Evidence map›Paper›PMID 21356367›Full record

ArticleThe American journal of pathology2011

β-Caryophyllene inhibits dextran sulfate sodium-induced colitis in mice through CB2 receptor activation and PPARγ pathway.

Allisson Freire Bento, Rodrigo Marcon, Rafael Cypriano Dutra, Rafaela Franco Claudino, Maíra Cola, Daniela Ferraz Pereira Leite, João B Calixto

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
107citing papers in PubMed, 1 pooled it
5.4field-weighted citation impact, top 4% 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

107 citing papers in PubMed, 1 synthesis or guideline pooled it, 226 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review

47 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

7 authors at 1 institution in 1 country.

Allisson Freire BentoDepartment of Pharmacology, Biological Sciences Center, Federal University of Santa Catarina Florianópolis, Santa Catarina, Brazil.
Rodrigo Marcon
Rafael Cypriano Dutra
Rafaela Franco Claudino
Maíra Cola
Daniela Ferraz Pereira Leite
João B Calixto
Universidade Federal de Santa Catarina · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cannabinoid receptor 2 (CB2) activation is suggested to trigger the peroxisome proliferator-activated receptor-γ (PPARγ) pathway, and agonists of both receptors improve colitis. Recently, the plant metabolite (E)-β-caryophyllene (BCP) was shown to bind to and activate CB2. In this study, we examined the anti-inflammatory effect of BCP in dextran sulfate sodium (DSS)-induced colitis and analyzed whether this effect was mediated by CB2 and PPARγ. Oral treatment with BCP reduced disease activity, colonic macro- and microscopic damage, myeloperoxidase and N-acetylglucosaminidase activities, and levels and mRNA expression of colonic tumor necrosis factor-α, IL-1β, interferon-γ, and keratinocyte-derived chemokine. BCP treatment also inhibited the activation of extracellular signal-regulated kinase 1/2, nuclear factor κB, IκB-kinase α/β, cAMP response element binding and the expression of caspase-3 and Ki-67. Moreover, BCP enhanced IL-4 levels and forkhead box P3 mRNA expression in the mouse colon and reduced cytokine levels (tumor necrosis factor-α, keratinocyte-derived chemokine, and macrophage-inflammatory protein-2) in a culture of macrophages stimulated with lipopolysaccharide. The use of the CB2 antagonist AM630 or the PPARγ antagonist GW9662 significantly reversed the protective effect of BCP. Confirming our results, AM630 reversed the beneficial effect of BCP on pro-inflammatory cytokine expression in IEC-6 cells. These results demonstrate that the anti-inflammatory effect of BCP involves CB2 and the PPARγ pathway and suggest BCP as a possible therapy for the treatment of inflammatory bowel disease.

Indexed as

AnimalsCaspase 3Caspase InhibitorsClaudin-4ColitisColonCyclic AMP Response Element-Binding ProteinCytokinesDextran SulfateExtracellular Signal-Regulated MAP KinasesI-kappa B KinaseInflammation MediatorsKi-67 AntigenLipopolysaccharidesMacrophage ActivationMacrophagescaryophylleneCaspase 3Caspase InhibitorsClaudin-4Cldn4 protein, mouseCreb1 protein, mouseCyclic AMP Response Element-Binding ProteinCytokinesDextran SulfateExtracellular Signal-Regulated MAP KinasesI-kappa B KinaseInflammation MediatorsKi-67 AntigenLipopolysaccharidesMembrane ProteinsNF-kappa BOxazolonePolycyclic SesquiterpenesPPAR gammaReceptor, Cannabinoid, CB2Sesquiterpenes

Identifiers

PMID21356367
PMCPMC3070571
OpenAlexW1977127420

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.