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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。
In this experiment, the hippocampal delayed neuronal death (DND) model was induced by ligating the bilateral common carotid artery of gerbils for 20 minutes and then perfused for 2 days or 7 days to detect the dorsal hippocampal Ca 2+ and lipid peroxides. Changes in the content, and the density of neurons in the hippocampal CA1 region were used as indicators to observe the effects of nimodipine and superoxide dismutase (SOD) on hippocampal DND. RESULTS: After 2 days of reperfusion, Ca 2+ and MDA content in dorsal hippocampus increased. Nimodipine and SOD both improved DND in hippocampal CA1 region and increased neuronal density in hippocampal CA1 region. This experiment suggests that lipid peroxides caused by Ca2+ and oxygen free radicals play an important role in the development of DND in hippocampus after transient cerebral ischemia. Calcium antagonists and free radical scavengers protect hippocampal DND effect.