摘要
本文采用Pulsinelli-Brierley4血管结扎致SD大鼠全脑缺血(10min)再灌流模型,分别观察了早期不同再灌流时间(12、24、48h)点上,大鼠海马CA1区神经元的超微结构以及再灌7d时光镜结构变化,同时观察了小檗碱对CA1区迟发性神经元坏死的影响。结果显示脑缺血再灌流早期,CA1区神经元超微结构发生明显改变,7d时光镜下绝大部分细胞脱失;而用药组大鼠海马CA1区神经元在相应时间点上超微结构变化相对较轻,7d时仍有绝大多数(82%)细胞存活,细胞密度为172±12.2个/mm,显著高于缺血对照组27±7.6个/mm,P<0.001。提示小檗碱对大鼠短暂脑缺血再灌流造成的海马CA1区迟发性神经元坏死具有显著的对抗作用。
The ultrastructural changes in the pyramidal neurons of the CA1 sector in hippocampus were studied after 12hours,24hours,48hours.reperfusion,also light structural changes after 7day.following a transient 10 min.cerebral ischemia induced by 4 vessel occlusion described by Pulsinelli-Brierly previously.The effect of berberine on delayed neuronal death in this model was observed simultaneously.The results showed that, at early reperfusion stages,the ultrastructural changes were apparent.After 7d,almost all neurons in CA1 were disappear,with the density 27±7.6/mm.But in berberine group,the subcellular changes were moderate,and after 7d reperfusim,most cells were intact,with the density of CA1 pyramidal neuron 172±12.2/mm.It is suggested that berberine effectirely protects neurons in CA1 from DND induced by transient cerebral ischemia followed by reperfusion.
出处
《中风与神经疾病杂志》
CAS
CSCD
北大核心
1996年第2期75-77,共3页
Journal of Apoplexy and Nervous Diseases
基金
广东省科委基金