论文部分内容阅读
目的：探讨超氧化物歧化酶（ＳＯＤ）对脑缺血再灌注损伤（Ｉ－Ｒ）大鼠皮层、海马、纹状体谷氨酸转运体功能的影响。方法：采用大鼠３个血管夹闭、松夹复制脑Ｉ－Ｒ损伤模型。利用脑组织突触膜颗粒对［３Ｈ］－Ｌ－谷氨酸摄入量的测定及分光光度法观察ＳＯＤ对皮层海马纹状体谷氨酸转运体功能、丙二醛（ＭＤＡ）含量及ＳＯＤ活性的影响。结果：Ｉ－Ｒ组谷氨酸转运体的功能及ＳＯＤ活性明显低于对照组（Ｐ＜００５，００１），ＭＤＡ含量明显高于对照组（Ｐ＜００５，００１）。ＳＯＤ＋Ｉ－Ｒ组大鼠谷氨酸转运体的功能及ＳＯＤ活性明显高于Ｉ－Ｒ组（Ｐ＜００５，００１）；ＭＤＡ含量明显低于Ｉ－Ｒ组（Ｐ＜００５，００１）。结论：ＳＯＤ可改善Ｉ－Ｒ后脑组织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 superoxide dismutase (SOD) on the function of glutamate transporter in cortex, hippocampus and striatum of cerebral ischemia-reperfusion injury (I-R) rats. Methods: Rat model of I-R injury was established by clipping and clamping the three blood vessels of rats. The contents of glutamate transporter, malondialdehyde (MDA) and the content of SOD in hippocampal striatum of cortex hippocampus were detected by measuring the intake of [3H] -L-glutamic acid by synaptosomal granules of brain tissue and spectrophotometry Effect of activity. Results: The function and SOD activity of glutamate transporter in I-R group were significantly lower than those in control group (P <005,001), MDA content was significantly higher than that in control group (P <005,001 ). The function and SOD activity of glutamate transporter in SOD + I-R group were significantly higher than those in I-R group (P <005,001); MDA content was significantly lower than that in I-R group (P <005 , 0 01). Conclusion: SOD can improve the function of glutamate transporter in I-R posterior brain tissue. Its mechanism may be related to the scavenging of free radicals.