摘要
本实验通过结扎沙土鼠双侧颈总动脉20分钟后再灌流2天或7天造成海马迟发性神经元死亡(DND)模型,检测背侧海马Ca^(2+)及脂质过氧化物含量的变化,并用海马CA_1区神经元密度作为指标,观察尼莫地平及超氧化物歧化酶(SOD)对海马DND的影响。结果:再灌流2天后背侧海马组织Ca^(2+)及MDA含量增加;尼莫地平及SOD均可改善海马CA_1区DND,使海马CA_1区神经元密度增加。本实验提示:Ca^(2+)及氧自由基导致的脂质过氧化物在短暂性脑缺血后海马DND的发生中起重要作用,钙拮抗剂及自由基清除剂对海马DND有保护作用。
DND in the gerbil hippocampus was performed by bilateral occlusion of carotid arteries for 20 min followed by reperfusion 2 or 7 days. The contents of Ca^(2+) and MDA in drosal hippocampus were measured after two days reperfusion. Neuronal density in CA1 sector of hippocampus was used as an parameter. Effects of nimodipine and Superoxide dismutase (SOD) on DND in hippocampus were observed after 7 days reperfusion.The results indicated that the levels of Ca^(2+) and MDA were increased significantly. DND in hippocampal CA1 sector was ameliorated by both nimodipine and SOD significantly. It was suggested that Ca^(2+) and Iipid peroxidation play an important role in the development of DND hippocampus after transient forebrain ischemia in gerbils. Calcium Antagonist and free radical scavenger have obvious protective effects on DND in hippocampus.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
1991年第6期605-608,共4页
Chinese Journal of Pathophysiology
基金
国家自然科学基金
关键词
脑缺血
海马
神经元
Transient cerebral ischemia
Hippocampus
Delayed neuronal death
Lipid peroxidation
