Isobolographic analysis of interaction between cyclooxygenase inhibitors and tramadol in acetic acid-induced writhing in mice.

Non-steroidal anti-inflammatory drugs (NSAIDs) and opioids are the most commonly used analgesics in the management of acute and chronic pain. Combined use of NSAIDs and opioids has been indicated for achieving better analgesia with reduced side effects. The present study was aimed at evaluating the combination of different NSAIDs, which inhibit cyclooxygenase (COX) enzymes and tramadol against acetic acid-induced writhing in mice.

Effect of selective inhibition of cyclooxygenase-2 on lipopolysaccharide-induced hyperalgesia.

Lipopolysaccharide (LPS) is known to increase the expression and release of various pro-inflammatory mediators, including cyclooxygenase-2 (COX-2) and produce hyperalgesia. It is also well known that prostaglandins (PGs), synthesised both in the periphery and centrally by COX isoforms, play a key role in sensitisation of nociceptors and nociceptive processing. To investigate the role of COX-2 in LPS-induced hyperalgesia, parecoxib, a selective COX-2-inhibiting pro-drug, was injected intravenously 30 min before assessing hyperalgesia induced by intraperitoneal or subcutaneous administration of LPS (50 microg/mouse or 25 microg/paw of rat, respectively).

Effect of U-74500A, a 21-aminosteroid on renal ischemia-reperfusion injury in rats.

Renal ischemia-reperfusion injury constitutes the most common pathogenic factor for acute renal failure and is the main contributor to renal dysfunction in allograft recipients and revascularization surgeries. Many studies have demonstrated that reactive oxygen species play an important role in ischemic acute renal failure. The aim of the present study was to investigate the effects of the synthetic antioxidant U-74500A, a 21-aminosteroid in a rat model of renal ischemia-reperfusion injury.

Oxidative stress-mediated renal dysfunction by cyclosporine A in rats: attenuation by trimetazidine.

Cyclosporine A (CsA) is one of the first line immunosuppressants employed in the management of solid organ transplantation and autoimmune diseases. The clinical utility of CsA is limited by the frequent occurrence of chronic nephrotoxicity, characterized by tubular atrophy, interstitial fibrosis and progressive renal impairment. The pathogenesis of CsA nephrotoxicity is still not well delineated.