• Souichi Ohta, Yasushi Iwashita, Hideaki Takada, Sadako Kuno, and Takashi Nakamura.
• Department of Orthopaedic Surgery, Kyoto University, Kyoto, Japan. sota@ea.mbn.or.jp
• Spine. 2005 May 15;30(10):1154-8.

Study DesignThe effect of edaravone, a novel free radical scavenger, was assessed functionally and histologically using a rat spinal cord contusion model.ObjectiveTo investigate the effect of edaravone on neuroprotection after spinal cord injury in rats.Summary Of Background DataThe spinal cord injury results in immediate physical damage (primary injury), followed by a prolonged neural tissue disorder (secondary injury). This secondary injury process has been suggested to be induced by lipid peroxidation. Edaravone has been reported to inhibit lipid peroxidation in cerebral ischemia models.MethodsSpinal cord injury at the T10 level was induced with a weight drop device (10 g weight, 25 mm height). Edaravone was administered intravenously as a bolus dose of 5 mg/kg at 5 minutes, 24 hours, and 48 hours after injury (edaravone-treated rats). In control rats, nothing was administered. Functional assessment was conducted weekly using the Basso-Beattie-Bresnahan locomotor rating scores. Histologically, a percentage of spared white matter area was calculated. The effects of intravenous administration of edaravone on lipid peroxide formation in rat spinal cord homogenate were examined using the thiobarbituric acid test for malonyldialdehyde production.ResultsSix weeks after injury, edaravone-treated rats showed significantly higher motor score and larger spared white matter area than control rats. The administration of edaravone attenuated malonyldialdehyde production in spinal cord homogenate by >45%.ConclusionEdaravone enhanced functional recovery and preserved more spinal cord tissue after spinal cord injury in rats. The attenuation of posttraumatic lipid peroxide formation by edaravone partially contributed to this enhancement.

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