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Effects of Pulsed Radiofrequency on a Standard Model of Muscle Injury in Rats

BACKGROUND: Pulsed radiofrequency (PRF) affects animal and plant tissues; however, the mechanism has not been defined. We hypothesized that the magnetic field produced by PRF exerts its effects by the magnetic sensitivity of transitions between spin states -a spin-correlated radical-pair mechanism (...

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Autores principales: Brasil, Luis Josino, Marroni, Norma, Schemitt, Elizângela, Colares, Josieli
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Kowsar 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7144246/
https://www.ncbi.nlm.nih.gov/pubmed/32309197
http://dx.doi.org/10.5812/aapm.97372
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author Brasil, Luis Josino
Marroni, Norma
Schemitt, Elizângela
Colares, Josieli
author_facet Brasil, Luis Josino
Marroni, Norma
Schemitt, Elizângela
Colares, Josieli
author_sort Brasil, Luis Josino
collection PubMed
description BACKGROUND: Pulsed radiofrequency (PRF) affects animal and plant tissues; however, the mechanism has not been defined. We hypothesized that the magnetic field produced by PRF exerts its effects by the magnetic sensitivity of transitions between spin states -a spin-correlated radical-pair mechanism (SCRPM)- which, in turn, affects the rates of chemical reactions with participation of paramagnetic species. OBJECTIVES: This study aimed to evaluate the effects of PRF on redox equilibrium and inflammatory status in a standard model of muscle injury in rats. METHODS: Twenty-four animals were subjected to a single impact trauma to the left quadriceps and the groups exposed and not exposed to PRF were compared. On day 7 of the experiment, the animals were killed and the quadriceps muscles were removed for analysis. RESULTS: There was a significant increase in the concentration of thiobarbituric acid reactive substances (TBARS) in the muscle of animals from the trauma group (+233%), and this increase was eliminated by PRF administration. Superoxide dismutase (SOD) activity was increased (+411%) by trauma, resulting in significantly higher consumption of catalase (-72%), while PRF administration brought both of these markers back to levels close to those of the control group. Trauma induced considerable production of interleukins TNF-α, IL-1β, and IL-6 (+215%, +262%, and +326% vs. controls, respectively) and these effects were also significantly reduced by PRF administration. CONCLUSIONS: In total, PRF inhibits oxidative stress and restores antioxidant enzymes to control levels and may block production of inflammatory markers in muscles of animals subjected to trauma. By modulating redox equilibrium, PRF treatment might block production of noxious mediators involved in development of trauma-induced injury.
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spelling pubmed-71442462020-04-17 Effects of Pulsed Radiofrequency on a Standard Model of Muscle Injury in Rats Brasil, Luis Josino Marroni, Norma Schemitt, Elizângela Colares, Josieli Anesth Pain Med Research Article BACKGROUND: Pulsed radiofrequency (PRF) affects animal and plant tissues; however, the mechanism has not been defined. We hypothesized that the magnetic field produced by PRF exerts its effects by the magnetic sensitivity of transitions between spin states -a spin-correlated radical-pair mechanism (SCRPM)- which, in turn, affects the rates of chemical reactions with participation of paramagnetic species. OBJECTIVES: This study aimed to evaluate the effects of PRF on redox equilibrium and inflammatory status in a standard model of muscle injury in rats. METHODS: Twenty-four animals were subjected to a single impact trauma to the left quadriceps and the groups exposed and not exposed to PRF were compared. On day 7 of the experiment, the animals were killed and the quadriceps muscles were removed for analysis. RESULTS: There was a significant increase in the concentration of thiobarbituric acid reactive substances (TBARS) in the muscle of animals from the trauma group (+233%), and this increase was eliminated by PRF administration. Superoxide dismutase (SOD) activity was increased (+411%) by trauma, resulting in significantly higher consumption of catalase (-72%), while PRF administration brought both of these markers back to levels close to those of the control group. Trauma induced considerable production of interleukins TNF-α, IL-1β, and IL-6 (+215%, +262%, and +326% vs. controls, respectively) and these effects were also significantly reduced by PRF administration. CONCLUSIONS: In total, PRF inhibits oxidative stress and restores antioxidant enzymes to control levels and may block production of inflammatory markers in muscles of animals subjected to trauma. By modulating redox equilibrium, PRF treatment might block production of noxious mediators involved in development of trauma-induced injury. Kowsar 2020-02-04 /pmc/articles/PMC7144246/ /pubmed/32309197 http://dx.doi.org/10.5812/aapm.97372 Text en Copyright © 2020, Author(s) http://creativecommons.org/licenses/by-nc/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 International License (http://creativecommons.org/licenses/by-nc/4.0/) which permits copy and redistribute the material just in noncommercial usages, provided the original work is properly cited.
spellingShingle Research Article
Brasil, Luis Josino
Marroni, Norma
Schemitt, Elizângela
Colares, Josieli
Effects of Pulsed Radiofrequency on a Standard Model of Muscle Injury in Rats
title Effects of Pulsed Radiofrequency on a Standard Model of Muscle Injury in Rats
title_full Effects of Pulsed Radiofrequency on a Standard Model of Muscle Injury in Rats
title_fullStr Effects of Pulsed Radiofrequency on a Standard Model of Muscle Injury in Rats
title_full_unstemmed Effects of Pulsed Radiofrequency on a Standard Model of Muscle Injury in Rats
title_short Effects of Pulsed Radiofrequency on a Standard Model of Muscle Injury in Rats
title_sort effects of pulsed radiofrequency on a standard model of muscle injury in rats
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7144246/
https://www.ncbi.nlm.nih.gov/pubmed/32309197
http://dx.doi.org/10.5812/aapm.97372
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