丹参酮IIa拮抗脊髓缺血再灌注损伤：干预谷氨酸释放的上游因素

目的：探讨丹参酮调控谷氨酸转运体功能对脊髓缺血再灌注损伤的作用。方法：88只SD 大鼠结扎腹主动脉，制作脊髓缺血再灌注损伤模型。按随机数字表法将动物分为假手术组（n=8），模型组（n=40）和丹参酮组（n=40）。分别在脊髓缺血再灌注损伤后0.5h、1h、4h、8h、12h相应时点检测各组谷氨酸转运体功能和Na+-K+−ATP酶活性。结果： ①大鼠脊髓组织谷氨酸转运体功能及Na+-K+−ATP酶活性在脊髓缺血再灌注损伤后0.5h后开始下降，4h后降到最低点，其后活性逐渐恢复，但12h后仍未及正常水平。②丹参酮组各观测点脊髓组织谷氨酸转运体功能及Na+-K+−ATP酶活性均较其它两组高。结论：①大鼠脊髓缺血再灌注损伤时脊髓谷氨酸转运体功能和Na+-K+−ATP酶活性均下降；②丹参酮可能通过保护脊髓谷氨酸转运体功能和Na+-K+−ATP酶活性的下降，从而减轻大鼠脊髓缺血再灌注损伤。

Observation of glutamate transporter function and Na+-K+−ATP enzyme via Tanshinone during ischemia/reperfusion injury of spinal cord

Objective: To examine function of tanshinone on glutamate transporter function of spinal cord during ischemia/reperfusion injury. Methods: A total of 88 Sprague Dawley rats anesthetized with an intraperitoneal injection of pentobarbital sodium which were randomly divided into a sham operation group (n=8), model group (n=40) and tanshinone group (n=40). Abdominal aorta occlusion was performed along the right renal arterial root using a Scoville-Lewis clamp to induce spinal cord ischemia. The spinal cord preparation was left undisturbed for 30 min before a baseline measurement. Completely ischemia was achieved by clamping the spinal cord and ischemia/reperfusion injury model of spinal cord was established. Abdominal aorta occlusion was not performed in the sham operation group. An intraperitoneal injection of tanshinone IIA sulfonic sodium solution 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. Thirty minutes after ischemia, glutamate transporter fuction and Na+-K+-ATP enzyme activity of spinal cord in the model group and the tanshinone group were detected at 0.5h, 1h, 4h, 8 and 12h following perfusion, with eight rats for each time point. Results: All 88 rats were included in the final analysis. Spinal cord of glutamate transporter function and Na+-K+-ATP enzyme activity decreased in the first half an hour during ischemia/reperfusion injury, reached to the minimum peak in the following 4h after reperfusion, then it increased gradually and did not reach to normal competence even in 12h. Glutamate transporter fuction and Na+-K+-ATP enzyme activity of spinal cord were higher in tanshinone groups than the model groups at each time point. Conclusions: In a rat model of spinal cord ischemia/reperfusion injury, glutamate transporter fuction and Na+-K+-ATP enzyme activity of spinal cord decreased. Tanshinone might reduce the speed of degrade the glutamate transporter function and Na+-K+-ATP enzyme activity which might reduce spinal cord ischemia/reperfusion injury.