摘要
研究采用小鼠反复脑缺血合并低血压模型 ,发现 7d时其脑内过氧化脂质(LPO)含量增高 ,SOD活力降低 ;1 0d时 ,海马CA1区神经元数量明显减少。抗呆合剂可对抗这种变化 ,减轻脑缺血再灌损伤 ,表明抗呆合剂的脑保护作用部分源于其自由基清除作用。
The cerebral ischemic and hypotensive mice treated by re perfusion were used to study the effects of Kangdai mixture (KM) on LPO, SOD and CA1 cells. The results showed that on the 7th day after re perfusion, SOD activity was inhibited, LPO production was increased, and about 81% of CA1 cells was damaged in the mice. After being treated with KM and nimodipine, SOD activity was increased, LPO production was decreased, and importantly, pyramidal cells in hippocampal CA1 region were protected from delayed neuronal death. About 87% of pyramidal cells survived in KM group and 49% in nimodipine group.
出处
《北京中医药大学学报》
CAS
CSCD
北大核心
1998年第6期23-26,共4页
Journal of Beijing University of Traditional Chinese Medicine
基金
国家中医药管理局资助课题! (No .9512 10 )