Department of Pharmacology, Rajarambapu College of Pharmacy, Kasegaon, Taluka: Walwa, Sangli, 415404, Maharashtra, India.
Eur J Clin Pharmacol. 2010 May;66(5):429-44. doi: 10.1007/s00228-010-0784-7. Epub 2010 Feb 13.
There is a large unmet medical need in the area of treatment of inflammatory pain initiated by tissue damage or inflammation that manifests as spontaneous pain and pain hypersensitivity (hyperalgesia).The current review focuses on the key mechanisms that produce hyperalgesia that accompanies inflammation. Also, the inflammatory mediators that interact with neurons to produce hyperalgesia are explored. As the dominant classes of analgesic drugs such as the NSAIDs and the opiates are limited by their side effects and tolerability, elucidation of the molecular mechanisms responsible for inflammatory pain provides novel opportunities for therapeutic approaches for managing inflammatory pain, with improved specificity, efficacy, and possibly with fewer toxic effects.
在治疗由组织损伤或炎症引起的炎症性疼痛方面存在着巨大的未满足的医疗需求,这种疼痛表现为自发性疼痛和痛觉过敏(痛觉超敏)。本综述重点介绍了产生伴随炎症的痛觉过敏的关键机制。此外,还探讨了与神经元相互作用产生痛觉过敏的炎症介质。由于非甾体抗炎药和阿片类药物等主要类别的镇痛药受到其副作用和耐受性的限制,阐明导致炎症性疼痛的分子机制为管理炎症性疼痛提供了新的治疗方法的机会,这些方法具有更好的特异性、疗效,并且可能毒性更小。