地塞米松对大鼠脑缺血—再灌注损伤时纹状体谷氨酸转运体转运功能的影响

目的 探讨地塞米松对大鼠脑缺血－再灌注损伤时、纹状体谷氨酸转运体的作用及其与自由基的关系。方法 采用三血管夹闭，松夹制作大鼠脑I－R模型。利用纹状体突触颗粒对3H－L－谷氨酸摄入量的测定及应用分光光度法观察了纹状体谷氨酸转运体，超氧化物歧化酶（SOD）活性及丙二醛（MDA）含量的变化。结果 与对照组相比，I－R组纹状体谷氨酸转运体功能及活性降低（P＜0.05、P＜0.01），MDA含量高（P＜0.01）。与I－R组相比，地塞米松组纹状体谷氨酸转运功能及SOD活性升高（P＜0.05、P＜0.01），MDA含量低（P＜0.01）。结论 地塞米松可改善I－R后纹状体谷氨酸转运体的功能，其机制可能与清除自由基有关。

Effect of dexamethasone on glutamate transporter function of striatum in the rats with the injury of cerebral ischemia-rePerfusion

Objective: To investigate the effect of dexamethasone on glutamate transporter function in striatum of ischemia reperfusion injury (I R) rats and its relationship with free radicals. Methods: A model of I R was established by clipping three arteries and then releasing to reperfuse blood into brain in rats. Glutamate transporter function, MDA content and SOD activity were studied by means of assay of 3H L glutamate uptake in striatum synaptosomes and spectrophotometry. Results: The striatum glutamate transporter function and SOD activity in I R group were significantly decreased (P<0 05,0 01) and content of MDA was increased (P<0 01), compared with that of the control group. Glutamate transporter function and SOD activity in dexamethasone group were increased (P<0 05,0 01) and content of MDA was decreased (P<0 01) compared with that of I R group. Conclusion: Dexamethasone can improve glutamate transporter function in striatum of I R rats. The mechanism might be related to the elimination of oxygen free radicals.