Exogenous carbon monoxide attenuates inflammatory responses in the small intestine of septic mice

Figure 3 Effects of tricarbonyldichlororuthenium (II) dimer carbon monoxide-releasing molecules on malondialdehyde, expression of interleukin-1β and tumor necrosis factor-α and nitrite production in the mid-ileum and mid-jejunum of septic mice. A: Mice were challenged with cecal ligation and perforation (CLP) and treated with tricarbonyldichlororuthenium (II) dimer. Malondialdehyde (MDA) in the mid-ileum and mid-jejunum was assessed 24 h following CLP injury; B: Tumor necrosis factor (TNF)-α levels in the mid-ileum and mid-jejunum was assessed 24 h following CLP injury; C: Interleukin (IL)-1β levels in the mid-ileum and mid-jejunum was assessed 24 h following CLP injury; D: Nitrite production in the mid-ileum and mid-jejunum was assessed 24 h following CLP injury. Results are mean ± SE, ^aP < 0.01 vs sham mice; ^cP < 0.05 vs CLP mice. CORM: Carbon monoxide-releasing molecule; iCORM: Inactivated-carbon monoxide-releasing molecule.