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目的探讨甘糖酯对脑缺血－再灌注损伤大鼠海马谷氨酸转运体功能的影响。②方法采用大鼠三血管夹闭、松夹制作脑缺血－再灌注损伤模型，利用海马突触膜颗粒对３Ｈ－Ｌ－谷氨酸摄入量的测定，观察了甘糖酯对谷氨酸转运体功能的影响，同时测定了脑组织丙二醛（ＭＤＡ）含量及超氧化物歧化酶（ＳＯＤ）活性的变化。③结果缺血－再灌注损伤时，大鼠海马谷氨酸转运体功能及ＳＯＤ活性明显降低，ＭＤＡ明显升高，与对照组比较差异均有显著性（ｔ＝３．６９１～５．４０６，Ｐ均＜０．０１）；应用甘糖酯组大鼠海马谷氨酸转运体功能及ＳＯＤ活性显著提高，ＭＤＡ含量降低，与缺血－再灌注损伤组相比，差异均有显著性（ｔ＝２．９３８～３．１２７，Ｐ均＜０．０５）。④结论甘糖酯可能通过清除自由基的作用，改善大鼠脑组织缺血－再灌注损伤时海马谷氨酸转运体的功能。
Objective To investigate the effect of glycol ester on the function of glutamate transporter in hippocampus after cerebral ischemia-reperfusion injury in rats. Methods The rat model of cerebral ischemia-reperfusion injury was established by occlusion of rat’s blood vessels in three vessels and pineal clips. The content of 3H-L-glutamic acid in hippocampal synaptic membrane granules was measured, Acid transporter function of the brain tissue at the same time measured the content of malondialdehyde (MDA) and superoxide dismutase (SOD) activity changes. Results After ischemia-reperfusion injury, glutamate transporter function and SOD activity in hippocampus of rats decreased significantly and MDA significantly increased compared with control group (t = 3.691-5.406, P <0.01). The glutamate transporter function and the activity of SOD in hippocampus were significantly increased and the content of MDA was decreased in the group treated with glycolose ester (P <0.01). Compared with the group of ischemia-reperfusion injury, the difference was significant = 2.938 ~ 3.127, P <0.05). ④ Conclusion Glycosides may improve the function of glutamate transporters in rat hippocampus during ischemia-reperfusion injury by eliminating free radicals.