| CO liberated from CORM-2 modulates the inflammatory response in the liver of thermally injured mice. | |
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MedLine Citation:
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PMID: 18203286 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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). |
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Authors:
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Bing-Wei Sun; Yan Sun; Zhi-Wei Sun; Xi Chen |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: World journal of gastroenterology : WJG Volume: 14 ISSN: 1007-9327 ISO Abbreviation: World J. Gastroenterol. Publication Date: 2008 Jan |
Date Detail:
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Created Date: 2008-01-18 Completed Date: 2008-04-24 Revised Date: 2009-11-18 |
Medline Journal Info:
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Nlm Unique ID: 100883448 Medline TA: World J Gastroenterol Country: China |
Other Details:
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Languages: eng Pagination: 547-53 Citation Subset: IM |
Affiliation:
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Department of Burns and Plastic Surgery, Affiliated Hospital, Jiangsu University, 438 Jiefang Rd. Zhenjiang 212001, Jiangsu Province, China. sunbinwe@hotmail.com |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Burns / complications*, immunology Carbon Monoxide / metabolism* Hepatitis / drug therapy*, etiology Inflammation Mediators / metabolism Liver / drug effects, immunology Male Mice Mice, Inbred C57BL Organometallic Compounds / pharmacokinetics* |
| Chemical | |
Reg. No./Substance:
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0/Inflammation Mediators; 0/Organometallic Compounds; 0/tricarbonyldichlororuthenium (II) dimer; 630-08-0/Carbon Monoxide |
| Comments/Corrections | |
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