Evidence map›Paper›PMID 32410045›Full record

ArticleNeurochemical research2020

A Novel Mechanism of Specialized Proresolving Lipid Mediators Mitigating Radicular Pain: The Negative Interaction with NLRP3 Inflammasome.

Yi-Hao Wang, Yan Li, Jun-Nan Wang, Qing-Xiang Zhao, Shuang Wen, Si-Cong Wang, Tao Sun

Abstract read
PubMed Publisher
In one paragraph

Article in Neurochemical research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 2 pooled it
1.5field-weighted citation impact, top 18% 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

18 citing papers in PubMed, 2 syntheses or guidelines pooled it, 20 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. The research progress and potential applications ofThe British journal of nutrition · 2025
    Review
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  7. Article
  8. Article
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  12. Maresin-1 and Inflammatory Disease.International journal of molecular sciences · 2022
    Review
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  15. Review
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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 3 institutions in 1 country.

Yi-Hao WangDepartment of Pain Management, Shandong Provincial Hospital Affiliated to Shandong University, Shandong University, 324 Jingwu Road, Jinan, 250021, Shandong, China.
Yan LiDepartment of Obstetrics and Gynecology, The Affiliated Hospital of Qingdao University, Qingdao, 266003, Shandong, China.
Jun-Nan WangDepartment of Pain Management, Shandong Provincial Hospital Affiliated to Shandong University, Shandong University, 324 Jingwu Road, Jinan, 250021, Shandong, China.
Qing-Xiang ZhaoDepartment of Pain Management, Shandong Provincial Hospital Affiliated to Shandong University, Shandong University, 324 Jingwu Road, Jinan, 250021, Shandong, China.
Shuang WenDepartment of Pain Management, Shandong Provincial Hospital Affiliated to Shandong University, Shandong University, 324 Jingwu Road, Jinan, 250021, Shandong, China.
Si-Cong WangDepartment of Pain Management, Shandong Provincial Hospital Affiliated to Shandong University, Shandong University, 324 Jingwu Road, Jinan, 250021, Shandong, China.
Tao SunDepartment of Pain Management, Shandong Provincial Hospital Affiliated to Shandong University, Shandong University, 324 Jingwu Road, Jinan, 250021, Shandong, China. suntaosdph@163.com.
Shandong Provincial Hospital · CNShandong University · CNQingdao University · CN

Funding

National Natural Science Foundation of China 81772443, 81972145
6 · The paper itself

Abstract

Inhibition of immune and inflammatory reaction induced by the expose of nucleus pulposus (NP) could effectively ameliorate neuropathic pain in the lumbar disc herniation. Maresin1 (MaR1), as a macrophage-derived mediator of inflammation resolution, displayed potent anti-inflammatory action. In the present study, we attempted to elucidate the impact of MaR1 on radicular pain and the interaction with NLRP3 inflammasome. We established a rat model of non-compressive lumbar disc herniation and different administration (MaR1 or Caspase-1 inhibitor) was given to them. The paw withdrawal latency (PWL) and paw withdrawal thresholds (PWTs) were observed to assess pain behaviors. The spinal cord horns were collected and the levels of IL-1β and IL-18 were measured by ELISA. The mRNA and protein expression levels of NLRP3 inflammasome components were tested by RT-PCR, western blot and immunohistochemistry. The endogenous MaR1 levels of the spinal cord were analyzed using LC-MS/MS. The application of NP in the models lead to mechanical and thermal hypersensitivity, increased IL-1β and IL-18 levels and expressions of NLRP3 inflammasome components, which were reversed markedly by administration of MaR1. Caspase-1 inhibition also improved mechanical hypersensitivity, decreased the expressions of inflammatory cytokines and restrained the activation of inflammasome. Meanwhile, Caspase-1 inhibitor promoted the endogenous MaR1 synthesis, which was hindered in the pain models. Altogether, our study indicated that the negative interaction between MaR1 and NLRP3 inflammasome mediated the inflammatory response in spinal dorsal horn, which involved in the pathogenesis of radicular pain.

Indexed as

AnalgesicsAnimalsAnti-Inflammatory AgentsCaspase 1Caspase InhibitorsDipeptidesDocosahexaenoic AcidsInflammasomesInflammationIntervertebral Disc DisplacementLow Back PainLumbar VertebraeMaleNeuralgiaNLR Family, Pyrin Domain-Containing 3 Proteinpara-Aminobenzoates7,14-dihydroxydocosa-4,8,10,12,16,19-hexaenoic acidAnalgesicsAnti-Inflammatory AgentsbelnacasanCaspase 1Caspase InhibitorsDipeptidesDocosahexaenoic AcidsInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, ratpara-AminobenzoatesCaspase-1 inhibitorEndogenous biosynthesisMaresin 1 (MaR1)NLRP3 inflammasomeRadicular pain

Identifiers

PMID32410045
OpenAlexW3024755462

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.