中文摘要：

目的观察毛冬青提取物（pubescent holly root extract,PHRE）对血管性痴呆（VD）模型小鼠学习记忆能力的影响,探讨其潜在的作用机制。方法采用反复夹闭、再通双侧颈总动脉同时尾静脉放血的方法制备小鼠痴呆模型,随后将小鼠随机分为假手术组,模型组,尼莫地平对照组（30 mg·kg-1）,毛冬青低、中、高剂量组（5,10,20 g·kg-1）,各组灌胃相应药物10 m L·kg-1,连续35 d,从第30天开始进行行为学检测,末次给药后收集大脑样本,HE染色观察病理学变化、免疫组化法及Western Blot法检测Bcl-2、Bax蛋白表达。结果与假手术组比较,模型组小鼠的恐惧记忆时间明显缩短,大脑海马区神经元细胞病变严重,海马区Bcl-2/Bax蛋白表达的比值降低,且主要分布于胞质。与模型组比较,各药物组小鼠的恐惧记忆时间明显延长,大脑海马区的组织病变情况改善,且海马区Bcl-2/Bax蛋白表达的比值显著增加。结论毛冬青提取物可能通过上调Bcl-2蛋白表达,下调Bax蛋白表达,减少细胞凋亡,保护神经细胞,从而改善血管性痴呆小鼠的学习记忆功能。

英文摘要：

Objective To explore the protective effect and mechanism of Radix Ilicis Pubescentis extract（RIPE）on memory and learning ability of mice model of vascular dementia（VD）. Methods Mice model of VD was established by repeatedly occlusion of common carotid artery and blood letting in caudal vein. The mice were evenly randomized into 6groups, namely sham operation group, model group, nimodipine positive group（30 mg·kg-1）, and low-dose,middle-dose and high-dose RIPE groups（in the dose of 5,10,20 g·kg-1respectively）. The corresponding drug was given by oral administration with 10 m L·kg-1for 35 d,and then the behavior tests were carried out on the 30 th day.The HE staining was used for the observation of the histopathological changes in the hippocampus,and the protein expression levels of Bcl-2 and Bax in the brain samples collected after the last administration were detected by immunocytochemistry and Western blotting. Results The VD model group exhibited a significant shortening of fear memory time,severe lesions in the neurons of the hippocampus,and decreased Bcl-2/Bax ratio mainly located in the cytoplasm as compared with the sham operation group. Compared with the model group,the fear memory time of RIPE groups and nimodipine group was markedly prolonged, the number of necrotic neurons was decreased, and the progressive increase of Bcl-2/Bax ratio was present. Conclusion PHRE improves the learning and memory ability of VD model mice, and the mechanism might be involved with the inhibition of the apoptosis of neurons in the hippocampus via up-regulating the expression of Bcl-2 and down-regulating Bax expression.