Evidence map›Paper›PMID 31957804›Full record

ArticleBioscience reports2020

Silencing of PTX3 alleviates LPS-induced inflammatory pain by regulating TLR4/NF-κB signaling pathway in mice.

Shuang Qi, Feng Zhao, Zinan Li, Feng Liang, Shanshan Yu

Open access · goldAbstract read
In one paragraph

Article in Bioscience reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

13 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
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  11. AXL Inhibits Proinflammatory Factors to Relieve Rheumatoid Arthritis Pain by Regulating the TLR4/NF-Evidence-based complementary and alternative medicine : eCAM · 2022
    Article
  12. Article
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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

5 authors at 1 institution in 1 country.

Shuang QiDepartment of Anesthesiology, China-Japan Union Hospital of Jilin University, Changchun City, Jilin Province 130033, P.R. China.
Feng ZhaoDepartment of Operating Room, China-Japan Union Hospital of Jilin University, Changchun City, Jilin Province 130033, P.R. China.
Zinan LiDepartment of Anesthesiology, China-Japan Union Hospital of Jilin University, Changchun City, Jilin Province 130033, P.R. China.
Feng LiangDepartment of Anesthesiology, China-Japan Union Hospital of Jilin University, Changchun City, Jilin Province 130033, P.R. China.
Shanshan YuDepartment of Anesthesiology, China-Japan Union Hospital of Jilin University, Changchun City, Jilin Province 130033, P.R. China.
Jilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pentraxin 3 (PTX3), an inflammatory marker and a pattern recognition receptor, plays an important role in promoting the progress of tumor and inflammatory diseases. However, the role of PTX3 in the pathogenesis of inflammatory pain diseases is rarely reported. The purpose of the present study is to investigate the effect of PTX3 on the progression of inflammatory pain and the special molecular mechanism. A mouse BV2 microglia cell activation-mediated inflammatory model was developed with Lipopolysaccharide (LPS) induction, and a mouse inflammatory pain model was established with LPS injection. The effect of PTX3 on microglia inflammatory activation was verified by measuring pro-inflammatory cytokines expression. The mechanical hyperalgesia testing, the thermal preference testing and the cold allodynia testing were used to measure the response of mice to mechanical pain, heat stimulation and cold stimulation, respectively. The results revealed that the expression of PTX3 was decreased in the LPS-induced inflammatory pain mice model. Silencing of PTX3 down-regulated LPS-induced inflammatory factors, including IL-6, NO and TNF-α, and alleviated LPS-induced inflammatory pain in BV2 cells. In addition, overexpression of TLR4 reversed the inhibitory effect of si-PTX3 on LPS-induced inflammatory response in BV2 cells. What is more, silencing of PTX3 inhibited TLR4/NF-κB signaling pathway. Collectively, it suggests that silencing of PTX3 alleviates LPS-induced inflammatory response of BV2 cells potentially by regulating the TLR4/NF-κB signaling pathway.

Indexed as

Pain ThresholdAnimalsBehavior, AnimalCell LineC-Reactive ProteinCytokinesDisease Models, AnimalHyperalgesiaInflammation MediatorsLipopolysaccharidesMaleMiceMicrogliaNerve Tissue ProteinsNF-kappa BNitric OxideC-Reactive ProteinCytokinesInflammation MediatorsLipopolysaccharidesNerve Tissue ProteinsNF-kappa BNitric OxidePentraxinsTlr4 protein, mouseToll-Like Receptor 4inflammationinflammatory painPTX3TLR4/NF-κB axis

Identifiers

PMID31957804
PMCPMC7000368
OpenAlexW3002805472

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Registered trials

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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.