CoChat
Sign Up
Cited by 288Pain Mechanisms and TreatmentsCannabis and Cannabinoid ResearchIon Channels and Receptors

The DOI matches its Crossref record; 67 of the 70 references it cites were found in a registry or an index.

The endogenous fatty acid amide, palmitoylethanolamide, has anti-allodynic and anti-hyperalgesic effects in a murine model of neuropathic pain: involvement of CB1, TRPV1 and PPARγ receptors and neurotrophic factors

Costa, Barbara, Comelli, Francesca, Bettoni, Isabella, Colleoni, Mariapia, Giagnoni, Gabriella·2008·Pain
DOI 10.1016/j.pain.2008.06.003
Open this paper in CoChat — free account

Abstract

Palmitoylethanolamide (PEA) is an endogenous lipid that is thought to be involved in endogenous protective mechanisms activated as a result of stimulation of inflammatory response. In spite of the well demonstrated anti-inflammatory properties of PEA, its involvement in controlling pain pathways still remains poorly characterized. On this basis, we tested the efficacy of PEA in vivo against a peculiar persistent pain, such as neuropathic one. PEA was administered i.p. to mice with chronic constriction injury of sciatic nerve (CCI) once a day for one week starting the day after the lesion. This therapeutic regimen evoked a relief of both thermal hyperalgesia and mechanical allodynia in neuropathic mice. Various selective receptor antagonists were used in order to clarify the relative contribution of cannabinoid, vanilloid and peroxisome proliferator-activated receptor to PEA-induced effects. The results indicated that CB(1), PPARgamma and TRPV1 receptors mediated the antinociception induced by PEA, suggesting that the most likely mechanism might be the so-called "entourage effect" due to the PEA-induced inhibition of the enzyme catalyzing the endocannabinoid anandamide (AEA) degradation that leads to an enhancement of its tissue levels thus increasing its analgesic action. In addition, the hypothesis that PEA might act through the modulation of local mast cells degranulation is sustained by our findings showing that PEA significantly reduced the production of many mediators such as TNFalpha and neurotrophic factors, like NGF. The findings presented here, in addition to prove the beneficial effects of PEA in chronic pain, identify new potential targets for analgesic medicine.

Overview

Integrity signals

Registry

Crossref · 10.1016/j.pain.2008.06.003

Cites

67 of 67 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Verification

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Citations

Cites

Flagged first, then by citations

3 of the 70 references couldn’t be matched to a known paper.

Research works printed but not linked: 1

  1. Jack, 1996, Aliamides: a new approach to the treatment of inflammation., Drug News Perspectives, 9, 93

Cited by

Sorted by citations

See all 288

Related

See all

Metadata

Authors
Costa, B., Comelli, F., Bettoni, I., Colleoni, M., & Giagnoni, G.
Affiliations
  • University of Milano-Bicocca (IT)
  • University of Milan (IT)
Corresponding author
Costa, Barbara
ORCID
Costa, Barbara
Venue
Pain
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
2008-10-31
Volume
139
Issue
3
Pages
541-550
ISSN
0304-3959 (ISSN-L)
DOI
10.1016/j.pain.2008.06.003
OpenAlex
W2162105352
Cited by
286
References
70
Citations by year
2026: 5 · 2025: 6 · 2024: 11 · 2023: 11 · 2022: 15 · 2021: 20 · 2020: 17 · 2019: 17 · 2018: 20 · 2017: 18 · 2016: 18 · 2015: 19 · 2014: 22 · 2013: 23 · 2012: 19
FWCI
10.41
Type
journal article
Language
en
Open access
closed
Locations
  • Pain (publishedVersion)
  • PubMed (publishedVersion)
  • BOA (University of Milano-Bicocca) (submittedVersion)
Topics
  • Health Sciences › Medicine › Physiology (medical) › Pain Mechanisms and Treatments
  • Health Sciences › Medicine › Pharmacology (medical) › Cannabis and Cannabinoid Research
  • Life Sciences › Neuroscience › Sensory Systems › Ion Channels and Receptors
Keywords
palmitoylethanolamide, neuropathic pain, chronic constriction injury, thermal hyperalgesia, mechanical allodynia, CB1 receptor, TRPV1 receptor, PPARγ, entourage effect, mast cell degranulation, TNF-α, nerve growth factor, neurotrophic factors, analgesic mechanism
MeSH terms
Amides, Animals, Cytoplasmic Granules, Drug Evaluation, Preclinical, Ethanolamines, Hot Temperature, Hyperalgesia, Ligation, Mast Cells, Nerve Growth Factors, Palmitic Acids, Physical Stimulation, Sciatic Nerve, Sciatica, Spinal Cord, Touch, Tumor Necrosis Factor-alpha, NF-kappa B, Analgesics, Non-Narcotic, Receptor, Cannabinoid, CB1, PPAR alpha, PPAR gamma, TRPV Cation Channels, Mice, Endocannabinoids

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review