摘要
脑缺血细胞损伤的原因之一为自由基大量形成和脂质过氧化的病理过程.本研究采用大脑中动脉插线法小鼠局灶性脑缺血模型,用DTNB直接法测定缺血脑组织GSH-px活性,TBA法测MDA含量,观察黄芪甲甙对缺血脑组织GSH-px活性和MDA含量的影响.结果表明,缺血脑GSH-px活性稍有降低,但无统计学意义;MDA含量显著升高;腹腔注射黄芪甲甙轻度增高GSH-px活性,但显著降低缺血脑组织中MDA含量.提示缺血脑组织发生明显的脂质过氧化反应,且脑组织潜在抗氧化能力降低.黄芪甲甙对清除自由基,保护缺血脑组织有一定作用.
Free radicals formation and lipid peroxidation were thought to potentiate ischemic brain cell injury. In the present study DTNB method and a-thiobarbituric acid method were applied to measure the activity of GSH-px and the concentration of MDA respectively following MCAO in mice. The results showed that there was no significant difference in cerebral GSHpx activity between ischemic group and sham operated group, while MDA concentration markedly increased in ischemic group compared with the sham operated group (P<0. 01). Injection of astragaloside I intraperitoneally at 1 hour before the MCAO mildly enhanced GSH-px activity, but markedly decreased MDA concentration (P<0. 01). These facts suggest that astragaloside I might protect the cerebral tissue against the free radical damage in ischemia.
出处
《中国临床神经科学》
1998年第3期146-148,共3页
Chinese Journal of Clinical Neurosciences
关键词
脑缺血
黄芪甲甙
丙二醛
Cerebral ischemia Mice Glutathione peroxidase (GSH-px)Malonyldialdehyde (MDA) Astragloside I
