Regulatory effect and mechanisms of carbon monoxide-releasing molecule II on hepatic energy metabolism in septic mice

Figure 8 Effect of carbon monoxide-releasing molecule II on hepatic lactate production in septic mice. Mice were challenged with cecal ligation and puncture (CLP) and treated with tricarbonyldichlororuthenium (II) dimer (CORM-2) or iCORM-2 as described in the Methods section. Lactate production in hepatic homogenates (A) and plasma (B) were assessed 24 h after CLP injury. When compared with the sham group, the CLP groups had significantly higher levels of lactic acid. After CORM-2 intervention, lactic acid levels in plasma and hepatic homogenates declined significantly. Results are presented as mean ± SD. ^bP < 0.01 vs sham mice; ^aP < 0.05 vs CLP mice.