AIM:To explore the effects of CO-releasing molecules tricarbonyldichlororuthenium(Ⅱ)dimer,CORM-2-liberated CO on attenuation of inflammatory responses in liver of an experimental animal model of thermal injury and to investigate the associated potential mechanisms.METHODS:Thirty-six mice were assigned to three groups in three respective experiments.In each experiment,mice in sham group(n=4)received sham thermal injury,whereas mice in burn group(n=4) received a 15%of total body surface area(TBSA)full-thickness thermal injury,and mice in burn+CORM-2 group(n=4)received the same thermal injury with immediate administration of CORM-2(8 mg/kg,iv).Hepatic tissue sections were stained with hematoxylin and eosin and examined under a light icroscope.Levels of aminotransferases(ALT and AST)and nitric oxide(NO) were measured by biochemical methods.Tumor necrosis factor-α(TNF-α)and interleukin(IL-1β)activity,and the protein expression of iNOS and HO-1 in serum and tissue homogenates were assessed.In in vitro experiments,Kupffer cells were stimulated with LPS(10μg/mL)for 4 h in the presence or absence of CORM-2(10-100μmol/L).Subsequently,the expression levels of TNF-αand NO production were assessed.RESULTS:Pro-inflammatory mediators(TNF-α,IL-1β,NO)in serum and liver homogenates of thermally injured mice were significantly reduced by CORM-2 administration.This was accompanied by a decrease in the expression of iNOS while an increase in the expression of HO-1 in the liver tissue.In parallel,the concentrations of TNF-αand NO in supernatants of LPS-stimulated Kupffer cells co-incubated with CORM-2 (10-100μmol/L)were also markedly decreased.Histological examination demonstrated that CORM-2 could attenuate the leukocytes infiltration to the liver tissue. CONCLUSION:CORM-released CO modulates liver inflammation and significantly protects liver injury in burn mice by inhibiting the expression of iNOS and NO production,down-regulating the expression of pro-inflammatory mediators(TNF-α,IL-1β). AIM: To explore the effects of CO-releasing molecules tricarbonyldichlororuthenium (II) dimer, CORM-2-liberated CO on attenuation of inflammatory responses in liver of an experimental animal model of thermal injury and to investigate the associated potential mechanisms. METHODS: Thirty- six mice were assigned to three groups in three experiments in each experiment, mice in sham group (n = 4) received sham thermal injury, mice in burn group (n = 4) received a 15% of total body surface area TBSA) full-thickness thermal injury, and mice in burn + CORM-2 group (n = 4) received the same thermal injury with immediate administration of CORM-2 (8 mg / kg, iv) .Hepatic tissue sections were stained with hematoxylin and eosin and examined under a light icroscope. Levels of aminotransferases (ALT and AST) and nitric oxide (NO) were measured by biochemical methods. Tumor necrosis factor-α (TNF-α) and interleukin (IL- protein expression of iNOS and HO-1 in serum and tissue homogenates were asses sed. In vitro experiments, Kupffer cells were stimulated with LPS (10 μg / mL) for 4 h in the presence or absence of CORM-2 (10-100 μmol / L) Pro-inflammatory mediators (TNF-α, IL-1β, NO) in serum and liver homogenates of thermally injured mice were significantly reduced by CORM-2 administration. This was accompanied by a decrease in the expression of iNOS while an increase in the expression of HO-1 in the liver tissue. In parallel, the concentrations of TNF-α and NO in supernatants of LPS-stimulated Kupffer cells co-incubated with CORM-2 (10-100 μmol / L) were also markedly decreased. Histological examination of that CORM-2 could attenuate the leukocytes infiltration to the liver tissue. CONCLUSION: CORM-released CO modulates liver inflammation and significantly protects liver injury in burn mice by inhibiting the expression of iNOS and NO production, down-regulating the expression of pro-inflammatory mediato rs (TNF-α, IL-1β).