BACKGROUND: Tanshinone has been previously shown to be involved in the prevention and treatment of cerebral ischemia/reperfusion injury. In addition, excitatory amino acid-mediated neurotoxicity may induce neuronal damage following spinal cord ischemia/reperfusion injury.OBJECTIVE: To explore the interventional effect of tanshinone on N-methyl-D-aspartate receptor 1 (NMDAR1) protein expression in a rat model of spinal cord ischemia/reperfusion injury.DESIGN, TIME AND SETTING: A randomized molecular biology experiment was conducted at the Traumatology & Orthopedics Laboratory of Fujian Hospital of Traditional Chinese Medicine (Key Laboratory of State Administration of Traditional Chinese Medicine) between September 2007 and May 2008. MATERIALS: A total of 88 Sprague Dawley rats were randomly divided into a sham operation (n = 8), model (n = 40), and tanshinone (n = 40) groups. Thirty minutes after ischemia, rats in the model and tanshinone groups were observed at hour 0.5, 1, 4, 8, and 12 following perfusion, with eight rats for each time point. METHODS: Abdominal aorta occlusion was performed along the right renal arterial root using a Scoville-Lewis clamp to induce spinal cord ischemia. Blood flow was recovered 30 minutes following occlusion to establish models of spinal cord ischemia/reperfusion injury. Abdominal aorta occlusion was not performed in the sham operation group. An intraperitoneal injection of tanshinone ⅡA sulfonic sodium solution (0.2 L/g) was administered to rats in the tanshinone group, preoperatively. In addition, rats in the sham operation and model groups were treated with an intraperitoneal injection of the same concentration of saline, preoperatively. MAIN OUTCOME MEASURES: NMDAR1 protein expression in the anterior h of the spinal cord, accumulative absorbance, average absorbance, and area of positive cells were detected in the three groups through immunohistochemistry. RESULTS: All 88 rats were included in the final analysis. (1) NMDAR1 protein expression increased following 30-minute ischemia/1-hour reperfusion injury to the spinal cord, and reached a peak 4 hours after reperfusion. (2) Accumulative absorbance and average absorbance of NMDAR1, as well as area of positive cells in the model group, were significantly greater than the sham operation group at each time point (P < 0.05). However, values in the tanshinone group were significantly less than the model group (P < 0.05). CONCLUSION: NMDAR1 protein expression was rapidly increased following spinal cord ischemia/reperfusion injury and reached a peak 4 hours following reperfusion. In addition, tanshinone downregulated NMDAR1 protein expression in the anterior h of the spinal cord.