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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| http://dx.doi.org/10.5812/aapm.97372 | DOI Listing |
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