中文摘要：

目的：观察原花青素对淀粉样β蛋白25‐35（Aβ25‐35）诱导的小鼠学习记忆损伤的影响。方法将30只雄性2月龄C57bl／6小鼠随机均分为五组：E组为空白对照；其余四组采用双侧侧脑室注射Aβ25‐35制备的小鼠学习记忆损伤模型后，D组为模型对照，A、B和C组分别用原花青素50、100和150 mg／kg灌胃，连续30 d。D组和E组采用灭菌双蒸水灌胃。采用Y迷宫测试小鼠短期学习记忆能力；HE染色观察小鼠海马CA1区神经元损伤情况；化学比色法测定小鼠血清中丙二醛（MDA）、羟自由基（OH －）、谷胱甘肽（GSH）、总抗氧化能力（T‐AOC）和超氧化物歧化酶（SOD）表达水平；Western blot测定硝基络氨酸（NTS）、过氧化物还原酶1（Prdx‐1）在小鼠海马组织中的表达。结果与D组比较，A、B和C组小鼠短期学习记忆能力较好，CA1区深染神经细胞比例呈剂量依赖性下降，血清GSH、T‐AOC和SOD含量增高，且海马组织中NTS表达水平降低，Prdx‐1表达水平升高（ P＜0．01或P＜0．05）。结论原花青素能改善Aβ25‐35诱导的小鼠氧化应激水平，从而减轻小鼠海马神经退行性病变和小鼠学习记忆损伤。

英文摘要：

Objective To investigate the effect of procyanidins on learning and memery dysfunction induced by amyloid beta protein 25‐35（Aβ25‐35 ） in mice .Methods Thirty male C57bl/6 mice at 2 months of age were equally and randomly assigned into 5 groups .The mice in group E were taken as blank control .After mice models with learning and memery dysfunction induced by intracerebroventricular injection of Aβ25‐35 were established ,the mice in groups of A ,B and C were given procyanidin 50 ,100 and 150 mg/kg by gastric gavage daily for 30 days ,which in group D were given saline as model control .The Y maze was used to test the ability of learning and memory . Neruonal damage in the hippocampus CA1 area of mice was observed by HE staining .Serum levels of malondialdehyde（MDA） ,hydroxyl free radicals（OH - ） ,glutathione（GSH） ,total antioxidant capacity （T‐AOC） and superoxide dismutase（SOD） were detected by chemical colorimetric method .Western blot was used to detect the expression of nitrocomplex amino acid （NTS） and peroxide reductase‐1 （Prdx‐1） in the hippocampus of mice .Results Compared with group D ,the mice in groups of A ,B and C showed better short‐term learning and memory ability ,dose‐dependently decreased proportion of hyperchromatic nerve cells in CA1 area ,increased serum levels of GSH ,T‐AOC and SOD ,reduced expression of NTS and increased expression of Prdx‐1 in the hippocampus（P〈0 .01 or P〈0 .05） . Conclusion Procyanidins could attenuate hippocampal neural degeneration and damage of learning and memory ability induced by Aβ25‐35 in mice .