CO-releasing molecules (CORM-2)-liberated CO attenuates leukocytes infiltration in the renal tissue of thermally injured mice.

Abstract

To determine whether the CO-releasing molecule -liberated CO attenuates infiltration of leukocytes in the renal tissue of thermally injured mice. 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, i.v.), 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-kBeta, expressions of ICAM-1 and HO-1 expression in renal tissues. Treatment of thermally injured mice with CORM-2 significantly attenuated PMN accumulation and prevented activation of NF-kBeta 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. CO delivered by CORM-2 attenuates leukocytes infiltration in the kidney of burned mice by interfering with NF-kBeta activation, protein expression of ICAM-1 and therefore suppressing endothelial cells pro-adhesive phenotype.