BACKGROUND: Although recent evidence suggests that cyclooxygenase-2 (COX-2) may contribute to the development and management of neuropathic pain, the efficacy of COX-2 inhibitor against neuropathic pain is still unclear. In this study, we investigated the effects of the systemic administration of the selective COX-2 inhibitor meloxicam at an early stage after nerve injury on the development of tactile allodynia in L5 single spinal-nerve injury in rats. METHODS: Twenty-four young male Sprague-Dawley rats received L5 single spinal-nerve injury. Nerve-injured rats (6 per group) received repeated intraperitoneal administrations of meloxicam (1, 2, or 4 mg/kg) or vehicle 0, 12, 24, and 36 hours after nerve injury. Tactile allodynia was quantified for 4 weeks by use of von Frey filaments. RESULTS: In animals given 2 mg/kg and 4 mg/kg, hind-paw withdrawal thresholds 4 weeks after nerve injury were significantly higher compared with those of the vehicle-treated animals. The area under the time-effect curve from preinjury to 4 weeks after nerve injury values were significantly higher in animals treated with 4 mg/kg of meloxicam compared with animals treated with vehicle. CONCLUSION: Systemic administration of 2 mg/kg and 4 mg/kg of meloxicam at an early stage after nerve injury attenuated the development of tactile allodynia. These results suggest that COX-2 may be at least in part involved in the development of tactile allodynia in an L5 single spinal-nerve injury model.
BACKGROUND: Although recent evidence suggests that cyclooxygenase-2 (COX-2) may contribute to the development and management of neuropathic pain, the efficacy of COX-2 inhibitor against neuropathic pain is still unclear. In this study, we investigated the effects of the systemic administration of the selective COX-2 inhibitor meloxicam at an early stage after nerve injury on the development of tactile allodynia in L5 single spinal-nerve injury in rats. METHODS: Twenty-four young male Sprague-Dawley rats received L5 single spinal-nerve injury. Nerve-injured rats (6 per group) received repeated intraperitoneal administrations of meloxicam (1, 2, or 4 mg/kg) or vehicle 0, 12, 24, and 36 hours after nerve injury. Tactile allodynia was quantified for 4 weeks by use of von Frey filaments. RESULTS: In animals given 2 mg/kg and 4 mg/kg, hind-paw withdrawal thresholds 4 weeks after nerve injury were significantly higher compared with those of the vehicle-treated animals. The area under the time-effect curve from preinjury to 4 weeks after nerve injury values were significantly higher in animals treated with 4 mg/kg of meloxicam compared with animals treated with vehicle. CONCLUSION: Systemic administration of 2 mg/kg and 4 mg/kg of meloxicam at an early stage after nerve injury attenuated the development of tactile allodynia. These results suggest that COX-2 may be at least in part involved in the development of tactile allodynia in an L5 single spinal-nerve injury model.