ArticleWorld journal of gastroenterology2008
CO liberated from CORM-2 modulates the inflammatory response in the liver of thermally injured mice.
Article in World journal of gastroenterology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 25 citations in OpenAlex.
- Chemical Reactivities of Two Widely Used Ruthenium-Based CO-Releasing Molecules with a Range of Biologically Important Reagents and Molecules.Analytical chemistry · 2021Article
- Burn injury induces histopathological changes and cell proliferation in liver of rats.World journal of hepatology · 2016Article
- Exogenous carbon monoxide suppresses Escherichia coli vitality and improves survival in an Escherichia coli-induced murine sepsis model.Acta pharmacologica Sinica · 2014Article
- Regulatory effect and mechanisms of carbon monoxide-releasing molecule II on hepatic energy metabolism in septic mice.World journal of gastroenterology · 2014Article
- A novel role of exogenous carbon monoxide on protecting cardiac function and improving survival against sepsis via mitochondrial energetic metabolism pathway.International journal of biological sciences · 2014Article
- Emerging concepts on the anti-inflammatory actions of carbon monoxide-releasing molecules (CO-RMs).Medical gas research · 2012Article
- Exogenous carbon monoxide attenuates inflammatory responses in the small intestine of septic mice.World journal of gastroenterology · 2012Article
- The therapeutic potential of carbon monoxide.Nature reviews. Drug discovery · 2010Review
- The Role of Nrf2 in Cellular Innate Immune Response to Inflammatory Injury.Toxicological research · 2009Review
- Bench-to-bedside review: Carbon monoxide--from mitochondrial poisoning to therapeutic use.Critical care (London, England) · 2009Review
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Authors and funding
4 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo 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.
methodsThirty-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.
resultsPro-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.
conclusionCORM-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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