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目的 探讨地塞米松对大鼠脑缺血－再灌注损伤（ｉｓｃｈｅｍ ｉａ－ｒｅｐｅｒｆｕｓｉｏｎ，Ｉ－Ｒ）时海马谷氨酸转运体功能的影响及其与自由基的关系。方法 采用大鼠三动脉夹闭、松夹制作脑Ｉ－Ｒ模型，利用海马突触膜颗粒对３Ｈ－Ｌ－谷氨酸摄入量的测定及分光光度法观察了海马谷氨酸转运体、超氧化物岐化酶（ｓｕｐｅｒｏｘｉｄｅ ｄｉｓｍ ｕｔａｓｅ，ＳＯＤ）活性及丙二醛（ｍ ａｌｏｎｄｉａｌｄｅｈｙｄｅ，ＭＤＡ）含量的变化。结果 与对照组相比，Ｉ－Ｒ组海马谷氨酸转运体的功能及ＳＯＤ活性降低（ｑ＝ ３．７５，５．７２；Ｐ＜ ０．０５，０．０１）；ＭＤＡ 含量升高（ｑ＝ ３．７９，Ｐ＜ ０．０５）。与Ｉ－Ｒ组相比，地塞米松组大鼠海马的谷氨酸转运体功能及ＳＯＤ活性回升（ｑ＝ ５．２１，３．５０，Ｐ＜ ０．０１，０．０５）；ＭＤＡ 含量回降（ｑ＝ ３．６１，Ｐ＜０．０５）。结论 地塞米松可改善Ｉ－Ｒ后海马谷氨酸转运体的功能，其机制可能与清除自由基有关
Objective To investigate the effect of dexamethasone on glutamate transporter function in hippocampus after cerebral ischemia-reperfusion (I-R) injury in rats and its relationship with free radicals. Methods Rat I-R model was made by clamping the three arteries of rats and making pineal clips. The content of 3H-L-glutamate in hippocampal synaptic membrane was measured and spectrophotometry was used to observe the changes of glutamate transporter, Changes of superoxide dismutase (SOD) activity and the content of malondialdehyde (MDA). Results Compared with the control group, the function and SOD activity of glutamate transporter in hippocampus were decreased in I-R group (q = 3.75,5.72; P <0.05,0.01); MDA content increased q = 3.79, P <0.05). Compared with I-R group, glutamate transporter function and SOD activity in hippocampus of dexamethasone group were significantly increased (q = 5.21, 3.50, P <0.01, 0.05) Fall back (q = 3.61, P <0.05). Conclusion Dexamethasone can improve the function of glutamate transporter in hippocampus after I-R, and its mechanism may be related to the scavenging of free radicals