O papel dos receptores opióides centrais no efeito antinociceptivo de um polissacarídeo sulfatado isolado da alga marinha solírea filiforms na hipernocicepcao induzida pela formalina na articulação temporomandibular de ratos

Abstract

The current study was designed to investigate the effect of sulfated polysaccharides from red seaweed Solieria filiformis (Fraction FII) in the inflammatory hypernociception in the temporomandibular joint (TMJ) of rats. Methods: Male Wistar rats (180–240 g). Rats were pretreated (30 min) with a subcutaneous injection (s.c.) of vehicle or FII (0.03, 0.3 or 3.0 mg/kg) followed by intra-TMJ injection of 1.5% Formalin or 5-hydroxytriptamine (5-HT, 225 µg/TMJ). In other set of experiments rats were pretreated (15 min) with an intrathecal injection of the non-selective opioid receptors Naloxone, or µ-opioid receptor antagonist CTOP, or δ-opioid receptor Naltridole hydrochloride, or -opioid receptor antagonist Nor-Binaltorphimine followed by injection of FII (s.c.). After 30 min, the animals were treated with an intra-TMJ injection of 1.5 % formalin. After TMJ treatment, behavioral nociception response was evaluated for a 45-min observation period, animals were terminally anesthetized and periarticular tissue, trigeminal ganglion and subnucleus caudalis (SC) were collected plasma extravasation and ELISA analysis. Results: Pretreatment with FII significantly reduced formalin- and serotonin-induced TMJ nociception (P<0.05: ANOVA, Bonferroni’s test). Pretreatment with FII significantly inhibit the plasma extravasation and inflammatory cytokines (TNF-α and IL-1β) release induced by 1.5% formalin in the TMJ (P<0.05). Pretreatment with intrathecal injection of Naloxone, CTOP, Naltridole or Nor-BNI blocked the antinociceptive effect of FII in the 1.5% formalin-induced TMJ nociception (P<0.05). In addition, FII was able to significantly increase the β-endorphin release in the subnucleus caudalis. Conclusions: The results suggest that FII has a potential antinociceptive and anti-inflammatory effect in the TMJ mediated by activation of opioid receptors in the subncucleus caudalis and inhibition of the release of inflammatory mediators in the periarticular tissue .