Evidence map›Paper›PMID 17339836›Full record

ArticleBritish journal of pharmacology2007

The carbon monoxide-releasing molecule CORM-2 inhibits the inflammatory response induced by cytokines in Caco-2 cells.

J Megías, J Busserolles, M J Alcaraz

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
4.3field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

47 citing papers in PubMed, 115 citations in OpenAlex.

  1. Therapeutic Gases in Biomedicine: Updates on Nitric Oxide and Beyond.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
  2. The Triple Crown: NO, CO, and HPharmacology & therapeutics · 2023
    Review
  3. Review
  4. Review
  5. [Carbon Monoxide and Pain Regulation: A Review].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2021
    Review
  6. Review
  7. Review
  8. Article
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  10. Review
  11. Repurposing Tin Mesoporphyrin as an Immune Checkpoint Inhibitor Shows Therapeutic Efficacy in Preclinical Models of Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2018
    Article
  12. Article
  13. Pinocembrin Suppresses HMolecular neurobiology · 2018
    Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

J MegíasDepartment of Pharmacology, University of Valencia, Burjasot, Valencia, Spain.
J Busserolles
M J Alcaraz
Universitat de València · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeRecent evidence indicates that carbon monoxide-releasing molecules (CO-RMs) exhibit potential anti-inflammatory properties. In the present study, we have investigated whether tricarbonyl dichloro ruthenium(II) dimer (CORM-2) can control the inflammatory response induced by cytokines in a human colonic epithelial cell line, Caco-2. EXPERIMENTAL APPROACH: Caco-2 cells were preincubated with CORM-2 for 30 minutes and then stimulated with interleukin (IL)-1beta, tumor necrosis factor-alpha and interferon-gamma for different times. Gene expression was analyzed by real-time PCR. Protein expression was investigated by Western blot and ELISA. Transcription factor activation was determined by the luciferase method. KEY

resultsWe have shown that CORM-2 significantly decreased the mRNA expression of nitric oxide synthase-2 (NOS-2) and the production of nitrite, in Caco-2 cells stimulated with cytokines. IL-8, IL-6 and metalloproteinase-7 (MMP-7) mRNA and protein were also significantly reduced by CORM-2. Time-course and small interfering RNA studies suggest that inhibition of IL-6 plays a role in the regulation of MMP-7 expression by CORM-2. These effects of CORM-2 can be dependent on the modulation of nuclear factor-kappaB (NF-kappaB), activator protein-1, CCAT/enhancer binding protein and the phosphorylated forms of NF-kappaB inhibitory protein-alpha, c-Jun N-terminal protein kinase 1/2, p38 and extracellular signal-regulated kinase 1/2. CONCLUSIONS AND IMPLICATIONS: CORM-2 can regulate a number of genes relevant in intestinal inflammation and cancer progression. These findings provide new insights into the anti-inflammatory properties and potential applications of this class of compounds.

Indexed as

Anti-Inflammatory AgentsCaco-2 CellsCarbon MonoxideCCAAT-Enhancer-Binding ProteinsCytokinesDose-Response Relationship, DrugEpithelial CellsGene ExpressionHumansI-kappa B ProteinsInflammationInterferon-gammaInterleukin-1betaInterleukin-6Interleukin-8Intestinal MucosaAnti-Inflammatory AgentsCarbon MonoxideCCAAT-Enhancer-Binding ProteinsCytokinesI-kappa B ProteinsInterferon-gammaInterleukin-1betaInterleukin-6Interleukin-8Matrix Metalloproteinase 7MMP7 protein, humanNF-kappa BNF-KappaB Inhibitor alphaNFKBIA protein, humanNitric Oxide Synthase Type IINOS2 protein, humanOrganometallic CompoundsRNA, MessengerTranscription Factor AP-1tricarbonyldichlororuthenium (II) dimerTumor Necrosis Factor-alpha

Identifiers

PMID17339836
PMCPMC2013913
OpenAlexW1484225253

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.