Evidence map›Paper›PMID 28928655›Full record

ArticleFrontiers in pharmacology2017

Effects of Simvastatin Beyond Dyslipidemia: Exploring Its Antinociceptive Action in an Animal Model of Complex Regional Pain Syndrome-Type I.

Graziela Vieira, Juliana Cavalli, Elaine C D Gonçalves, Tainara R Gonçalves, Larissa R Laurindo, Maíra Cola, Rafael C Dutra

Open access · goldAbstract read
In one paragraph

Article in Frontiers in pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.8field-weighted citation impact, top 27% 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

11 citing papers in PubMed, 16 citations in OpenAlex.

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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 1 institution in 1 country.

Graziela VieiraLaboratory of Autoimmunity and Immunopharmacology (LAIF), Department of Health Sciences, Center of Araranguá, Federal University of Santa CatarinaAraranguá, Brazil.
Juliana CavalliLaboratory of Autoimmunity and Immunopharmacology (LAIF), Department of Health Sciences, Center of Araranguá, Federal University of Santa CatarinaAraranguá, Brazil.
Elaine C D GonçalvesLaboratory of Autoimmunity and Immunopharmacology (LAIF), Department of Health Sciences, Center of Araranguá, Federal University of Santa CatarinaAraranguá, Brazil.
Tainara R GonçalvesLaboratory of Autoimmunity and Immunopharmacology (LAIF), Department of Health Sciences, Center of Araranguá, Federal University of Santa CatarinaAraranguá, Brazil.
Larissa R LaurindoLaboratory of Autoimmunity and Immunopharmacology (LAIF), Department of Health Sciences, Center of Araranguá, Federal University of Santa CatarinaAraranguá, Brazil.
Maíra ColaLaboratory of Autoimmunity and Immunopharmacology (LAIF), Department of Health Sciences, Center of Araranguá, Federal University of Santa CatarinaAraranguá, Brazil.
Rafael C DutraLaboratory of Autoimmunity and Immunopharmacology (LAIF), Department of Health Sciences, Center of Araranguá, Federal University of Santa CatarinaAraranguá, Brazil.
Universidade Federal de Santa Catarina · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Simvastatin is a lipid-lowering agent that blocks the production of cholesterol through inhibition of 3-hydroxy-methyl-glutaryl coenzyme A (HMG-CoA) reductase. In addition, recent evidence has suggested its anti-inflammatory and antinociceptive actions during inflammatory and pain disorders. Herein, we investigated the effects of simvastatin in an animal model of complex regional pain syndrome-type I, and its underlying mechanisms. Chronic post-ischemia pain (CPIP) was induced by ischemia and reperfusion (IR) injury of the left hind paw. Our findings showed that simvastatin inhibited mechanical hyperalgesia induced by CPIP model in single and repeated treatment schedules, respectively; however simvastatin did not alter inflammatory signs during CPIP model. The mechanisms underlying those actions are related to modulation of transient receptor potential (TRP) channels, especially TRMP8. Moreover, simvastatin oral treatment was able to reduce the nociception induced by acidified saline [an acid-sensing ion channels (ASICs) activator] and bradykinin (BK) stimulus, but not by TRPA1, TRPV1 or prostaglandin-E2 (PGE2). Relevantly, the antinociceptive effects of simvastatin did not seem to be associated with modulation of the descending pain circuits, especially noradrenergic, serotoninergic and dopaminergic systems. These results indicate that simvastatin consistently inhibits mechanical hyperalgesia during neuropathic and inflammatory disorders, possibly by modulating the ascending pain signaling (TRPM8/ASIC/BK pathways expressed in the primary sensory neuron). Thus, simvastatin open-up new standpoint in the development of innovative analgesic drugs for treatment of persistent pain, including CRPS-I.

Indexed as

inflammatory painischemia-reperfusionneuropathic painsimvastatinTRPM8 channel

Identifiers

PMID28928655
PMCPMC5591456
OpenAlexW2751573048

What OpenQuestion holds

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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.