Far infrared-emitting ceramics decrease Freund's adjuvant-induced inflammatory hyperalgesia in mice through cytokine modulation and activation of peripheral inhibitory neuroreceptors.

Ralph Fernando Rosas; Aline Armiliato Emer; Ana Paula Batisti; Daniela Dero Ludtke; Bruna Lenfers Turnes; Franciane Bobinski; Francisco José Cidral-filho; Daniel Fernandes Martins

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Far infrared-emitting ceramics decrease Freund's adjuvant-induced inflammatory hyperalgesia in mice through cytokine modulation and activation of peripheral inhibitory neuroreceptors.

Author: Ralph Fernando ROSAS ^{1
,

2} ; Aline Armiliato EMER ^{1
,

2} ; Ana Paula BATISTI ^{1
,

2} ; Daniela Dero LUDTKE ^{1
,

2} ; Bruna Lenfers TURNES ^{1
,

3} ; Franciane BOBINSKI ^{1
,

2} ; Francisco José CIDRAL-FILHO ^{1
,

2} ; Daniel Fernandes MARTINS ^{1
,

4}
Author Information

1. Experimental Neuroscience Laboratory (LaNEx), University of Southern Santa Catarina, Palhoça 88137-272, Santa Catarina, Brazil
2. Postgraduate Program in Health Sciences, University of Southern Santa Catarina, Palhoça 88137-272, Santa Catarina, Brazil.
3. Laboratory of Bioenergetics and Oxidative Stress (LABOX), Federal University of Santa Catarina, Florianópolis 88049-000, Santa Catarina, Brazil.
4. Postgraduate Program in Health Sciences, University of Southern Santa Catarina, Palhoça 88137-272, Santa Catarina, Brazil. Electronic address: daniel.martins4@unisul.br.
Publication Type:Journal Article
Keywords: Adenosine; Cannabinoid; Far infrared-emitting ceramics; Inflammatory pain; Integrative therapy; Opioid receptors
From: Journal of Integrative Medicine 2018;16(6):396-403
CountryChina
Language:English
Abstract:
OBJECTIVEThe present study aimed to evaluate the analgesic and anti-inflammatory effects of far infrared-emitting ceramics (cFIRs) in a model of persistent inflammatory hyperalgesia and to elucidate the possible mechanisms of these effects.
METHODSMice were injected with complete Freund's adjuvant (CFA) and treated with cFIRs via placement on a pad impregnated with cFIRs on the bottom of the housing unit for different periods of time. Mice underwent mechanical hyperalgesia and edema assessments, and tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and IL-10 levels were measured. Twenty-four hours after CFA injection and 30 min before cFIR treatment, mice were pretreated with a nonselective adenosinergic antagonist, caffeine, the selective adenosine receptor A antagonist, 1,3-dipropyl-8-cyclopentylxanthine (DPCPX), the selective cannabinoid receptor type 1 antagonist, AM281, the selective cannabinoid receptor type 2 antagonist, AM630, or the nonselective opioid receptor antagonist, naloxone, and mechanical hyperalgesia was assessed.
RESULTScFIRs statistically (P < 0.05) decreased CFA-induced mechanical hyperalgesia ((82.86 ± 5.21)% in control group vs (56.67 ± 9.54)% in cFIR group) and edema ((1699.0 ± 77.8) μm in control group vs (988.7 ± 107.6) μm in cFIR group). cFIRs statistically (P < 0.05) reduced TNF-α ((0.478 ± 0.072) pg/mg of protein in control group vs (0.273 ± 0.055) pg/mg of protein in cFIR group) and IL-1β ((95.81 ± 3.95) pg/mg of protein in control group vs (80.61 ± 4.71) pg/mg of protein in cFIR group) levels and statistically (P < 0.05) increased IL-10 ((18.32 ± 0.78) pg/mg of protein in control group vs (25.89 ± 1.23) pg/mg of protein in cFIR group) levels in post-CFA-injected paws. Peripheral pre-administration of inhibitory neuroreceptor antagonists (caffeine, DPCPX, AM281, AM630 and naloxone) prevented the analgesic effects of cFIRs (P < 0.05).
CONCLUSIONThese data provide additional support for the use of cFIRs in the treatment of painful inflammatory conditions and contribute to our understanding of the neurobiological mechanisms of the therapeutic effects of cFIRs.