Evidence map›Paper›PMID 25205418›Full record

ArticleBritish journal of pharmacology2015

Palmitoylethanolamide, a naturally occurring lipid, is an orally effective intestinal anti-inflammatory agent.

Francesca Borrelli, Barbara Romano, Stefania Petrosino, Ester Pagano, Raffaele Capasso, Diana Coppola, Giovanni Battista, Pierangelo Orlando, Vincenzo Di Marzo, Angelo A Izzo

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
106citing papers in PubMed, 2 pooled it
9.8field-weighted citation impact, top 2% 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

106 citing papers in PubMed, 2 syntheses or guidelines pooled it, 173 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Periodontitis Salivary Microbiota Exacerbates Murine Rheumatoid Arthritis via Gut Dysbiosis and Immune Dysregulation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Review

46 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

10 authors at 4 institutions in 1 country.

Francesca BorrelliDepartment of Pharmacy, University of Naples Federico II, Naples, Italy.
Barbara Romano
Stefania Petrosino
Ester Pagano
Raffaele Capasso
Diana Coppola
Giovanni Battista
Pierangelo Orlando
Vincenzo Di Marzo
Angelo A Izzo
University of Naples Federico II · ITNational Research Council · ITOspedale dei Pellegrini · ITInstitute of Protein Biochemistry · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposePalmitoylethanolamide (PEA) acts via several targets, including cannabinoid CB1 and CB2 receptors, transient receptor potential vanilloid type-1 (TRPV1) ion channels, peroxisome proliferator-activated receptor alpha (PPAR α) and orphan G protein-coupled receptor 55 (GRR55), all involved in the control of intestinal inflammation. Here, we investigated the effect of PEA in a murine model of colitis. EXPERIMENTAL APPROACH: Colitis was induced in mice by intracolonic administration of dinitrobenzenesulfonic acid (DNBS). Inflammation was assessed by evaluating inflammatory markers/parameters and by histology; intestinal permeability by a fluorescent method; colonic cell proliferation by immunohistochemistry; PEA and endocannabinoid levels by liquid chromatography mass spectrometry; receptor and enzyme mRNA expression by quantitative RT-PCR. KEY

resultsDNBS administration caused inflammatory damage, increased colonic levels of PEA and endocannabinoids, down-regulation of mRNA for TRPV1 and GPR55 but no changes in mRNA for CB1 , CB2 and PPARα. Exogenous PEA (i.p. and/or p.o., 1 mg·kg(-1) ) attenuated inflammation and intestinal permeability, stimulated colonic cell proliferation, and increased colonic TRPV1 and CB1 receptor expression. The anti-inflammatory effect of PEA was attenuated or abolished by CB2 receptor, GPR55 or PPARα antagonists and further increased by the TRPV1 antagonist capsazepine. CONCLUSIONS AND IMPLICATIONS: PEA improves murine experimental colitis, the effect being mediated by CB2 receptors, GPR55 and PPARα, and modulated by TRPV1 channels.

Indexed as

Administration, OralAmidesAnimalsAnti-Inflammatory AgentsBenzenesulfonatesCapsaicinColitisColonDisease Models, AnimalEndocannabinoidsEthanolaminesIntestinal AbsorptionMaleMice, Inbred ICROleic AcidsPalmitic AcidsAmidesAnti-Inflammatory AgentsBenzenesulfonatesCapsaicincapsazepinedinitrobenzenesulfonic acidEndocannabinoidsEthanolaminesGPR55 protein, mouseOleic AcidsOleylethanolamidepalmidrolPalmitic AcidsPeroxidasePPAR alphaReceptor, Cannabinoid, CB1Receptor, Cannabinoid, CB2Receptors, CannabinoidRNA, MessengerTRPV1 protein, mouseTRPV Cation Channels

Identifiers

PMID25205418
PMCPMC4280974
OpenAlexW1531212045

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.