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作 者:任晓燕[1] 葛宝林[1] 曲忠森[1] 张玉敏[1]
机构地区:[1]青岛大学医学院病理生理学教研室,266021
出 处:《临床神经病学杂志》1999年第5期263-265,共3页Journal of Clinical Neurology
基 金:国家自然科学基金
摘 要:目的 探讨超氧化物歧化酶(SOD)对缺血-再灌注损伤(I-R) 大鼠纹状体谷氨酸转运体功能(GTF)的影响。方法 采用大鼠三血管夹闭、松夹制作脑I-R损伤模型。利用脑组织突触膜颗粒对3 H-L-谷氨酸摄入量的测定及分光光度法观察GTF的改变,同时测定组织丙二醛(MDA)的含量及SOD活性的变化。结果 与对照组相比,I-R 组GTF及SOD活性明显降低(P< 0.01,0.05),MDA 含量明显升高(P< 0.01)。与I-R组相比,SOD组大鼠GTF及SOD活性明显提高(P< 0.05);MDA 含量明显降低(P< 0.01)。结论 SOD可改善I-R后纹状体GTF,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 the striatum glutamate transporter in rats with injury of cerebral ischemia reperfusion. Methods A model of ischemia reperfusion injury (IR) was made by clipping three arteries and then by releasing them to reperfuse blood into the ischemic brain in rats. Glutamate transporter functions were studied by means of assay of 3 H L glutamate uptake in synaptosomes, GTF was observed by spectrophotometry, meantime MDA contents and SOD activities were measured. Results Glutamate transporter function and SOD activity in I R group were significantly decreased ( P <0 01,0 05), the content of MDA was significantly increased ( P <0 01) while compared with control group. Glutamate transporter function and SOD activity in SOD group were siginficantly increased ( P <0.05); MDA content was significantly decreased (P <0.01) while compared with I R group. Conclusion SOD could improve glutamate transporter function in I R rats. The mechanism might be related to eli minate free radicals.
分 类 号:R743.3[医药卫生—神经病学与精神病学]
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