Evidence map›Paper›PMID 22918683›Full record

ArticleDigestive diseases and sciences2013

Attenuation of acetic acid-induced gastric ulcer formation in rats by glucosylceramide synthase inhibitors.

Manabu Nakashita, Hidekazu Suzuki, Soichiro Miura, Takao Taki, Keita Uehara, Tohru Mizushima, Hiroshi Nagata, Toshifumi Hibi

Abstract read
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In one paragraph

Article in Digestive diseases and sciences, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

11 citing papers in PubMed, 14 citations in OpenAlex.

  1. Chemical components and protective effects ofWorld journal of gastroenterology · 2023
    Article
  2. Protective Effect of Ocotillol, the Derivate of Ocotillol-Type Saponins inInternational journal of molecular sciences · 2020
    Article
  3. Article
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  5. Antiulcer Activity and Potential Mechanism of Action of the Leaves ofOxidative medicine and cellular longevity · 2018
    Article
  6. Oxidative medicine and cellular longevity · 2017
    Article
  7. Article
  8. Article
  9. Gastroduodenal mucosal defense.Current opinion in gastroenterology · 2013
    Review
  10. Article
  11. Gastro-protective effect ofAvicenna journal of phytomedicine
    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 1 country.

Manabu NakashitaDivision of Gastroentrology and Hepatology, Department of Internal Medicine, School of Medicine, Keio University, 35 Shinanomachi, Shinjuku-ku, Tokyo, 160-8582, Japan.
Hidekazu Suzuki
Soichiro Miura
Takao Taki
Keita Uehara
Tohru Mizushima
Hiroshi Nagata
Toshifumi Hibi
Keio University · JPkeiyu Hospital · JPNational Defense Medical College · JPOtsuka (Japan) · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionCeramide has been suggested to play a role in apoptosis during gastric ulcerogenesis. The present study is designed to investigate whether accumulated ceramide could serve as the effector molecules of ulcer formation in a rat model of acetic acid-induced gastric ulcer.

methodsThe effect of fumonisin B1, an inhibitor of ceramide synthase, and of d,l,-threo-1-phenyl-2-hexadecanoylamino-3-morpholino-1-propanol (PPMP) and N-butyldeoxynojirimycin (NB-DNJ), both inhibitors of glucosylceramide synthase, on the accumulation of ceramide and formation of gastric ulcer were examined in the rat model of acetic acid-induced gastric ulcer.

resultsFumonisin B1 attenuated acetic acid-induced gastric ulcer formation, associated with a decrease in the number of apoptotic cells. Our results showed that it is neither the C18- nor the C24-ceramide itself, but the respective metabolites that were ulcerogenic, because PPMP and NB-DNJ attenuated gastric mucosal apoptosis and the consequent mucosal damage in spite of their reducing the degradation of ceramide.

conclusionThe ceramide pathway, in particular, the metabolites of ceramide, significantly contributes to acetic acid-induced gastric damage, possibly via enhancing apoptosis. On the other hand, PPMP and NB-DNJ treatment attenuated gastric mucosal apoptosis and ulcer formation despite increasing the ceramide accumulation, suggesting that it was not the ceramides themselves, but their metabolites that contributed to the ulcer formation in the acetic acid-induced gastric ulcer model.

Indexed as

1-DeoxynojirimycinAcetic AcidAnimalsApoptosisDisease Models, AnimalEnzyme InhibitorsFumonisinsGastric MucosaGlucosylceramidesGlucosyltransferasesG(M3) GangliosideHumansMaleMorpholinesRatsRats, Sprague-Dawley1-Deoxynojirimycin1-phenyl-2-palmitoylamino-3-morpholino-1-propanolAcetic Acidceramide glucosyltransferaseEnzyme Inhibitorsfumonisin B1FumonisinsGlucosylceramidesGlucosyltransferasesG(M3) GangliosidemiglustatMorpholinesSphingolipids

Identifiers

PMID22918683
OpenAlexW2080921481

What OpenQuestion holds

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Read underepoch 390

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.