Evidence map›Paper›PMID 20084447›Full record

ReviewInflammation2010

Different mechanisms in formation and prevention of indomethacin-induced gastric ulcers.

Halis Suleyman, Abdulmecit Albayrak, Mehmet Bilici, Elif Cadirci, Zekai Halici

Abstract readComparative StudyReview
PubMed Publisher
In one paragraph

Review in Inflammation, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed, 1 pooled it
6.7field-weighted citation impact, top 3% 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

79 citing papers in PubMed, 1 synthesis or guideline pooled it, 215 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Pyroptosis in gastric mucosal injury‑related diseases (Review).International journal of molecular medicine · 2025
    Review
  8. Article
  9. Review
  10. Antiulcer activity ofOpen veterinary journal · 2025
    Review
  11. Review
  12. Review
  13. Article
  14. In Vitro Protective Effects of a Standardized Extract ofAntioxidants (Basel, Switzerland) · 2024
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

19 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

5 authors at 1 institution in 1 country.

Halis SuleymanFaculty of Medicine, Department of Pharmacology, Ataturk University, Erzurum, Turkey. suleyman@atauni.edu.tr
Abdulmecit Albayrak
Mehmet Bilici
Elif Cadirci
Zekai Halici
Atatürk University · TR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Indomethacin is an indol derivative, non-steroidal, anti-inflammatory drug with anti-inflammatory, analgesic, and antipyretic effects. Indomethacin became the first-choice drug to produce an experimental ulcer model as a result of having a higher ulcerogenic potential than other non-steroidal anti-inflammatory drugs (NSAIDs). There have been several conflicting reports about the ulcerogenic mechanism of indomethacin; the mechanism is still unclear. It has been suggested that indomethacin induces gastric damage via inhibiting the release of protective factors like cyclooxygenase-1 (COX-1), prostaglandin E2 (PGE2), bicarbonate, and mucus; increasing aggressive factors like acid; and increasing oxidant parameters while decreasing antioxidant parameters. Classic antiulcer drugs are known to produce antiulcer effects by activating against indomethacin (increasing PGE2, mucus, and bicarbonate production; inhibiting acid secretion; decreasing oxidant parameters; and increasing antioxidants). However, some antiulcer drugs have been shown to inhibit indomethacin-induced ulcers without affecting acid and mucus secretion or oxidant parameters, as well as to inhibit the production of protective factors like COX-1, PGE2, and bicarbonate, and to reduce antioxidant parameters. In order to resolve the contradictions in the abovementioned data, this review hypothesized a relationship between indomethacin-induced ulcers and alpha 2 adrenergic receptors. It is suggested that blockage of alpha 2 adrenergic receptors may be responsible for the increase in the aggressive factors induced by indomethacin, and stimulation of alpha 2 adrenergic receptors may be responsible for the increase of protective factors induced by antiulcer drugs.

Indexed as

AnimalsAnti-Inflammatory Agents, Non-SteroidalAnti-Ulcer AgentsBicarbonatesCyclooxygenase InhibitorsDinoprostoneGastric AcidGastric MucosaHumansIndomethacinModels, BiologicalMucusNitric OxideOxidation-ReductionOxidative StressProstaglandin AntagonistsAnti-Inflammatory Agents, Non-SteroidalAnti-Ulcer AgentsBicarbonatesCyclooxygenase InhibitorsDinoprostoneIndomethacinNitric OxideProstaglandin AntagonistsReceptors, Adrenergic, alpha-2

Identifiers

PMID20084447
OpenAlexW1990425813

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.