Evidence map›Paper›PMID 24083240›Full record

ArticleBioMed research international2013

Acetylsalicylic Acid reduces the severity of dextran sodium sulfate-induced colitis and increases the formation of anti-inflammatory lipid mediators.

Thomas Köhnke, Beate Gomolka, Süleyman Bilal, Xiangzhi Zhou, Yanping Sun, Michael Rothe, Daniel C Baumgart, Karsten H Weylandt

Open access · hybridAbstract read
In one paragraph

Article in BioMed research international, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 2 pooled it
2.3field-weighted citation impact, top 11% 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

15 citing papers in PubMed, 2 syntheses or guidelines pooled it, 27 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Diagnostic imaging advances in murine models of colitis.World journal of gastroenterology · 2016
    Review
  11. Article
  12. Article
  13. Review
  14. A review on chemical-induced inflammatory bowel disease models in rodents.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2014
    Review
  15. Article
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

8 authors at 4 institutions in 2 countries.

Thomas KöhnkeDepartment of Gastroenterology, Hepatology and Endocrinology, Virchow-Hospital, Charité Medical School, Free and Humboldt-University of Berlin, 13353 Berlin, Germany ; Laboratory for Lipid Medicine and Technology, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA.
Beate Gomolka
Süleyman Bilal
Xiangzhi Zhou
Yanping Sun
Michael Rothe
Daniel C Baumgart
Karsten H Weylandt
Harvard University · USBrigham and Women's Hospital · USHumboldt-Universität zu Berlin · DELipidomix (Germany) · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The role of non-steroidal anti-inflammatory drugs in inflammatory bowel disease is controversial, as they have been implicated in disease aggravation. Different from other cyclooxygenase inhibitors, acetylsalicylic acid (ASA) enhances the formation of anti-inflammatory and proresolution lipoxins derived from arachidonic acid as well as resolvins from omega-3 polyunsaturated fatty acids such as docosahexaenoic acid (DHA). In this study, we examined the effect of ASA on murine dextran sodium sulfate colitis. A mouse magnetic resonance imaging (MRI) protocol and post mortem assessment were used to assess disease severity, and lipid metabolites were measured using liquid chromatography-coupled tandem mass spectrometry. Decreased colitis activity was demonstrated by phenotype and MRI assessment in mice treated with ASA, and confirmed in postmortem analysis. Analysis of lipid mediators showed sustained formation of lipoxin A4 and an increase of DHA-derived 17-hydroxydocosahexaenoic acid (17-HDHA) after treatment with ASA. Furthermore, in vitro experiments in RAW264.7 murine macrophages demonstrated significantly increased phagocytosis activity after incubation with 17-HDHA, supporting its proresolution effect. These results show a protective effect of ASA in a murine colitis model and could give a rationale for a careful reassessment of ASA therapy in patients with inflammatory bowel disease and particularly ulcerative colitis, possibly combined with DHA supplementation.

Indexed as

AnimalsAnti-Inflammatory AgentsAspirinColitisDextran SulfateDocosahexaenoic AcidsFemaleLipidsMagnetic Resonance ImagingMiceMice, Inbred C57BLPhagocytosis17-hydroxy-4,7,10,13,15,19-docosahexaenoic acidAnti-Inflammatory AgentsAspirinDextran SulfateDocosahexaenoic AcidsLipids

Identifiers

PMID24083240
PMCPMC3780524
OpenAlexW2161905271

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.