摘要
目的观察银杏叶提取物对拟血管性痴呆大鼠海马CA1区神经细胞的保护作用。方法反复夹闭再通大鼠双侧颈总动脉同时腹腔注射硝普钠制造拟血管性痴呆大鼠模型,采用Morris水迷宫和尼氏染色方法分别观察大鼠空间学习记忆能力及海马CA1区细胞形态学改变和细胞数目。结果模型组大鼠在1个月、2个月和4个月不同时间点测得的Morris水迷宫逃避潜伏期(EL)均较假手术组明显延长(P<0.01),药物组EL显著均短于模型组,但仍长于假手术组(P<0.05或0.01);各时间点模型组海马CA1区锥体细胞及其树突丢失,药物组锥体细胞数多于模型组。结论EGb761对海马CA1区的保护作用可能是其改善VD大鼠学习记忆障碍的重要机制。
Objective Observe the effects of EGb761 to protect the cells in the CAI area in hippoeampus of the vascular dementia rats. Methods VD rat models, established by repeatedly cerebral ischemia/reperfusion,were randomly divided into two groups：model group and EGb761 treated group （both n = 30） ,and another 30 condition-matched rats were selected as the sham-operated group. Spatial learning and memory ability and the microcosmic changes and the number of neurons in CAI area in different groups were assayed by Morris water maze （MWM） task and Nissl stain slices through microscopy respectively. Results The MWM escape latency （EL） of lnodel group were highl） longer than that of the sham-operated group （ P 〈 0.01 ） , while the EL of EGb761-treated group was significantly shorter than that of model group, but still longer than that of the sham-operated group at 1m,2m and 4m after VD modeling operation（ P 〈 0.05 or 0.01 ） . At different time points, the loss of pyramidal neurons and shortened apical dendrite of neurons were revealed in hippocampal CA1 area in the VD model group,while the rats in the EGb761-treated groups have more cells in the CAI area in hippocampus than those in the VD model group. Conclusion EGb761 couht protect the cells in the CA1 area in hippoealnpus,which may be one of important mechanisms of EGb761 in improving learning and memory dysfunction of VD rats.
出处
《潍坊医学院学报》
2006年第6期423-425,I0003,共4页
Acta Academiae Medicinae Weifang
基金
山东省教育厅科研基金资助项目(No:J01K09)
