首页> 中文期刊>中国老年学杂志 >两种血管性痴呆模型大鼠学习记忆能力与海马自由基代谢的比较

两种血管性痴呆模型大鼠学习记忆能力与海马自由基代谢的比较

     

摘要

Objective To observe the learning and memory function and the changes of free radical metabolism in hippocampus of two kinds of vascular dementia (VD) rats induced by middle cerebral artery occlusion (MCAO) and common carotid artery (CCA). Methods Rat models with MCAO were established by line embolism method. Rat models with CCA were prepared by a permanent ligation of the bilateral common carotid artery (2-VO) . Then, the learning and memory function of rat models were detected by Morris water maze ( MWM) , and the content changes of GSH-Px, SOD, MDA in hippocampus of rat models were tested by biochemical method. Results The escape latency and swimming length in the hidden-platform acquisition training with MWM were significantly prolonged in MCAO and CCA models when rats were swimming trained on 1 ~4 d (P <0. 01 or P <0. 05). The extended escape latency and swimming length were appeared earlier in CCA models than those of MCAO models (P <0. 01 or P <0. 05) , and the dP/dT and crossing circle times were decreased in MCAO models(P<0.05,P<0.01). The content of MDA was increased, the contents of SOD and GSH-Px were reduced in hippocampus of MCAO and CCA models (P < 0. 05, P < 0. 01). But in the 2 kinds of models, there were not any significant differences in the content changes of MDA, SOD and GSH-Px. Conclusions The spatial memory is decreased significantly in CCA model, and the memory retention is poor in MCAO model. The metabolism of MDA, SOD and GSH-Px contribute to pathological process of VD induced by MCAO and CCA.%目的 观察两种拟血管性痴呆(VD)模型大鼠学习记忆能力及海马组织自由基代谢变化.方法 采用线栓法和双侧颈总动脉结扎法分别制备大脑中动脉梗死(MCAO)和慢性脑低灌注型(CCA)VD模型,Morris水迷宫检测痴呆大鼠的学习记忆功能,生化法检测模型大鼠海马组织中谷胱甘肽过氧化物酶(GSH-Px)、超氧化物歧化酶(SOD)、丙二醛(MDA)的含量变化.结果 在训练的1~4 d,MCAO模型和CCA模型大鼠逃避潜伏期和游泳路径延长(P<0.05,P<0.01),CCA模型出现逃避潜伏期和游泳路径延长的时间早于MCAO模型(P<0.05,P <0.01);MCAO模型大鼠的dP/dT和穿环次数均明显减少(P<0.05,P<0.01);MCAO模型与CCA模型大鼠海马组织MDA含量明显增加,SOD、GSH-Px的含量则明显下降(P <0.05,P<0.01),两种模型MDA、SOD、GSH-Px含量变化无显著差别.结论 CCA模型大鼠空间记忆能力下降明显,而MCAO模型记忆保持能力较差,MDA、SOD、GSH-Px代谢参与了MCAO和CCA所致血管性痴呆的病理过程.

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