Evidence map›Paper›PMID 25855977›Full record

ArticlePloS one2015

Novel epigallocatechin-3-gallate (EGCG) derivative as a new therapeutic strategy for reducing neuropathic pain after chronic constriction nerve injury in mice.

Xavier Xifró, Laura Vidal-Sancho, Pere Boadas-Vaello, Carlos Turrado, Jordi Alberch, Teresa Puig, Enrique Verdú

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

20 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Flavonoids in the Treatment of Neuropathic Pain.Current pain and headache reports · 2021
    Review
  9. Review
  10. Review
  11. Review
  12. Antioxidant and Cytoprotective Effects of (-)-Epigallocatechin-3-(3″-International journal of molecular sciences · 2019
    Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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

7 authors at 2 institutions in 1 country.

Xavier XifróGrupo de Investigación de Anatomía Clínica, Embriología, Neurociencia y Oncología Molecular (NEOMA), Departamento de Ciencias Médicas, Facultad de Medicina, Universitat de Girona (UdG), Girona, Spain; Departament de Biologia Cel·lular, Immunologia i Neurociències, Facultat de Medicina, Universitat de Barcelona, Barcelona, Spain; Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, Spain; Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Madrid, Spain.
Laura Vidal-SanchoGrupo de Investigación de Anatomía Clínica, Embriología, Neurociencia y Oncología Molecular (NEOMA), Departamento de Ciencias Médicas, Facultad de Medicina, Universitat de Girona (UdG), Girona, Spain; Departament de Biologia Cel·lular, Immunologia i Neurociències, Facultat de Medicina, Universitat de Barcelona, Barcelona, Spain; Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, Spain; Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Madrid, Spain.
Pere Boadas-VaelloGrupo de Investigación de Anatomía Clínica, Embriología, Neurociencia y Oncología Molecular (NEOMA), Departamento de Ciencias Médicas, Facultad de Medicina, Universitat de Girona (UdG), Girona, Spain.
Carlos TurradoLaboratorio de Química Médica, Departamento de Química Orgánica I, Facultad de Ciencias Químicas, Universidad Complutense de Madrid (UCM), Madrid, Spain.
Jordi AlberchDepartament de Biologia Cel·lular, Immunologia i Neurociències, Facultat de Medicina, Universitat de Barcelona, Barcelona, Spain; Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, Spain; Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Madrid, Spain.
Teresa PuigGrupo de Investigación de Anatomía Clínica, Embriología, Neurociencia y Oncología Molecular (NEOMA), Departamento de Ciencias Médicas, Facultad de Medicina, Universitat de Girona (UdG), Girona, Spain.
Enrique VerdúGrupo de Investigación de Anatomía Clínica, Embriología, Neurociencia y Oncología Molecular (NEOMA), Departamento de Ciencias Médicas, Facultad de Medicina, Universitat de Girona (UdG), Girona, Spain.
University of Girona · ESUniversidad Complutense de Madrid · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuropathic pain is common in peripheral nerve injury and often fails to respond to ordinary medication. Here, we investigated whether the two novel epigallocatechin-3-gallate (EGCG) polyphenolic derivatives, compound 23 and 30, reduce the neuropathic pain in mice chronic constriction nerve injury (CCI). First, we performed a dose-response study to evaluate nociceptive sensation after administration of EGCG and its derivatives 23 and 30, using the Hargreaves test at 7 and 21 days after injury (dpi). We daily administered EGCG, 23 and 30 (10 to 100 mg/Kg; i.p.) during the first week post-CCI. None of the doses of compound 23 caused significant pain diminution, whereas 50mg/kg was optimal for both EGCG and 30 to delay the latency of paw withdrawal. With 50 mg/Kg, we showed that EGCC prevented the thermal hyperalgesia from 7 to 21 dpi and compound 30 from 14 to 56 dpi. To evaluate the molecular mechanisms underpinning why EGCG and compound 30 differentially prevented the thermal hyperalgesia, we studied several biochemical parameters in the dorsal horn of the spinal cord at 14 and 56 dpi. We showed that the effect observed with EGCG and compound 30 was related to the inhibition of fatty acid synthase (FASN), a known target of these polyphenolic compounds. Additionally, we observed that EGCG and compound 30 reduced the expression of CCI-mediated inflammatory proteins and the nuclear localization of nuclear factor-kappa B at 14 dpi, but not at 56 dpi. We also strongly detected a decrease of synaptic plasma membrane levels of N-methyl-D-asparte receptor 2B in CCI-mice treated with compound 30 at 56 dpi. Altogether, compound 30 reduced the chronic thermal hyperalgesia induced by CCI better than the natural compound EGCG. Thus, our findings provide a rationale for the preclinical development of compound 30 as an agent to treat neuropathic pain.

Indexed as

AnimalsCatechinCell MembraneCytokinesFatty AcidsFatty Acid Synthase, Type IGene Expression RegulationHyperalgesiaMaleMiceNeuralgiaPainPain ThresholdPeripheral Nerve InjuriesSpinal Cord InjuriesCatechinCytokinesepigallocatechin gallateFatty AcidsFatty Acid Synthase, Type I

Identifiers

PMID25855977
PMCPMC4391943
OpenAlexW2044311891

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.