Volume 11, Issue 3 (Fall 2007)                   Physiol Pharmacol 2007, 11(3): 228-237 | Back to browse issues page

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Abstract:   (18204 Views)
Introduction: Neuropathic pain may be due to a primary insult to the peripheral or central nervous system. In this situation, Hyperalgesia and Allodynia are the results of prostaglandins and cytokines release in the spinal cord. It seems that immune cells play an importat role in the induction and maintenance of chronic pain. Compared to selective CoxII inhibitors, nimesulide, a highly selective CoxII inhibitor, effectively reduced hyperalgesia due to peripherally administration of inflammatory agents like formalin. In this study we investigate the effect of nimesulide on pain behavior and CoxII expression in macrophage and microglial cells in neuropathic pain condition. Methods: Male Wistar rats (n=6, 150-200 g) using Bennet & Xie model of neuropathic pain were divided in different groups:1- CCI saline 2- Sham saline (control), 3- CCI drugs.Nimesulide 1.25,2.5and 5mg/kg were used. 42 º C water for thermal hyperalgesia and Von Frey Filaments for mechanical allodynia, respectively, were used as pain behaviour tests. Experiments were performed on day before and 1,3,5,7,10,14days post injury. At day 14 rats who received nimesulide 5 mg/kg were killed and CoxII was assessed in macrophages and microglial cells. ANOVA and T-test were used for statistical analysis and % of SD control was used for enzyme expression. Results: Nimesulide 2.5,5mg/kg reduced hyperalgesia and allodynia. Nimesulide 5mg/kg also reduced CoxII expression in macrophages and microglial cells compared to CCIsaline group. Conclusion: Nimesulide reduced hyperalgesia due to nerve inflammation. CoxII- induced PGs activates a wide range of immune cells like macrophages and microglia. It seems that nimesulide a highly selective Cox2 inhibitor can reduce effectively chronic inflammatory pain. َ
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