RESUMO
OBJECTIVE: Warm water immersion therapy (WWIT) has been widely used in the treatment of various clinical conditions, with analgesic and anti-inflammatory effects. However, its mechanism of action has not been fully investigated. The present study analyzed the role of spinal inhibitory neuroreceptors in the antihyperalgesic effect of WWIT in an experimental model of inflammatory pain. METHODS: Mice were injected with complete Freund's adjuvant (CFA; intraplantar [i.pl.]). Paw withdrawal frequency to mechanical stimuli (von Frey test) was used to determine: (1) the effect of intrathecal (i.t.) preadministration of naloxone (a non-selective opioid receptor antagonist; 5⯵g/5⯵l), (2); AM281 (a selective cannabinoid receptor type 1 [CB1] antagonist; 2⯵g/5⯵l), (3); and 1,3-dipropyl-8-cyclopentylxanthine (DPCPX; a selective adenosine A1 receptor antagonist; 10â¯nmol/5⯵l), on the antihyperalgesic (pain-relieving) effect of WWIT against CFA-induced hyperalgesia. RESULTS: Intrathecal naloxone, AM281, and DPCPX significantly prevented the antihyperalgesic effect of WWIT. This study suggests the involvement of spinal (central) receptors in the antihyperalgesic effect of WWIT in a model of inflammatory pain. CONCLUSIONS: Taken together, these results suggest that opioid, CB1, and A1 spinal receptors might contribute to the pain-relieving effect of WWIT.
Assuntos
Naloxona/efeitos adversos , Células Receptoras Sensoriais/efeitos dos fármacos , Animais , Adjuvante de Freund/efeitos adversos , Hiperalgesia/fisiopatologia , Imersão , Inflamação , Camundongos , Antagonistas de Entorpecentes/efeitos adversos , Manejo da Dor , Água , Xantinas/química , Xantinas/farmacologiaRESUMO
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 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-1ß (IL-1ß) and IL-10 levels were measured. Twenty-four hours after CFA injection and 30â¯min before cFIR treatment, mice were pretreated with a nonselective adenosinergic antagonist, caffeine, the selective adenosine receptor A1 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. RESULTS: cFIRs statistically (Pâ¯<â¯0.05) decreased CFA-induced mechanical hyperalgesia ((82.86⯱â¯5.21)% in control group vs (56.67⯱â¯9.54)% in cFIR group) and edema ((1699.0⯱â¯77.8) µm in control group vs (988.7⯱â¯107.6)⯵m in cFIR group). cFIRs statistically (Pâ¯<â¯0.05) reduced TNF-α ((0.478⯱â¯0.072)â¯pg/mg of protein in control group vs (0.273⯱â¯0.055)â¯pg/mg of protein in cFIR group) and IL-1ß ((95.81⯱â¯3.95)â¯pg/mg of protein in control group vs (80.61⯱â¯4.71)â¯pg/mg of protein in cFIR group) levels and statistically (Pâ¯<â¯0.05) increased IL-10 ((18.32⯱â¯0.78)â¯pg/mg of protein in control group vs (25.89⯱â¯1.23)â¯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 (Pâ¯<â¯0.05). CONCLUSION: These 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.
Assuntos
Cerâmica/química , Citocinas/imunologia , Adjuvante de Freund/efeitos adversos , Hiperalgesia/imunologia , Hiperalgesia/terapia , Células Receptoras Sensoriais/imunologia , Animais , Cerâmica/efeitos da radiação , Citocinas/genética , Modelos Animais de Doenças , Humanos , Hiperalgesia/induzido quimicamente , Raios Infravermelhos , Interleucina-10/genética , Interleucina-10/imunologia , Interleucina-1beta/genética , Interleucina-1beta/imunologia , Masculino , Camundongos , Manejo da Dor , Nervos Periféricos/imunologia , Fator de Necrose Tumoral alfa/genética , Fator de Necrose Tumoral alfa/imunologiaRESUMO
Although training programs with regular eccentric (ECC) exercise are more commonly used for improving muscular strength and mobility, ECC exercise effects upon functional recovery of the sciatic nerve has not yet been determined. After sciatic nerve crush, different mice groups were subjected to run on the treadmill for 30 min at a speed of 6, 10, or 14 m/min with - 16° slope, 5 days per week, over 8 weeks. During the training time, neuropathic pain-like behavior (mechanical and cold hyperalgesia) was assessed and functional recovery was determined with the grip strength test and the Sciatic Functional and Static indexes (SFI and SSI). After 9 weeks, triceps surae muscle weight and morphological alterations were assessed. Tumor necrosis factor alpha (TNF-α), interleukin-1ß (IL-1ß), interleukin-4 (IL-4), interleukin-1Ra (IL-1Ra), insulin-like growth factor-1 (IGF-1) levels, and markers pro- and anti-inflammatory and regeneration, respectively, were quantified in the muscle and sciatic nerve on day 14 post-crushing. Exercised groups presented less neuropathic pain-like behavior and better functional recovery than non-exercised groups. Biochemically, ECC exercise reduced TNF-α increase in the muscle. ECC exercise increased sciatic nerve IGF-1 levels in sciatic nerve crush-subjected animals. These findings provide new evidence indicating that treatment with ECC might be a potential approach for neuropathy induced by peripheral nerve injury.