CAJ | 학술논문

目的观察缺血后处理(Ischemic postconditioning)对全脑缺血损伤后神经元结构可塑性及记忆的影响,从形态学的角度对缺血后处理的保护作用机制进行探讨.方法 SD成年雄性大鼠36只,随机数字表法分为为假手术组、全脑缺血15 min组、全脑缺血+后处理组,每组12只,处理方式为缺血/再灌注各15 s,循环3次.每组6只以Morris水迷宫观察学习记忆,重复性方差分析处理数据,另外6只以高尔基(golgi)银染观察神经元形态与树突棘密度变化,使用方差分析进行统计分析.结果缺血后处理组逃避潜伏期较全脑缺血组明显缩短(第3天P=0.014,第4天P=0.040第5天P=0.001),缺血后处理组树突棘密度较全脑缺血组明显增多(F=562.820,P＜0.01) 结论缺血后处理对脑缺血所致的记忆损伤有明显的保护作用,其机制可能与减少树突棘的损伤有关.
목적 관찰결혈후처리(Ischemic postconditioning)대전뇌결혈손상후신경원결구가소성급기억적영향,종형태학적각도대결혈후처리적보호작용궤제진행탐토.방법 SD성년웅성대서36지,수궤수자표법분위위가수술조、전뇌결혈15 min조、전뇌결혈+후처리조,매조12지,처리방식위결혈/재관주각15 s,순배3차.매조6지이Morris수미궁관찰학습기억,중복성방차분석처리수거,령외6지이고이기(golgi)은염관찰신경원형태여수돌극밀도변화,사용방차분석진행통계분석.결과 결혈후처리조도피잠복기교전뇌결혈조명현축단(제3천P=0.014,제4천P=0.040제5천P=0.001),결혈후처리조수돌극밀도교전뇌결혈조명현증다(F=562.820,P＜0.01) 결론결혈후처리대뇌결혈소치적기억손상유명현적보호작용,기궤제가능여감소수돌극적손상유관.
Objective To observe the effect of ischemic postconditioning on neuron structure plasticity and memory after global cerebral ischemia injury in rats and discuss the protection mechanism from aspect of Morphology. Methods A total of 36 SD male rats were randomly divided into sham operation group, global cerebral ischemia for 15 min group and global cerebral ischemia plus postconditioning group, 12 rats per group. The pullsinelli 4 vessel occlusion was applied to produce the models of global cerebral ischemia reperfusion injury, common carotid arteries (CCA) occlusion with 15 min and postconditioning with three cycles, of 15 sec release and 15 sec occlusion (15s/15s). Six rats from each group were evaluated by Morris Maze test for the ability of space learning and memory and the other six rats were evaluated by golgi stain for morphologic change of neuron. Results The ischemic postcondtioning group showed significant shorter mean escape latency compared with the sham operated group ( at day 3, P =0. 014; at day 4, P =0.040; at day 5, P =0.001 ). The density of dendritic spine in ischemic postcondtioning group was increased more significantly compared with ischemic group ( F = 562. 820,P ＜ 0. 01 ). Conclusion Ischemic postconditioning has obvious protective effect on cerebral ischemiainduced memory impairment, which may be related to alleviation of dendritic spine injury.