摘要
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。
AIM:To investigate the effect of superoxide dismutase(SOD) on the function of glutamate transporter in rats with injury of cerebral ischemia-reperfusion.METHODS:A model of ischemia-reperfusion injury(I-R) was performed by clipping three arteries and then by releasing them to reperfuse blood into ischemic brain in rats. Glutamate transporter functions were studied by means of assay of L-glutamate uptake in synaptosomes, and malondialdehyde (MDA) contents and SOD activities in cerebral contex, hippocampus ,striatum by spectrophotometry.RESULTS:Glutamate transporter function and SOD activity in I-R group significantly decreased ( P <0 05, P< 0 01);content of MDA significantly increased( P <0 05, P< 0 01) compared with control group. Glutamate transporter function and SOD activity in SOD group significantly increased ( P <0 05, P< 0 01);MDA content significantly decreased( P <0 05, P< 0 01) compared with I-R group.CONCLUSION:SOD can improve glutamate transporter function of I-R rats. The mechanism might be related to eliminate free radicals.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
1999年第7期601-603,共3页
Chinese Journal of Pathophysiology
基金
国家自然科学基金
