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Ohiective: To observe the role and mechanism of Coreleasing molecule (CORM)-2 in lung injury induced by ischemia-reperfusion (IR) of hind limbs in rats.Methods: A rat model of lung injury induced by IR of hind limbs was established.A total of 40 Sprague Dawley (SD) rats were randomly divided into 5 groups (n=8):sham,shanl+CORM-2,IR,IR+CORM-2and IR+dimethyl sulfoxide (DMSO).Rats in the IR group received hind limb ischemia for 2 hours and reperfusion for 2 hours,rats in the sham group underwent sham surgery without infrarenal aorta occlusion.rats in the IR+CORM-2 group and in the sham+CORM-2 group were given CORM-2 (10 pmol/kg in travenous bolus) 5 minutes before reperfusion or at the corresponding time points.while rats in the IR+DMSO group was treated with the same dose of vehicle (DMSO) at the same time.The lung tissue structure,polymorphonuclear neutrophil (PMN) count,wet-to-dry weight ratio (W/D),malondialdehyde (MDA) content,myeloperoxidase (MPO) activity,intercellular adhesion molecule-1 (ICAM-1) expression,I κ Bo degradation and nuclear factor (NF)-κB activity in the lungs were assessed.Results: As compared with the sham group.lung PMNs number,W/D,MDA content,MPO activity,ICAM-1 expression and NF-κB activity significantly increased in the IR group,but the level of I κ Bo decresed (P＜0.01).Compared with the IR group,lung PMNs number,W/D,MDA content.MPO activity and ICAM-1 expression significantly decreased in the IR+COMR-2 group (P＜0.01),while the level of I κ Ba increased.Conclusions: These data demonstrate that CORM-2 attenuates limb IR-induced lung injury through inhibiting ICAM-1 protein expression.NF-κ B pathway and the leukocytes sequestration in the lungs following limb IR in rats,suggesting that CORM-2 may be used as a therapeutic agent against lung injury induced by limb IR.