Abstract

Pain and inflammation are considered strongly associated. The greater pain behavior was demonstrated in animals with greater amount of inflammation. Tissue or nerve injury results in the release of various inflammatory mediators such as prostaglandins, bradykinin, proinflammatory cytokines, chemokines, histamine, serotonin and nerve growth factors from the site of injury. These inflammatory mediators play a critical role in both integrating the inflammatory response and mediating pain hypersensitivity. This review highlights the role of prostaglandins and proinflammatory cytokines in the pain sensitization and its underlying mechanisms, emphasizing the evidence that these molecules are potential targets to develop novel drugs and therapies for the treatment of both inflammation and pain in clinic.

Keywords: Inflammation, pain, prostaglandins, proinflammatory cytokines, hyperalgesia, bradykinin, COX, Tetrodotoxin (TTX) resistant, Tumor- necrosis factor- alpha (TNF- ), GlucocortiCoids