Evidence map›Paper›PMID 11991626›Full record

ArticleDigestive diseases and sciences2002

16,16-Dimethyl prostaglandin E2 inhibits indomethacin-induced small intestinal lesions through EP3 and EP4 receptors.

Tomonori Kunikata, Akiko Tanaka, Tohru Miyazawa, Shinichi Kato, Koji Takeuchi

Abstract read
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In one paragraph

Article in Digestive diseases and sciences, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 9% 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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 94 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
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  12. Review
  13. NSAID-Gut Microbiota Interactions.Frontiers in pharmacology · 2020
    Review
  14. Observational
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  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

5 authors at 1 institution in 1 country.

Tomonori KunikataDepartment of Pharmacology and Experimental Therapeutics, Kyoto Pharmaceutical University, Yamashina, Japan.
Akiko Tanaka
Tohru Miyazawa
Shinichi Kato
Koji Takeuchi
Kyoto Pharmaceutical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We evaluated the effect of various PGE analogs specific to EP receptor subtypes on indomethacin-induced small intestinal lesions in rats and investigated the relationship of EP receptor subtype with the PGE action using EP receptor knockout mice. Animals were administered indomethacin subcutaneously, and they were killed 24 hr later. 16,16-dimethyl prostaglandin E2 (dmPGE2) or various EP agonists were administered intravenously 10 min before indomethacin. Indomethacin caused hemorrhagic lesions in the rat small intestine, accompanied with an increase in intestinal motility and the number of enteric bacteria as well as iNOS and MPO activities. Prior administration of dmPGE2 dose-dependently prevented intestinal lesions, together with inhibition of those functional changes. These effects of dmPGE2 were mimicked by prostanoids (ONO-NT-012 and ONO-AE1-329), only specific to EP3 or EP4 receptors, although the intestinal motility was inhibited only by ONO-AE1-329. Intestinal mucus secretion and fluid accumulation were decreased by indomethacin but enhanced by dmPGE2, ONO-NT-012, and ONO-AE1-329 at the doses that prevented intestinal lesions. Indomethacin also caused intestinal lesions in both wild-type and knockout mice lacking EP1 or EP3 receptors, yet the protective action of dmPGE2 was observed in wild-type and EP1 receptor knockout mice but not the mice lacking EP3 receptors. These results suggest that the intestinal cytoprotective action of PGE2 against indomethacin is mediated by EP3/EP4 receptors and that this effect is functionally associated with an increase of mucus secretion and enteropooling as well as inhibition of intestinal hypermotility, the former two processes mediated by both EP3 and EP4 receptors, and the latter by EP4 receptors.

Indexed as

Cyclooxygenase InhibitorsIndomethacin16,16-Dimethylprostaglandin E2AnimalsColony Count, MicrobialGastrointestinal MotilityIntestinal DiseasesIntestinal MucosaIntestine, SmallMaleMiceMice, KnockoutMucusNitric Oxide SynthaseNitric Oxide Synthase Type IIPeroxidase16,16-Dimethylprostaglandin E2Cyclooxygenase InhibitorsIndomethacinNitric Oxide SynthaseNitric Oxide Synthase Type IINos2 protein, mouseNos2 protein, ratPeroxidasePtger3 protein, mousePtger3 protein, ratPtger4 protein, mousePtger4 protein, ratReceptors, Prostaglandin EReceptors, Prostaglandin E, EP3 SubtypeReceptors, Prostaglandin E, EP4 Subtype

Identifiers

PMID11991626
OpenAlexW270039881

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.