CO liberated from CORM-2 modulates the inflammatory response in the liver of thermally injured mice

Figure 1 Histologic results of liver tissue after staining with hematoxylin and eosin (HE, × 100). Mice were challenged with thermal injury and immediately intravenously injected with CORM-2 (8 mg/kg). A: Sham group; B: Burn group; C: Burn + CORM-2 group.

Figure 2 Effect of CORM-2 on TNF-a and IL-1β levels in serum and tissue homogenates of burn-challenged mice. Data are expressed as mean ± SE of three experiments (three mice per group). ^aP < 0.05 vs burn group; ^cP < 0.05 vs sham group.

Figure 3 Effects of CORM-2 on protein expression of iNOS and HO-1 in the liver of burn-challenged mice. Protein expressions of iNOS and HO-1 were performed by Western blotting at 24 h after thermal injury. A: Representative experiment; B and C: Quantitative results (average absorbance, A₅₄₀) of three. ^aP < 0.05 vs burn group; ^cP < 0.05 vs sham group.

Figure 4 Effects of CORM-2 on NO level in serum and tissue homogenates of burn-challenged mice. Measurement of NO level was performed by a microplate assay using Griess reagent at 24 h after thermal injury. NO levels both in serum and tissue homogenates of thermally injured mice were markedly increased, but significantly inhibited by in vivo administration of CORM-2. ^aP < 0.05 vs burn group; ^cP < 0.05 vs sham group.

Figure 5 Effect of CORM-2 on levels of NO and TNF-α in supernatants of Kupffer cells stimulated with LPS. Kupffer cells were co-incubated with LPS and different concentrations of CORM-2 (10-100 mmol/L) for 4 h. All values are expressed as means ± SE (n = 3). ^bP < 0.01 vs control; ^aP < 0.05 vs LPS group.