PMID- 18203286
OWN - NLM
STAT- MEDLINE
DCOM- 20080424
LR  - 20211020
IS  - 1007-9327 (Print)
IS  - 1007-9327 (Linking)
VI  - 14
IP  - 4
DP  - 2008 Jan 28
TI  - CO liberated from CORM-2 modulates the inflammatory response in the liver of 
      thermally injured mice.
PG  - 547-53
AB  - AIM: To explore the effects of CO-releasing molecules 
      [tricarbonyldichlororuthenium (II) dimer, CORM-2]-liberated CO on attenuation of 
      inflammatory responses in liver of an experimental animal model of thermal injury 
      and to investigate the associated potential mechanisms. METHODS: Thirty-six mice 
      were assigned to three groups in three respective experiments. In each 
      experiment, mice in sham group (n=4) received sham thermal injury, whereas mice 
      in burn group (n=4) received a 15% of total body surface area (TBSA) 
      full-thickness thermal injury, and mice in burn+CORM-2 group (n=4) received the 
      same thermal injury with immediate administration of CORM-2 (8 mg/kg, iv). 
      Hepatic tissue sections were stained with hematoxylin and eosin and examined 
      under a light microscope. Levels of aminotransferases (ALT and AST) and nitric 
      oxide (NO) were measured by biochemical methods. Tumor necrosis factor-alpha 
      (TNF-alpha) and interleukin (IL-1beta) activity, and the protein expression of 
      iNOS and HO-1 in serum and tissue homogenates were assessed. In in vitro 
      experiments, Kupffer cells were stimulated with LPS (10 microg/mL) for 4 h in the 
      presence or absence of CORM-2 (10-100 micromol/L). Subsequently, the expression 
      levels of TNF-alpha and NO production were assessed. RESULTS: Pro-inflammatory 
      mediators (TNF-alpha, IL-1beta, NO) in serum and liver homogenates of thermally 
      injured mice were significantly reduced by CORM-2 administration. This was 
      accompanied by a decrease in the expression of iNOS while an increase in the 
      expression of HO-1 in the liver tissue. In parallel, the concentrations of 
      TNF-alpha and NO in supernatants of LPS-stimulated Kupffer cells co-incubated 
      with CORM-2 (10-100 micromol/L) were also markedly decreased. Histological 
      examination demonstrated that CORM-2 could attenuate the leukocytes infiltration 
      to the liver tissue. CONCLUSION: CORM-released CO modulates liver inflammation 
      and significantly protects liver injury in burn mice by inhibiting the expression 
      of iNOS and NO production, down-regulating the expression of pro-inflammatory 
      mediators (TNF-alpha, IL-1beta).
FAU - Sun, Bing-Wei
AU  - Sun BW
AD  - Department of Burns and Plastic Surgery, Affiliated Hospital, Jiangsu University, 
      438 Jiefang Rd. Zhenjiang 212001, Jiangsu Province, China. sunbinwe@hotmail.com
FAU - Sun, Yan
AU  - Sun Y
FAU - Sun, Zhi-Wei
AU  - Sun ZW
FAU - Chen, Xi
AU  - Chen X
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - World J Gastroenterol
JT  - World journal of gastroenterology
JID - 100883448
RN  - 0 (Inflammation Mediators)
RN  - 0 (Organometallic Compounds)
RN  - 0 (tricarbonyldichlororuthenium (II) dimer)
RN  - 7U1EE4V452 (Carbon Monoxide)
SB  - IM
MH  - Animals
MH  - Burns/*complications/immunology
MH  - Carbon Monoxide/*metabolism
MH  - Hepatitis/*drug therapy/etiology
MH  - Inflammation Mediators/metabolism
MH  - Liver/drug effects/immunology
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Organometallic Compounds/*pharmacokinetics
PMC - PMC2681145
EDAT- 2008/01/19 09:00
MHDA- 2008/04/25 09:00
PMCR- 2008/01/28
CRDT- 2008/01/19 09:00
PHST- 2008/01/19 09:00 [pubmed]
PHST- 2008/04/25 09:00 [medline]
PHST- 2008/01/19 09:00 [entrez]
PHST- 2008/01/28 00:00 [pmc-release]
AID - 10.3748/wjg.14.547 [doi]
PST - ppublish
SO  - World J Gastroenterol. 2008 Jan 28;14(4):547-53. doi: 10.3748/wjg.14.547.