Evidence map›Paper›PMID 15880142›Full record

ArticleBritish journal of pharmacology2005

Carbon monoxide-releasing molecules (CO-RMs) attenuate the inflammatory response elicited by lipopolysaccharide in RAW264.7 murine macrophages.

Philip Sawle, Roberta Foresti, Brian E Mann, Tony R Johnson, Colin J Green, Roberto Motterlini

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 127 papers.

0numbers the graph read from it
0cells of the map it votes in
127citing papers in PubMed
10.5field-weighted citation impact, top 1% 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

127 citing papers in PubMed, 387 citations in OpenAlex.

  1. Article
  2. Article
  3. Carbon Monoxide in an Experimental Model of Chronic Pelvic Pain Syndrome: The Effects of CORM-A1 on Pain and Anxiety-Related Behaviors.Pathophysiology : the official journal of the International Society for Pathophysiology · 2025
    Article
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  12. Click chemistry and drug delivery: A bird's-eye view.Acta pharmaceutica Sinica. B · 2023
    Review
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  14. Article
  15. Article
  16. Article
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67 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Philip SawleDepartment of Surgical Research, Vascular Biology Unit, Northwick Park Institute for Medical Research, Harrow, Middlesex.
Roberta Foresti
Brian E Mann
Tony R Johnson
Colin J Green
Roberto Motterlini
Northwick Park Institute for Medical Research · GBUniversity of Sheffield · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The enzyme heme oxygenase-1 (HO-1) is a cytoprotective and anti-inflammatory protein that degrades heme to produce biliverdin/bilirubin, ferrous iron and carbon monoxide (CO). The anti-inflammatory properties of HO-1 are related to inhibition of adhesion molecule expression and reduction of oxidative stress, while exogenous CO gas treatment decreases the production of inflammatory mediators such as cytokines and nitric oxide (NO). CO-releasing molecules (CO-RMs) are a novel group of substances identified by our group that are capable of modulating physiological functions via the liberation of CO. We aimed in this study to examine the potential anti-inflammatory characteristics of CORM-2 and CORM-3 in an in vitro model of lipopolysaccharide (LPS)-stimulated murine macrophages. Stimulation of RAW264.7 macrophages with LPS resulted in increased expression of inducible NO synthase (iNOS) and production of nitrite. CORM-2 or CORM-3 (10-100 microM) reduced nitrite generation in a concentration-dependent manner but did not affect the protein levels of iNOS. CORM-3 also decreased nitrite levels when added 3 or 6 h after LPS exposure. CORM-2 or CORM-3 did not cause any evident cytotoxicity and produced an increase in HO-1 expression and heme oxygenase activity; this effect was completely prevented by the thiol donor N-acetylcysteine. CORM-3 also considerably reduced the levels of tumor necrosis factor-alpha, another mediator of the inflammatory response. The inhibitory effects of CORM-2 and CORM-3 were not observed when the inactive compounds, which do not release CO, were coincubated with LPS. These results indicate that CO liberated by CORM-2 and CORM-3 significantly suppresses the inflammatory response elicited by LPS in cultured macrophages and suggest that CO carriers can be used as an effective strategy to modulate inflammation.

Indexed as

AnimalsCarbon MonoxideCell LineCell SurvivalGlutathioneHeme Oxygenase-1Heme Oxygenase (Decyclizing)InflammationLipopolysaccharidesMacrophagesMembrane ProteinsMiceNitric Oxide SynthaseNitric Oxide Synthase Type IINitritesOrganometallic CompoundsCarbon MonoxideGlutathioneHeme Oxygenase-1Heme Oxygenase (Decyclizing)Hmox1 protein, mouseLipopolysaccharidesMembrane ProteinsNitric Oxide SynthaseNitric Oxide Synthase Type IINitritesNos2 protein, mouseOrganometallic Compoundstricarbonylchloro(glycinato)ruthenium(II)tricarbonyldichlororuthenium (II) dimerTumor Necrosis Factor-alpha

Identifiers

PMID15880142
PMCPMC1576195
OpenAlexW2094470927

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.