摘要
目的：研究迟发性神经元坏死与脂质过氧化水平的关系以及脑梗通对海马丙二醛（ＭＤＡ）含量的影响。方法：采用大鼠四血管阻断的脑缺血模型，观察脑缺血再灌注后皮层、海马和纹状体ＭＤＡ含量的动态变化。ＭＤＡ用硫代巴比妥酸法测定。结果：仅海马ＭＤＡ含量于再灌注后２４ｈ明显升高，并持续到７２ｈ。结论：再灌注后，脂质过氧化水平升高，脑梗通可阻止这种升高，提示脑梗通可能通过抑制脂质过氧化而保护神经细胞免受损害。
Objective:To explore the relation between delayed neuronal death and degree of lipid peroxidation;and to study the effect of Naogengtong on Malodialdehyde(MDA)contents in hippocampus.Methods:The dynamic change of the MDA contents in cortex,hippocampus and striatum after transient cerebral ischemia in 4 vessel occlusion model of rats,were measured by TBA method.Results:The MDA contents increased only in hippocampus 24 hours after reperfusion till 72 hours,which could be decreased by Naogengtong .Conclusion: Naogengtong may protect neurons against the ischemic injury by inhibiting lipid peroxidation.
出处
《中日友好医院学报》
1997年第2期101-104,共4页
Journal of China-Japan Friendship Hospital
基金
卫生部"八五"攻关课题
关键词
大鼠.Wister
脑缺血
海马
丙二醛
药.中草
rats,Wister
cerebral ischemia
hippocampus
malodialdehyde
drugs,Chinese herbal
