Evidence map›Paper›PMID 20193086›Full record

ArticleMolecular pain2010

Nitric oxide synthase modulates CFA-induced thermal hyperalgesia through cytokine regulation in mice.

Yong Chen, Michael K Boettger, Andreas Reif, Angelika Schmitt, Nurcan Uçeyler, Claudia Sommer

Open access · goldAbstract read
In one paragraph

Article in Molecular pain, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
5.0field-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

38 citing papers in PubMed, 91 citations in OpenAlex.

  1. Article
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  18. Effects of chronic nitric oxide synthase inhibition on V'ONaunyn-Schmiedeberg's archives of pharmacology · 2017
    Article
  19. Article
  20. The role of nitric oxide on the oxytocin induce analgesia in mice.Iranian journal of basic medical sciences · 2016
    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

6 authors at 1 institution in 1 country.

Yong ChenDepartment of Neurology, University of Würzburg, Josef-Schneider-Str 11, 97080 Würzburg, Germany. Chen_Y@klinik.uni-wuerzburg.de
Michael K Boettger
Andreas Reif
Angelika Schmitt
Nurcan Uçeyler
Claudia Sommer
University of Würzburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAlthough it has been largely demonstrated that nitric oxide synthase (NOS), a key enzyme for nitric oxide (NO) production, modulates inflammatory pain, the molecular mechanisms underlying these effects remain to be clarified. Here we asked whether cytokines, which have well-described roles in inflammatory pain, are downstream targets of NO in inflammatory pain and which of the isoforms of NOS are involved in this process.

resultsIntraperitoneal (i.p.) pretreatment with 7-nitroindazole sodium salt (7-NINA, a selective neuronal NOS inhibitor), aminoguanidine hydrochloride (AG, a selective inducible NOS inhibitor), L-N(G)-nitroarginine methyl ester (L-NAME, a non-selective NOS inhibitor), but not L-N(5)-(1-iminoethyl)-ornithine (L-NIO, a selective endothelial NOS inhibitor), significantly attenuated thermal hyperalgesia induced by intraplantar (i.pl.) injection of complete Freund's adjuvant (CFA). Real-time reverse transcription-polymerase chain reaction (RT-PCR) revealed a significant increase of nNOS, iNOS, and eNOS gene expression, as well as tumor necrosis factor-alpha (TNF), interleukin-1 beta (IL-1beta), and interleukin-10 (IL-10) gene expression in plantar skin, following CFA. Pretreatment with the NOS inhibitors prevented the CFA-induced increase of the pro-inflammatory cytokines TNF and IL-1beta. The increase of the anti-inflammatory cytokine IL-10 was augmented in mice pretreated with 7-NINA or L-NAME, but reduced in mice receiving AG or L-NIO. NNOS-, iNOS- or eNOS-knockout (KO) mice had lower gene expression of TNF, IL-1beta, and IL-10 following CFA, overall corroborating the inhibitor data.

conclusionThese findings lead us to propose that inhibition of NOS modulates inflammatory thermal hyperalgesia by regulating cytokine expression.

Indexed as

AnimalsCytokinesDisease Models, AnimalEnzyme InhibitorsFreund's AdjuvantGene Expression Regulation, EnzymologicHyperalgesiaInflammation MediatorsInterleukin-10Interleukin-1betaIsoenzymesMaleMiceMice, Inbred C57BLMice, KnockoutNG-Nitroarginine Methyl EsterCytokinesEnzyme InhibitorsFreund's AdjuvantInflammation MediatorsInterleukin-10Interleukin-1betaIsoenzymesNG-Nitroarginine Methyl EsterNitric OxideNitric Oxide SynthaseNitric Oxide Synthase Type INitric Oxide Synthase Type IINitric Oxide Synthase Type IIINos1 protein, mouseNos2 protein, mouseNos3 protein, mouseRNA, MessengerTumor Necrosis Factor-alpha

Identifiers

PMID20193086
PMCPMC2838835
OpenAlexW2160571965

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LicenceCC BY
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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.