Evidence map›Paper›PMID 28300788›Full record

ArticleNutrients2017

Protective Effect of Protocatechuic Acid on TNBS-Induced Colitis in Mice Is Associated with Modulation of the SphK/S1P Signaling Pathway.

Irene Crespo, Beatriz San-Miguel, José Luis Mauriz, Juan José Ortiz de Urbina, Mar Almar, María Jesús Tuñón, Javier González-Gallego

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Nutrients, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

32 citing papers in PubMed, 71 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 1 country.

Irene CrespoInstitute of Biomedicine (IBIOMED), University of León, 24071 León, Spain. icreg@unileon.es.
Beatriz San-MiguelInstitute of Biomedicine (IBIOMED), University of León, 24071 León, Spain. bsanv@unileon.es.
José Luis MaurizInstitute of Biomedicine (IBIOMED), University of León, 24071 León, Spain. jl.mauriz@unileon.es.
Juan José Ortiz de UrbinaPharmacy Service, Complejo Asistencial Universitario de León, 24071 León, Spain. jortiz@saludcastillayleon.es.
Mar AlmarInstitute of Biomedicine (IBIOMED), University of León, 24071 León, Spain. malmg@unileon.es.
María Jesús TuñónInstitute of Biomedicine (IBIOMED), University of León, 24071 León, Spain. mjtung@unileon.es.
Javier González-GallegoInstitute of Biomedicine (IBIOMED), University of León, 24071 León, Spain. jgonga@unileon.es.
Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas · ESUniversidad de León · ESComplejo Asistencial Universitario de Palencia · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

(1) Background: The present study aimed to investigate whether beneficial effects of protocatechuic acid (PCA) are associated with inhibition of the SphK/S1P axis and related signaling pathways in a 2,4,6-trinitrobenzenesulfonic acid (TNBS) model of inflammatory bowel disease; (2) Methods: Colitis was induced in male Balb/c mice by intracolonic administration of 2 mg of TNBS. PCA (30 or 60 mg/kg body wt) was given intraperitoneally daily for five days; (3) Results: Administration of PCA prevented the macroscopic and microscopic damage to the colonic mucosa, the decrease in body weight gain and the increase in myeloperoxidase activity induced by TNBS. PCA-treated mice exhibited a lower oxidized/reduced glutathione ratio, increased expression of antioxidant enzymes and Nrf2 and reduced expression of proinflammatory cytokines. Following TNBS treatment mRNA levels, protein concentration and immunohistochemical labelling for SphK1 increased significantly. S1P production and expression of S1P receptor 1 and S1P phosphatase 2 were significantly elevated. However, there was a decreased expression of S1P lyase. Furthermore, TNBS-treated mice exhibited increased phosphorylation of AKT and ERK, and a higher expression of pSTAT3 and the NF-κB p65 subunit. PCA administration significantly prevented those changes; (4) Conclusions: Data obtained suggest a contribution of the SphK/S1P system and related signaling pathways to the anti-inflammatory effect of PCA.

Indexed as

Signal TransductionAnimalsColitisColonCyclooxygenase 2Disease Models, AnimalDose-Response Relationship, DrugDown-RegulationGlutathioneHydroxybenzoatesInterleukin-1betaIntestinal MucosaMaleMiceMice, Inbred BALB CNF-kappa BCyclooxygenase 2GlutathioneHydroxybenzoatesInterleukin-1betamembrane-bound transcription factor peptidase, site 1NF-kappa BPeroxidasePhosphotransferases (Alcohol Group Acceptor)Proprotein Convertasesprotocatechuic acidPtgs2 protein, mouseSerine EndopeptidasesSphingosine KinaseStat3 protein, mouseSTAT3 Transcription FactorTrinitrobenzenesulfonic AcidTumor Necrosis Factor-alphacolitisinflammationprotocatechuic acidsphingolipidsSphK/S1P signaling

Identifiers

PMID28300788
PMCPMC5372951
OpenAlexW2596638439

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.