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

作     者：Ralph Fernando Rosas Aline Armiliato Emer Ana Paula Batisti Daniela Dero Ludtke Bruna Lenfers Turnes Franciane Bobinski Francisco Jose Cidral-Filho daniel fernandes martins 

作者机构：Experimental Neuroscience Laboratory(LaNEx)University of Southern Santa CatarinaPalhoca 88137-272Santa CatarinaBrazil Postgraduate Program in Health SciencesUniversity of Southern Santa CatarinaPalhoca 88137-272Santa CatarinaBrazil Laboratory of Bioenergetics and Oxidative Stress(LABOX)Federal University of Santa CatarinaFlorianopolis 88049-000Santa CatarinaBrazil 

出 版 物：《Journal of Integrative Medicine》 (结合医学学报（英文版）)

年 卷 期：2018年第16卷第6期

页      面：396-403页

核心收录：

学科分类：1001[医学-基础医学(可授医学、理学学位)] 100104[医学-病理学与病理生理学] 10[医学] 

基　　金：supported by grants from the National Council of Scientific and Technological Development(CNPq)grant#14/2013 the Santa Catarina State Foundation in Support of Research and Innovation(FAPESC)grant#04/2012 the Coordination of Higher Education Personnel Improvement(CAPES) the UNISUL Scientific Initiation Program(PUIC),Brazil 

主　　题：Adenosine Cannabinoid Far infrared-emitting ceramics Integrative therapy Inflammatory pain Opioid receptors 

摘      要：Objective： The 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. Methods： Mice were injected with complete Freund＇s adjuvant （CFA） and treated with cFIRs via place- ment 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 hyperalge- sia was assessed. Results： cFIRs 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） gm in control group vs （988.7±107.6） gm 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-113 （（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 cF1Rs （P 〈 0.05）.Conclusion： These data provide additional support for the use of cFIRs in the treatment of painful in