中文摘要：

AIM:To investigate the possible mechanisms of exogenous carbon monoxide-releasing moleculeⅡ(CORM-2)intervention on hepatic energy metabolism in experimental sepsis.METHODS:Forty-eight C57BL/6 mice were randomly divided into four groups(n=12):sham group;cecal ligation and puncture(CLP)group;CLP+CORM-2group and CLP+iCORM-2(inactive CORM-2)group.Survival rates were determined after 72 h.Twenty-four similarly treated mice(n=6 in each group)were assayed for post-operative continuous blood glucose in the first 36 h.Thirty-six similarly treated mice(n=9in each group)underwent micro-positron emission tomography(PET)scanning after tail vein injection of18Ffluorodeoxyglucose(FDG)24 h after operation.Plasma and liver specimens were collected for assay of liver pathology,alanine transaminase(ALT)and aspartate transaminase(AST)activities.Hepatic glucokinase activity,lactic acid levels and mitochondrial swelling were also determined.RESULTS:Improved survival was observed in CORM-2treated mice.Both the CLP and CLP+CORM-2 groups had sustained low blood glucose levels within the first post-operative 36 h.18F-FDG micro-PET images showed abnormally high levels of hepatic glucose metabolism(standardized uptake value)in the CLP group(2.76±0.39 vs 0.84±0.14,P【0.01),which declined to normal levels after CORM-2 intervention(1.29±0.32 vs2.76±0.39,P【0.05).glucokinase activity was markedly increased in the CLP group(6.38±0.56 U/g vs 4.60±0.21 U/g,P【0.01),but was normal after CORM-2intervention(4.74±0.14 U/g vs 6.38±0.56 U/g,P【0.05).CORM-2 suppressed plasma lactic acid levels(4.02±0.02 mmol/L vs 7.72±2.37 mmol/L,P【0.05)and protected hepatic mitochondria in CLP mice.CORM-2 intervention also reduced elevated plasma AST(199.67±11.08 U/L vs 379.67±16.34 U/L,P【0.05)and ALT(63.67±12.23 U/L vs 112.67±9.74 U/L,P【0.05)activities in CLP mice.CONCLUSION:The release of CO molecules by CORM-2 protects mitochondria and maintains a stable level of hepatic glucose metabolism.Thus,CORM-2 improves liver function and survi

英文摘要：

AIM: To investigate the possible mechanisms of exogenous carbon monoxide-releasing molecule II (CORM-2) intervention on hepatic energy metabolism in experimental sepsis.