Background. Heme oxygenase-1 (HO-1), an oxidative stress-response gene up-regulated by various physiological and exogenous stimuli, has cytoprotective activities. Ischemic postconditioning (Postcon) can protect an organ from ischemia-reperfusion (I/R) injury. In the present study, we investigated the potential contributions of HO-1 to Postcon-dependent protection against I/R injury in rat liver transplantation models. Materials and methods. Adult male Sprague-Dawley rats were randomly divided into four groups: sham group with laparotomy for liver exposure; I/R group with 24-hour cold ischemia of the donor liver; Postcon group with the same treatment as the I/R group plus ischemic Postcon; and zinc protoporphyrin (ZnPP HO-1 inhibitor) + Postcon group treated the same as the Postcon cohort with donors pretreated using ZnPP 24 hours before the I/R injury. We measured liver tissue and peripheral blood samples collected at 6 hours after reperfusion and serum transaminase levels, histopathology, liver tissue malondialdehyde (MDA) content, superoxide dismutase (SOD) activity and HO-1 expression in the liver. Results. Postcon significantly diminished the elevation of serum transaminases levels after I/R injury when compared with I/R and ZnPP+Postcon groups. Postcon treated rats showed significantly lower MDA production and higher SOD activity. HO-1 was induced in rat livers exposed to Postcon; its levels were obviously overexpressed after 6 hours in Postcon rats. Inhibiting the expression of HO-1, negated the protective effects of Postcon. Conclusions. Induction of HO-1 in the Postcon condition played a protective role against hepatic I/R injury and enhanced the early antioxidative activity. The protective effects of Postcon were significantly associated with greater intrahepatic HO-1 expression.