Background/Aims: Ischemic postconditioning (Postcon) is a phenomenon that intermittent interruptions of blood flow in the early phase of reperfusion can protect organ against ischemia/reperfusion (I/R) injury. The potential application of postconditioning to liver is not available. In the present study, we investigated the effects of Postcon in liver I/R injury in rat liver transplantation models. Methodology: Adult male Sprague-Dawley rats were randomly allocated to three groups including sham group without I/R, I/R group with 24h cold ischemic donor liver before orthotopic liver transplantation, and Postcon group treated the same as I/R group and 6 cycles of 60s ischemia and 60s reperfusion at the onset of reperfusion. Peripheral blood samples were collected after reperfusion. Serum transaminases level, plasma cytokines concentration, histopathology, liver tissues malondialdehyde (MDA) level and superoxide dismutase (SOD) activity were measured. The heme oxygenase-1 (HO-1) expression levels of liver were evaluated. Results: Serum transaminases level and plasma cytokines concentration significantly decreased in Postcon group as compared to I/R group. Postcon treatment reduced MDA production and increased SOD activity compared with the I/R group. The HO-1 expression levels of liver were significantly higher in Postcon rats than in the I/R group at the end of reperfusion. Conclusions: These results indicate that Postcon ameliorates liver I/R injury. This protective effect is likely mediated by up-regulation of HO-1 expression.