Evidence map›Paper›PMID 24349609›Full record

ArticleOxidative medicine and cellular longevity2013

Carbon monoxide attenuates dextran sulfate sodium-induced colitis via inhibition of GSK-3β signaling.

Md Jamal Uddin, Sun-oh Jeong, Min Zheng, Yingqing Chen, Gyeong Jae Cho, Hun Taeg Chung, Yeonsoo Joe

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

21 citing papers in PubMed, 39 citations in OpenAlex.

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  12. HInflammopharmacology · 2018
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  16. Nicotine protects against DSS colitis through regulating microRNA-124 and STAT3.Journal of molecular medicine (Berlin, Germany) · 2017
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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

7 authors at 3 institutions in 2 countries.

Md Jamal UddinSchool of Biological Sciences, University of Ulsan, Ulsan 680-749, Republic of Korea.
Sun-oh JeongSchool of Biological Sciences, University of Ulsan, Ulsan 680-749, Republic of Korea.
Min ZhengSchool of Biological Sciences, University of Ulsan, Ulsan 680-749, Republic of Korea ; Department of Thoracic and Cardiovascular Surgery, Affiliated Hospital of Yanbian University, Yanji 133000, China.
Yingqing ChenSchool of Biological Sciences, University of Ulsan, Ulsan 680-749, Republic of Korea.
Gyeong Jae ChoDepartment of Anatomy, School of Medicine, Institute of Health Sciences, Gyeongsang National University, Jinju 660-701, Republic of Korea.
Hun Taeg ChungSchool of Biological Sciences, University of Ulsan, Ulsan 680-749, Republic of Korea.
Yeonsoo JoeSchool of Biological Sciences, University of Ulsan, Ulsan 680-749, Republic of Korea.
University of Ulsan · KRGyeongsang National University · KRYanbian University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endogenous carbon monoxide (CO) is produced by heme oxygenase-1 (HO)-1 which mediates the degradation of heme into CO, iron, and biliverdin. Also, CO ameliorates the human inflammatory bowel diseases and ulcerative colitis. However, the mechanism for the effect of CO on the inflammatory bowel disease has not yet been known. In this study, we showed that CO significantly increases survival percentage, body weight, colon length as well as histologic parameters in DSS-treated mice. In addition, CO inhalation significantly decreased DSS induced pro-inflammatory cytokines by inhibition of GSK-3β in mice model. To support the in vivo observation, TNF-α, iNOS and IL-10 after CO and LiCl treatment were measured in mesenteric lymph node cells (MLNs) and bone marrow-derived macrophages (BMMs) from DSS treated mice. In addition, we determined that CO potentially inhibited GSK-3β activation and decreased TNF-α and iNOS expression by inhibition of NF-κB activation in LPS-stimulated U937 and MLN cells pretreated with CO. Together, our findings indicate that CO attenuates DSS-induced colitis via inhibition of GSK-3β signaling in vitro and in vivo. Importantly, this is the first report that investigated the molecular mechanisms mediated the novel effects of CO via inhibition GSK-3β in DSS-induced colitis model.

Indexed as

Signal TransductionAnimalsBody WeightBone Marrow CellsCarbon MonoxideCell LineColitisColonCytokinesDextran SulfateGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHumansInflammation MediatorsLymph NodesMacrophagesCarbon MonoxideCytokinesDextran SulfateGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGSK3B protein, humanGsk3b protein, mouseInflammation MediatorsNitric Oxide Synthase Type IITumor Necrosis Factor-alpha

Identifiers

PMID24349609
PMCPMC3848334
OpenAlexW2079649227

What OpenQuestion holds

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LicenceCC BY
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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.