Taurine Enhances Antinociception Produced by a COX-2 Inhibitor in an Inflammatory Pain Model
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Taurine Enhances Antinociception Produced by a COX-2 Inhibitor in an Inflammatory Pain Model Beatriz de Rienzo-Madero,1 Ulises Coffeen,1 Karina Simón-Arceo,1 Francisco Mercado,1 Orlando Jaimes,1 Lucía Magis-Weinberg,1 Bernardo Contreras,1 and Francisco Pellicer1,2
Abstract—The temporal activation of the sensory systems, especially in pain, determines intermediate states that define the future of the response to sensory stimulation. In this work, we interfere pharmacologically with those states that produce peripheral and central sensitisation after an acute inflammatory process, inhibiting at the periphery the COX-2 with celecoxib and using taurine (glycine A receptor agonist) for central pain relief. We tested the paw withdrawal reflex latencies to thermo- and mechanonociception after the induction of an acute inflammatory process with carrageenan. Celecoxib at low doses [0.13 and 1.3 mg/kg, intraperitoneal (i.p.)] in combination with taurine (300 mg/kg, i.p.) produces a decrease of the nociceptive response in thermo- and mechanonociception, as compared with the effect of both drugs alone. We propose that the enhancement of the analgesic effect of celecoxib in combination with taurine could be due the simultaneous action of these drugs at both, peripheral and central levels. KEY WORDS: taurine; glycine A receptor; celecoxib; COX-2 inhibitor; pain; inflammation.
from minutes to days [2]. This condition is related to plastic changes that are well defined in the sensory receptor as well as in second-order neurons [3, 4]. Both of the aforementioned conditions can be manipulated at different stages to achieve better therapeutic control of the nociceptive input. Inflammatory pain is associated with the release of arachidonic acid and its derivatives which activate and sensitise peripheral nociceptors. Additionally, cyclooxygenase and prostaglandins play a role in the transmission and maintenance of acute pain at the spinal cord level. Selective COX-2 inhibitors are capable of diminishing neuronal hyperexcitability in the spinal cord when given systemically [5]. Also, when administered intraventricularly once the inflammation is established, they decrease mechanonociception-related allodynia [6]. This process activates a series of neuronal pathways that lead to central sensitisation and the development of chronic pain [3]. The sensitisation process is possible, in part, through the action of excitatory amino acids, particularly glutamate, and modulated by the inhibitory amino acids glycine, GABA and taurine (Tau). Both systems are triggered by a nociceptive stimulus; however, the release of inhibitory amino acids is smaller and shorter than that
INTRODUCTION The duration of the period in which a sensory system remains activated determines the intermediate state which, in turn, influences the sensory response. This fact becomes especially important in the processes that define pain. In experimental models, acute pain lasts from milliseconds to several seconds. Also, acute pain classically has the antialgesic flexion reflex as its beh
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