Propargylglycine decreases neuro-immune interaction inducing pain response in temporomandibular joint inflammation model

Publication date: Available online 8 October 2019Source: Nitric OxideAuthor(s): Emanuela G. Garattini, Bruna M. Santos, Daniele Ferrari, Camila Porto, Heloísa D.C. Francescato, Terezila M. Coimbra, Christie R.A. Leite-Panissi, Luiz G.S. Branco, Glauce C. NascimentoAbstractThe mechanisms underlying temporomandibular disorders following orofacial pain remain unclear. Hydrogen sulfide (H2S), a newly identified gasotransmitter, has been reported to modulate inflammation. Cystathionine γ-lyase (CSE) is responsible for the systemical production of H2S, which exerts both pro- and antinociceptive effects through inflammation. In the current study, we investigated whether the endogenous H2S production pathway contributes to arousal and maintenance of orofacial inflammatory pain, through the investigation of the effects of a CSE inhibitor, propargyglycine (PAG), in a rat CFA (Complete Freund Adjuvant)-induced temporomandibular inflammation model to mimic persistent pain in the orofacial region. For this, rats received either CFA or saline in the temporomandibular joints (TMJs), and after 3 or 14 days, they received a single injection of PAG or saline and were evaluated for nociception with the von Frey and formalin test. Also, pro-inflammatory cytokines, tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β) were analyzed in TMJs and trigeminal ganglion (TG). In this last one, glial cells reactivity was also verified. Endogenous H2S production rate were measured in both, TMJ...
Source: Nitric Oxide - Category: Chemistry Source Type: research