Introduction: Oleic acid (OA) induces morphologic and cellular changes of lung similar to those observed in human acute lung injury (ALI) in animal models. Human serum albumin (HSA) shows a protecting effect from OA induced lung injury in animal model. However the pathophysiology of HSA on OA-induced lung injury was not fully revealed. Material & Methods: We measured IL-1β, IL-6 in serum and histopathology changes of lung. Five groups (sham, HSA, OA, OA-HSA and OA-DAHK) were determined. ALI/ARDS was induced by intravenous (IV) administration of OA. The OA-HSA and OA-DAHK groups consecutively received IV HSA after OA infusion each. Blood samples were collected prior injection and 12, 24 hours after IV infusion independent of the time of HSA and DAHK infusion. Results: The serum levels of IL-1βand IL-6 were increased in OA group, and the administration of HSA and DAHK significantly reduced serum IL-6 level at 12 hours (p<0.05). The effect of treatment were not differed OA-HSA from OA-DAHK group.Lung histopathology failed to show significant differences among OA, OA-HAS and OA-DAHK groups. Conclusion: HSA and DAHK attenuate oleic acid induces elevation of serum IL-6 levels in OA-induced ALI/ARDS rat model. Our data suggest that protective role of DAHKrepresent the protective effect of HSA is originated from the fatty acid binding effect of N-terminal part OA-induced lung injury.