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作 者:胡小吾[1] 王文仲[1] 赵孟尧[1] 缪明永[2] 赵麟[2] 丁自强[3]
机构地区:[1]上海第二军医大学长海医院神经外科,200433 [2]上海第二军医大学生化教研室,200433 [3]上海第二军医大学病生教研室,200433
出 处:《临床神经科学》1997年第1期13-16,共4页Chinese Journal of Clinical Neurosciences
摘 要:把SD大鼠分成正常组、生理盐水治疗的损伤对照组及GM_1治疗的损伤治疗组。结果发现对照组伤后8h和16h。脑线粒体呼吸功能明显降低,治疗组则明显好转。对照组皮层神经元细胞和线粒体超微结构有明显损害,治疗组损害明显减轻。其可能机制与GM_1保护膜脂和膜酶活性,维持膜内外离子平衡,减轻水肿及减少自由基形成等有关。Sprague-Dawley rats were divided into three groups; normal group, 0. 9% sodium chloride solution-treated control group and GM1 treated group. The results showed that mito-chondrial respiratory function significantly decreased in control group on 8th and 16th hour after injury, while markedly increased in GMj treated group, which were similar to those in normal group. Cortical neurons and their mitochondrial ultrastructure of control group were severely damaged, but the pathological changes in GMj treated group were much milder. The possible mechanism is that GM1 protects changes in the plasma membrane hpids, and membrane enzyme activity and reduces ionic imbalance, edema and free radical formation.
关 键 词:神经节苷脂 脑损伤 治疗 脑细胞 呼吸功能 结构
分 类 号:R651.150.5[医药卫生—外科学]
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