Objective: To determine whether the CO-releasing molecule-liberated CO attenuates infiltration of leukocytes in the renal tissue of thermally injured mice.

Materials and methods: Twenty-eight mice were assigned to four groups. Mice in sham group (n= 7) were underwent sham thermal injury, whereas mice in burn group (n= 7) received 15% total body surface area (TBSA) full-thickness thermal injury. Mice in burn+ CORM-2 group (n= 7) underwent thermal injury followed by immediate administration of CORM-2 (8mg/kg, iv), whereas mice in burn+ iCORM-2 group (n= 7) underwent thermal injury followed by administration of iCORM-2 (an inactive compound used as negative control). Histological alterations and granulocytes infiltration in kidney were assessed alongised PMN accumulation, activation of NF-ĸΒ, expressions of ICAM-1 and HO-1 expression in renal tissues.

Results: Treatment of thermally injured mice with CORM-2 significantly attenuated PMN accumulation and prevented activation of NF-ĸΒ in the kidney. This was accompanied by a decrease of the expression of ICAM-1 and an increase in HO-1 expression. In parallel, burn-induced granulocytes infiltration in renal tissue was markedly decreased by treatment with CORM-2.

Conclusions: CO delivered by CORM-2 attenuates leukocytes infiltration in the kidney of burned mice by interfering with NF-ĸΒ activation, protein expression of ICAM-1 and therefore suppressing endothelial cells pro-adhesive phenotype.