Evidence map›Paper›PMID 21086163›Full record

ArticleDigestive diseases and sciences2011

Carbon monoxide liberated from carbon monoxide-releasing molecule exerts an anti-inflammatory effect on dextran sulfate sodium-induced colitis in mice.

Tomohisa Takagi, Yuji Naito, Kazuhiko Uchiyama, Takahiro Suzuki, Ikuhiro Hirata, Katsura Mizushima, Hisato Tsuboi, Natsuko Hayashi, Osamu Handa, Takeshi Ishikawa and 4 more

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Article in Digestive diseases and sciences, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

37 citing papers in PubMed, 77 citations in OpenAlex.

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  6. Protective effect ofFrontiers in microbiology · 2022
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  17. Effect ofEvidence-based complementary and alternative medicine : eCAM · 2019
    Article
  18. Heme oxygenase-1 prevents murine intestinal inflammation.Journal of clinical biochemistry and nutrition · 2018
    Article
  19. Review
  20. Review
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

14 authors at 1 institution in 1 country.

Tomohisa TakagiMolecular Gastroenterology and Hepatology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, 465 Kajii-cho, Kawaramachi-Hirokoji, Kamigyo-ku, Kyoto 602-8566, Japan.
Yuji Naito
Kazuhiko Uchiyama
Takahiro Suzuki
Ikuhiro Hirata
Katsura Mizushima
Hisato Tsuboi
Natsuko Hayashi
Osamu Handa
Takeshi Ishikawa
Nobuaki Yagi
Satoshi Kokura
Hiroshi Ichikawa
Toshikazu Yoshikawa
Kyoto Prefectural University of Medicine · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEndogenous carbon monoxide (CO) is one of the three products of heme degradation by heme oxygenase-1 (HO-1) and exerts novel anti-inflammatory and anti-apoptotic effects as a gaseous second messenger. The purpose of this investigation was to determine whether exogenous CO could modulate intestinal inflammation.

methodsAcute colitis was induced with 2% DSS in male C57BL/6 mice. CO-releasing molecule-2 (CORM-2; tricarbonyldichlororuthenium(II) dimer) was intraperitoneally administered twice daily and the disease activity index (DAI) was determined. We measured tissue-associated myeloperoxidase (MPO) activity as an index of neutrophil infiltration, and the production of keratinocyte chemoattractant (KC) and tumor necrosis factor-α (TNF-α) protein in the intestinal mucosa. In an in-vitro study, young adult mouse colonic epithelial (YAMC) cells were incubated with TNF-α, and KC mRNA/protein expression and nuclear translocation of nuclear factor-kappa B (NF-κB) were measured with or without CORM-2 treatment.

resultsAfter DSS administration, DAI score increased in a time-dependent manner, and this increase was ameliorated by CORM-2 treatment. Increases in MPO activity and in the production of KC and TNF-α after DSS administration were significantly inhibited by CORM-2. TNF-α-induced KC production in YAMC cells was also inhibited by CORM-2 treatment. Further, nuclear translocation of NF-κB in YAMC cells was inhibited by CORM-2.

conclusionCORM-liberated CO significantly inhibited inflammatory response in murine colitis by inhibition of cytokine production in the colonic epithelium. These results suggest that CO could become a new therapeutic molecule for inflammatory bowel disease.

Indexed as

AnimalsAnti-Inflammatory Agents, Non-SteroidalCarbon MonoxideChemotactic FactorsColitisColonDextran SulfateFemaleGene Expression RegulationMiceMice, Inbred C57BLOrganometallic CompoundsPeroxidaseTumor Necrosis Factor-alphaAnti-Inflammatory Agents, Non-SteroidalCarbon MonoxideChemotactic FactorsDextran SulfateOrganometallic CompoundsPeroxidasetricarbonyldichlororuthenium (II) dimerTumor Necrosis Factor-alpha

Identifiers

PMID21086163
OpenAlexW2066109560

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Registered trials

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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.