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作 者:曲忠森[1] 任晓燕[1] 葛宝林[1] 张玉敏[1] 徐珞[1]
机构地区:[1]青岛大学医学院病理生理学教研室,青岛266021
出 处:《中国神经免疫学和神经病学杂志》1999年第3期161-164,共4页Chinese Journal of Neuroimmunology and Neurology
基 金:国家自然科学基金
摘 要: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。Objective To investigate the effect of dexamethasone on glutamate transporter function in hippocampus of ischemia reperfusion injuny (I R) rats and the relationship to free radicals. Method A model of I R was established by clipped three arteries and then released to reperfuse blood into brain in rats. Glutamate transporter function, MDA content and SOD activity were studied by means of assay of 3H L glutamate uptake in hippocampal synaptosomes and spectrophotometry. Results The hippocampus glutamate transporter function and SOD activity in I R group were significantly decreased ( q =3 75, 5 72, P <0 05, 0 01) and content of MDA were increased ( q =3 79, P <0 05) , compared with control group. Glutamate transporter function and SOD activity in dexamethasone group were increased ( q =5 21, 3 50, P <0 01, 0 05) and content of MDA were decreased ( q =3 61, P <0 05) compared with I R group. Conclusion Dexamethasone could improve glutamate transporter function in hippcampus of I R rats. The mechanism might be related to elimination of oxygen free radicals.$$$$
分 类 号:R743.310.5[医药卫生—神经病学与精神病学]
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