Neuropathic pain represents a serious complication arising from a spectrum of disorders that precipitate lesions within the central and peripheral nervous systems. This disabling pain can persist for years, severely diminishing the quality of life of the affected individuals. The treatment options available for neuropathic pain at present have limited efficacy. Moreover, the adverse effects associated with these options restrict their application. The exact etiological mechanisms underlying the pathogenesis of neuropathic pain remain unclear. However, neuroinflammatory processes mediated by the immune system play significant roles in the initiation and progression of neuropathic pain in various models. The nucleotide-binding domain and leucine-rich repeat pyrin-containing protein-3 (NLRP3) inflammasome, a pivotal element of the innate immune system, plays an indispensable role in the pathophysiological mechanisms of central and peripheral neuropathic pain. However, the precise mechanisms facilitating its activation in disparate neuropathic pain conditions remain to be elucidated. Gaining insights into the regulatory mechanisms affecting NLRP3 inflammasome activation in diverse neuropathic pain-associated disorders will aid in developing novel therapeutic avenues. Therefore, this review summarizes the current knowledge on the role of the NLRP3 inflammasome in the pathophysiology of several neuropathic pain-related conditions, such as diabetic neuropathic pain, chemotherapy-induced neuropathic pain, peripheral nerve compression, central nervous system neuropathic pain, radiculopathy, and morphine analgesic tolerance. In addition, this review also discusses the possible use of this inflammasome as a therapeutic target to alleviate the pain-related symptoms of these diseases.

Background: Intra-abdominal adhesions are fibrous bands that develop after abdominal surgery or inflammation and cause mortality and morbidity following surgeries. This study aimed to assess the effects of bupivacaine, saline and two doses of lidocaine, after peritoneal lavage and to compare their effects in reducing abdominal adhesions in rat. Methods: In a blinded, randomised, placebo-controlled clinical trial, 50 female rats were anaesthetised and the parietal peritoneum was scratched to induce punctate bleeding. The rats were randomly assigned to five groups: saline, lidocaine 2% (3 and 6 mg/kg), bupivacaine 0.25% (2 mg/kg) and control (no irrigation). The peritoneal cavity was irrigated with the appropriate solution during laparotomy. Two weeks later, re-laparotomy was performed. The quantity, quality, severity and scores of adhesions were recorded and compared. Results: The quantity and quality of adhesions were significantly higher in the control group than in the lidocaine (6 mg/kg) and bupivacaine groups. The quality of the adhesions was higher in the normal saline group than in the lidocaine (6 mg/kg) and bupivacaine groups. The severity of adhesions between the lidocaine 3 and 6 mg/kg groups and between the lidocaine 3 mg/ kg and saline groups was lower than that in the control group. Conclusion: Using lidocaine (6 mg/kg) and bupivacaine lavage in first laparotomy reduces abdominal peritoneal obstruction because of the formation of adhesion bands.