanted mice were observed, which might be contributed in part to the reduced hepatocyte apoptosis. Hepatic VE-821 regeneration is an important component of the recovery process occurred after liver injury, and the improvement of hepatocyte proliferating capacity could be of critical importance in CCl4-induced cirrhosis. In liver regeneration, the existence of liver specific growth factors has been extensively studied. HGF, as the most effective mitogen, inhibits liver injury by stimulating hepatocyte proliferation in addition to protecting hepatocyte from apoptosis. In the present study, we confirmed the hAMCs transplantation induced higher expression of HGF protein in CCl4-induced liver injury. In additional to a decreased hepatocyte apoptosis, we also found a more significant hepatocyte proliferation in hAMC group relative to control group. Therefore, the improvement of liver functions by the hAMCs transplantation was partially contributed to enhancing hepatocyte proliferation. One of the unique responses of the injured liver is hepatocyte replication and regeneration. However, somatic cells have a limited capacity for replication owing to lack of the telomerase enzyme. Increased hepatocyte senescence has been confirmed in cirrhosis and has been shown to correlate with the ductular reaction and portal fibrosis in chronic hepatitis C and with clinical severity. So far, SA-b-gal activity has been used as a marker of cellular senescence. In this study, profound hepatocyte senescence was confirmed after CCl4-induce liver injury as SA-bgal activity was detected frequently in hepatocyte in CCl4-treated liver. Whereas, hAMCs transplantation depressed cellular senescence in livers. NAD-dependent deacetylase Sirt protein play an important role in the survival of cell. The upregulation of Sirt1 could promote cellular proliferation, reducing senescence and apoptosis. In addition, oxidant stress has been demonstrated to inducing cellular senescence and apoptosis. In the present study, SOD activity, an anti-oxidant enzyme, was noticeable higher in hAMCs group than control group. Previous studies have demonstrated that hAMCs can differentiate into hepatocyte lineage cells in vitro. In our study, hAMCs were successfully transplanted via spleen into hepatic cirrhosis model to prevent histopathological changes. These cells survived and scattered in the liver at 4 weeks after the transplantation. Moreover, they also differentiate into albuminexpressing or a-fetoprotein–expressing hepatocyte. Therefore, the effect of hAMCs on reducing fibrogenesis partially likely relies on the differentiation of these cells into hepatocytes in vivo. In summary, these results suggest that hAMCs transplantation significantly decrease the fibrosis formation and progression of CCl4-induced cirrhosis, providing a new approach for the treatment of fibrotic liver disease.