Evidence map›Paper›PMID 23066659›Full record

ArticleBMC gastroenterology2012

A possible involvement of Nrf2-mediated heme oxygenase-1 up-regulation in protective effect of the proton pump inhibitor pantoprazole against indomethacin-induced gastric damage in rats.

Ho-Jae Lee, Young-Min Han, Eun-Hee Kim, Yoon-Jae Kim, Ki-Baik Hahm

Open access · goldAbstract read
In one paragraph

Article in BMC gastroenterology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

14 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Proton pump inhibitors modulate esophageal epithelial barrier function and crosstalk with eosinophils.Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Proton pump inhibitors in IPF: beyond mere suppression of gastric acidity.QJM : monthly journal of the Association of Physicians · 2016
    Review
  11. Article
  12. Review
  13. Article
  14. 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 2 institutions in 1 country.

Ho-Jae LeeLab of Chemoprevention, Lee Gil Ya Cancer and Diabetes Institute, Gachon University, Incheon 406-840, Korea.
Young-Min Han
Eun-Hee Kim
Yoon-Jae Kim
Ki-Baik Hahm
CHA University · KRGachon University Gil Medical Center · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundProton pump is an integral membrane protein that is ubiquitous ATP binding cassette (ABC) involved in many transport processes in all living organisms, among which a specialized form of pump, so called p-type proton pump, exists in the parietal cells of stomach. Though proton pump inhibitors (PPIs) are frequently prescribed to prevent nonsteroidal anti-inflammatory drugs (NSAIDs)-induced gastric damage, the acid suppressive actions do not suffice to explain.

methodsIn order to document the effects of pantoprazole, one of PPIs, on the NSAIDs-induced gastric damage, in vitro and in vivo studies were performed. Immunocytochemistry, Western blot analysis, electrophoretic mobility shift assay and RT-PCR were conducted to evaluate the induction of heme oxygenase-1 (HO-1) through Nrf2 activation in normal gastric mucosal RGM-1 cells or in vivo stomach tissues from rats treated with indomethacin and/or pantoprazole.

resultsPantoprazole activated Nrf2 through inactivation of Keap1, after which the expression of HO-1 was significantly increased in a dose-dependent manner in RGM-1 cells. Increased ARE-DNA binding activity was observed maximally at 1 h with 300 μM of pantoprazole. The expression of HO-1 induced by pantoprazole was significantly associated with the increased in vitro tube formation (P < 0.05) and angiogenic factors including VEGF, bFGF, and HIF-1α. Indomethacin markedly increased the expressions of TNF-α, IL-1ß, IL-8, NOX-1, ICAM-1 and VCAM, whereas pantoprazole significantly decreased the expressions of indomethacin-induced these inflammatory mediators in accord with pantoprazole-induced HO-1 (P < 0.05) as documented with HO-1 inhibitor. In vivo model of indomethacin-induced gastric damage could validate in vitro-drawn results that pantoprazole remarkably protected against indomethacin-induced gastric damage, in which zinc protoporphyrin (5 mg/kg, ip) significantly abolished the protective efficacy of pantoprazole.

conclusionThese results demonstrate that Nrf2-mediated HO-1 induction of PPIs afforded a significant protective effect against NSAIDs-induced gastric damage beyond acid suppressive actions.

Indexed as

2-PyridinylmethylsulfinylbenzimidazolesAnalysis of VarianceAnimalsCells, CulturedEnzyme InductionEnzyme InhibitorsFibroblast Growth Factor 2Heme Oxygenase (Decyclizing)Hypoxia-Inducible Factor 1, alpha SubunitIndomethacinIntercellular Adhesion Molecule-1Interleukin-1betaInterleukin-8Intracellular Signaling Peptides and ProteinsKelch-Like ECH-Associated Protein 1NADH, NADPH Oxidoreductases2-PyridinylmethylsulfinylbenzimidazolesEnzyme InhibitorsFibroblast Growth Factor 2Heme Oxygenase (Decyclizing)Hypoxia-Inducible Factor 1, alpha SubunitIndomethacinIntercellular Adhesion Molecule-1Interleukin-1betaInterleukin-8Intracellular Signaling Peptides and ProteinsKEAP1 protein, ratKelch-Like ECH-Associated Protein 1NADH, NADPH OxidoreductasesNADPH Oxidase 1Nfe2l2 protein, ratNF-E2-Related Factor 2PantoprazoleProton Pump InhibitorsProtoporphyrinsTumor Necrosis Factor-alphaVascular Cell Adhesion Molecule-1Vascular Endothelial Growth Factor Azinc protoporphyrin

Identifiers

PMID23066659
PMCPMC3548718
OpenAlexW2037912913

What OpenQuestion holds

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LicenceCC BY
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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.