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

Figure 4 Effect of carbon monoxide-releasing molecule II on fludeoxyglucose uptake in the liver of 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. ¹⁸F-fludeoxyglucose (FDG) was administered by tail vein injection at a dose of 20 μCi followed by micro-positron emission tomography scanning and measurement of ¹⁸F-FDG biodistribution. Compared with the normal control group, the CLP group of mice showed significant increases in the level of hepatic glucose metabolism, and these increases were suppressed by CORM-2 intervention. A: Representative images of liver FDG uptake; B: The mean standardized radioactive uptake values in liver tissue; C: Quantification of ¹⁸F-FDG biodistribution. ^bP < 0.01 vs sham mice; ^dP < 0.01 vs CLP mice.