中文摘要：

目的研究天珠散对脑缺血所致的血管性痴呆（VD）大鼠学习记忆相关指标的影响。方法双侧颈总动脉永久性结扎复制脑缺血所致学习记忆障碍大鼠模型,天珠散连续ig给药63 d,以Morris水迷宫实验检测大鼠学习记忆能力,脑海马组织HE染色和Nissl染色观察病理变化,免疫组织化学法检测大鼠海马微管相关蛋白-2（MAP-2）、突触素-1（SYN-1）表达。结果 Morris水迷宫实验,从第2天开始,模型组大鼠逃避潜伏期明显长于假手术组（P〈0.05、0.01）,尼莫地平组和天珠散给药组大鼠逃避潜伏期较模型组不同程度缩短（P〈0.05、0.01）。HE染色显示模型组大鼠脑海马CA1、CA3区神经细胞出现变形、坏死,尼莫地平、天珠散能减轻神经细胞损伤。Nissl染色显示,天珠散能增加海马CA1、CA3区尼氏体含量。尼莫地平能显著提高大鼠脑海马MAP-2表达,天珠散有增加MAP-2表达的趋势。SYN-1在不同区域表达结果不同,CA1、齿状回区模型组增加,CA3区下降,天珠散具有增加CA3区SYN-1表达趋势。结论天珠散能通过减轻脑组织神经细胞的损伤、促进神经递质的合成,调节MAP-2、SYN-1表达,改善慢性低灌注型VD大鼠的学习记忆能力。

英文摘要：

Objective To investigate the therapeutic effects of Tianzhusan （TZS） on the related indexes of learning and memory impairment of rats with vascular dementia （VD） caused by cerebral ischemia. Methods The rats＇ models were prepared by a permanent ligation of the bilateral common carotid arteries. After ig administration for 63 d, the learning and memory abilities of rats were observed with Morris water maze, the pathological changes in hippocampus were detected with HE staining and Nissl staining, and the expression levels ofmicrotubule associated protein-2 （MAP-2） and synaptophysin-1 （SYN-1） in hippocampus were evaluated by immunohistochemistry. Results The latent period of rots in the model group was longer than that in the control group obviously （P 〈 0.05）. However, the latent period of rats in Nimodipine and TZS groups was shortened after ig administration by different degrees. HE staining showed that the neuronal cells appeared necrosis and deformation in CA1 and CA3 areas ofhippocampus of rats in the model group, while Nimodipine and TZS could reduce these injuries. Nissl staining showed that TZS could increase the number of Nissl bodies in CA1 and CA3 areas of hippocampus. Nimodipine and TZS could improve the expression level of MAP-2 in hippocampus. The rats in the model group had a high expression of SYN-1 in CA1 and dentate gyrns areas, but a low expression in CA3 area. Nevertheless, TZS could increase the expression of SYN-1 in CA3 area. Conclusion TZS could improve the learning and memory abilities of VD rats by relieving the damage of neuronal cell, promoting the synthesis of neurotransmitters, and regulating the expression levels of MAP-2 and SYN- 1.