Evidence map›Paper›PMID 26310614›Full record

ArticleScientific reports2015

Potential analgesic effects of a novel N-acylethanolamine acid amidase inhibitor F96 through PPAR-α.

Longhe Yang, Long Li, Ling Chen, Yanting Li, Huixia Chen, Yuhang Li, Guangnian Ji, Donghai Lin, Zuguo Liu, Yan Qiu

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
5.9field-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

24 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. LiposomalRSC advances · 2020
    Article
  11. Article
  12. Article
  13. International journal of molecular sciences · 2019
    Article
  14. Article
  15. PPARs and pain.British journal of pharmacology · 2019
    Review
  16. Article
  17. Frontiers in pharmacology · 2019
    Article
  18. Article
  19. Article
  20. Molecular mechanism of activation of the immunoregulatory amidase NAAA.Proceedings of the National Academy of Sciences of the United States of America · 2018
    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

10 authors at 1 institution in 1 country.

Longhe YangMedical College, Xiamen University, Xiamen, Fujian 361005, P. R. China.
Long LiMedical College, Xiamen University, Xiamen, Fujian 361005, P. R. China.
Ling ChenMedical College, Xiamen University, Xiamen, Fujian 361005, P. R. China.
Yanting LiMedical College, Xiamen University, Xiamen, Fujian 361005, P. R. China.
Huixia ChenMedical College, Xiamen University, Xiamen, Fujian 361005, P. R. China.
Yuhang LiMedical College, Xiamen University, Xiamen, Fujian 361005, P. R. China.
Guangnian JiMedical College, Xiamen University, Xiamen, Fujian 361005, P. R. China.
Donghai LinDepartment of Chemistry and The Key Laboratory for Chemical Biology of Fujian Province, College of Chemistry and Chemical Engineering, Xiamen University, Xiamen, Fujian 361005, P. R. China.
Zuguo LiuMedical College, Xiamen University, Xiamen, Fujian 361005, P. R. China.
Yan QiuMedical College, Xiamen University, Xiamen, Fujian 361005, P. R. China.
Xiamen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pharmacological blockade of N-acylethanolamine acid amidase (NAAA) activity is an available approach for inflammation and pain control through restoring the ability of endogenous PEA. But the recently reported NAAA inhibitors suffer from the chemical and biological unstable properties, which restrict functions of NAAA inhibition in vivo. It is still unrevealed whether systematic inhibition of NAAA could modulate PEA-mediated pain signalings. Here we reported an oxazolidinone imide compound 3-(6-phenylhexanoyl) oxazolidin-2-one (F96), which potently and selectively inhibited NAAA activity (IC50 = 270 nM). Intraperitoneal (i.p.) injection of F96 (3-30 mg/kg) dose-dependently reduced ear edema and restored PEA levels of ear tissues in 12-O-Tetradecanoylphorbol-13-acetate (TPA) induced ear edema models. Furthermore, F96 inhibited acetic acid-induced writhing and increased spared nerve injury induced tactile allodynia thresholds in a dose-dependent manner. Pharmacological effects of F96 (10 mg/kg, i.p.) on various animal models were abolished in PPAR-α(-/-) mice, and were prevented by PPAR-α antagonist MK886 but not by canabinoid receptor type 1 (CB1) antagonist Rimonabant nor canabinoid receptor type 2 (CB2) antagonist SR144528. Zebrafish embryos experiments showed better security and lower toxicity for F96 than ibuprofen. These results revealed that F96 might be useful in treating inflammatory and neuropathic pain by NAAA inhibition depending on PPAR-α receptors.

Indexed as

Acetic AcidAmidohydrolasesAnalgesicsAnimalsDisease Models, AnimalEarEdemaEnzyme InhibitorsEthanolaminesFatty AcidsHEK293 CellsHumansMaleMiceMice, Inbred C57BLNeuralgia3-(6-phenylhexanoyl)oxazolidin-2-oneAcetic AcidamidaseAmidohydrolasesAnalgesicsEnzyme InhibitorsEthanolaminesFatty AcidsN-acylethanolaminesOxazolidinonesPPAR alpha

Identifiers

PMID26310614
PMCPMC4550851
OpenAlexW2405727557

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.