Abstract
The neurochemical mechanisms underlying neuropathic pain (NP) are related to peripheral and central sensitization caused by the release of inflammatory mediators in the peripheral damaged tissue and ectopic discharges from the injured nerve, leading to a hyperexcitable state of spinal dorsal horn neurons. The aim of this work was to clarify the role played by cyclooxygenase (COX) in the lesioned peripheral nerve in the development and maintenance of NP by evaluating at which moment the non-steroidal anti-inflammatory drug indomethacin, a non-selective COX inhibitor, attenuated mechanical allodynia after placing one loose ligature around the nervus ischiadicus, an adaptation of Bennett and Xie's model in rodents. NP was induced in male Wistar rats by subjecting them to chronic constriction injury (CCI) of the nervus ischiadicus, placing one loose ligature around the peripheral nerve, and a sham surgery (without CCI) was used as control. Indomethacin (2 mg/kg) or vehicle was intraperitoneally and acutely administered in each group of rats and at different time windows (1, 2, 4, 7, 14, 21, and 28 days) after the CCI or sham surgical procedures, followed by von Frey's test for 30 min. The data showed that indomethacin decreased the mechanical allodynia threshold of rats on the first, second, and fourth days after CCI (P<0.05). These findings suggested that inflammatory mechanisms are involved in the induction of NP and that COX-1 and COX-2 are involved in the induction but not in the maintenance of NP.
Highlights
According to the International Association for the Study of Pain (IASP), pain is an unpleasant sensory and emotional experience associated with actual or potential tissue injury or described regarding such damage [1]
We have recently reported an improvement in this procedure in a laboratory animal model of Neuropathic pain (NP), inducing constriction injury (CCI) of the right nervus ischiadicus through a single loose ligature in an adaptation of the NP model described by Bennett and Xie in 1988 [9,10,11]
We evaluated whether indomethacin, an Non-steroidal anti-inflammatory drugs (NSAIDs) that inhibits the cyclooxygenase 1 and 2 (COX-1 and COX-2) enzymes, can attenuate mechanical allodynia in an adapted CCI model of NP generated by placing a single loose ligature around a peripheral nerve
Summary
According to the International Association for the Study of Pain (IASP), pain is an unpleasant sensory and emotional experience associated with actual or potential tissue injury or described regarding such damage [1]. Pain is a signal to prevent further lesion or to avoid tissue injury. Neuropathic pain (NP) is related to the reaction of nervous system tissue to neural damage. NP can be induced by lesions of the peripheral nervous system. COX 1 and 2 enzymes and neuropathic pain induction (PNS) caused by tumor invasion, metabolic diseases, infection, neurotoxic chemicals, and mechanical trauma leading to pathophysiological changes in either the PNS or the central nervous system (CNS) [3]. NP is an unpleasant and debilitating condition that causes a severe impact on the quality of life of patients [6]. The management of patients affected by NP is complicated, involving a multidisciplinary team for alleviating symptoms and available treatments are frequently ineffective
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