Evidence map›Paper›PMID 25469038›Full record

ArticleWorld journal of gastroenterology2014

Alleviated mucosal and neuronal damage in a rat model of Crohn's disease.

Petra Talapka, Lajos István Nagy, Alexandra Pál, Marietta Zita Poles, Anikó Berkó, Mária Bagyánszki, László Géza Puskás, Éva Fekete, Nikolett Bódi

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in World journal of gastroenterology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
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

9 citing papers in PubMed.

  1. Intestinal muscularis in health and disease.Communications biology · 2026
    Review
  2. Review
  3. Imaging the enteric nervous system.Frontiers in neuroanatomy · 2025
    Review
  4. Article
  5. Altered Caecal Neuroimmune Interactions in the Neuroligin-3Frontiers in cellular neuroscience · 2020
    Article
  6. Nitrergic Enteric Neurons in Health and Disease-Focus on Animal Models.International journal of molecular sciences · 2019
    Review
  7. Article
  8. Article
  9. 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

9 authors.

Petra TalapkaPetra Talapka, Alexandra Pál, Marietta Zita Poles, Anikó Berkó, Mária Bagyánszki, Éva Fekete, Nikolett Bódi, Department of Physiology, Anatomy and Neuroscience, Faculty of Sciences and Informatics, University of Szeged, H-6726 Szeged, Hungary.
Lajos István NagyPetra Talapka, Alexandra Pál, Marietta Zita Poles, Anikó Berkó, Mária Bagyánszki, Éva Fekete, Nikolett Bódi, Department of Physiology, Anatomy and Neuroscience, Faculty of Sciences and Informatics, University of Szeged, H-6726 Szeged, Hungary.
Alexandra PálPetra Talapka, Alexandra Pál, Marietta Zita Poles, Anikó Berkó, Mária Bagyánszki, Éva Fekete, Nikolett Bódi, Department of Physiology, Anatomy and Neuroscience, Faculty of Sciences and Informatics, University of Szeged, H-6726 Szeged, Hungary.
Marietta Zita PolesPetra Talapka, Alexandra Pál, Marietta Zita Poles, Anikó Berkó, Mária Bagyánszki, Éva Fekete, Nikolett Bódi, Department of Physiology, Anatomy and Neuroscience, Faculty of Sciences and Informatics, University of Szeged, H-6726 Szeged, Hungary.
Anikó BerkóPetra Talapka, Alexandra Pál, Marietta Zita Poles, Anikó Berkó, Mária Bagyánszki, Éva Fekete, Nikolett Bódi, Department of Physiology, Anatomy and Neuroscience, Faculty of Sciences and Informatics, University of Szeged, H-6726 Szeged, Hungary.
Mária BagyánszkiPetra Talapka, Alexandra Pál, Marietta Zita Poles, Anikó Berkó, Mária Bagyánszki, Éva Fekete, Nikolett Bódi, Department of Physiology, Anatomy and Neuroscience, Faculty of Sciences and Informatics, University of Szeged, H-6726 Szeged, Hungary.
László Géza PuskásPetra Talapka, Alexandra Pál, Marietta Zita Poles, Anikó Berkó, Mária Bagyánszki, Éva Fekete, Nikolett Bódi, Department of Physiology, Anatomy and Neuroscience, Faculty of Sciences and Informatics, University of Szeged, H-6726 Szeged, Hungary.
Éva FeketePetra Talapka, Alexandra Pál, Marietta Zita Poles, Anikó Berkó, Mária Bagyánszki, Éva Fekete, Nikolett Bódi, Department of Physiology, Anatomy and Neuroscience, Faculty of Sciences and Informatics, University of Szeged, H-6726 Szeged, Hungary.
Nikolett BódiPetra Talapka, Alexandra Pál, Marietta Zita Poles, Anikó Berkó, Mária Bagyánszki, Éva Fekete, Nikolett Bódi, Department of Physiology, Anatomy and Neuroscience, Faculty of Sciences and Informatics, University of Szeged, H-6726 Szeged, Hungary.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimTo establish a rat model suitable to investigate the repetitive relapsing inflammations (RRI) characteristic to Crohn's disease.

methodsColitis was induced by 2,4,6-trinitrobenzenesulfonic acid (TNBS). RRI were mimicked by repeating administrations of TNBS. Tissue samples were taken from control, once, twice and three times treated rats from the inflamed and adjacent non-inflamed colonic segments at different timepoints during the acute intestinal inflammation. The means of the ulcerated area were measured to evaluate the macroscopic mucosal damage. The density of myenteric neurons was determined on whole mounts by HuC/HuD immunohistochemistry. Heme oxygenase-1 (HO-1) expression was evaluated by molecular biological techniques.

resultsTNBS-treated rats displayed severe colitis, but the mortality was negligible, and an increase of body weight was characteristic throughout the experimental period. The widespread loss of myenteric neurons, and marked but transient HO-1 up-regulation were demonstrated after the first TNBS administration. After repeated doses the length of the recovery time and extent of the ulcerous colonic segments were markedly decreased, and the neuronal loss was on a smaller scale and was limited to the inflamed area. HO-1 mRNA level was notably greater than after a single dose and overexpression was sustained throughout the timepoints examined. Nevertheless, the HO-1 protein up-regulation after the second TNBS treatment proved to be transient. Following the third treatment HO-1 protein expression could not be detected.

conclusionExperimentally provoked RRI may exert a protective preconditioning effect against the mucosal and neuronal damage. The persistent up-regulation of HO-1 mRNA expression may correlate with this.

Indexed as

AnimalsColitisColonCrohn DiseaseDisease Models, AnimalHeme Oxygenase (Decyclizing)Intestinal MucosaMaleMyenteric PlexusRats, Sprague-DawleyRecurrenceRemission InductionRNA, MessengerTime FactorsTrinitrobenzenesulfonic AcidUp-RegulationHeme Oxygenase (Decyclizing)Hmox1 protein, ratRNA, MessengerTrinitrobenzenesulfonic AcidCrohn’s diseaseExperimental rat modelHeme oxygenase-1Myenteric neuronsRepetitive relapsing inflammation

Identifiers

PMID25469038
PMCPMC4248213

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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.