中文摘要：

目的：构建β淀粉样蛋白1-42（Aβ1-42）联合D-半乳糖（D-gal）致痴呆模型,探讨枫叶黄酮抗氧化作用的分子机制。方法：36只成年雄性Sprague Dawley（SD）大鼠随机分为3组：假手术组、模型组、治疗组。采用侧脑室注射β淀粉样蛋白1-42（Aβ1-42）联合腹腔注射D半乳糖（D-gal）构建SD大鼠痴呆模型后经枫叶黄酮治疗,采用Morris水迷宫实验（MWM）检测大鼠学习记忆能力;用化学比色法检测大脑皮质丙二醛（MDA）和内源性巯醇抗氧化物（酶）：谷胱甘肽还原酶（glutathione reductase,GR）、谷胱甘肽（glutathione,GSH）、谷胱甘肽过氧化酶（glutathione peroxidase,GSH-PX）、超氧化物歧化酶（superoxide dismutase,SOD）的含量;免疫印迹法检测大脑皮质中丝裂原活化蛋白激酶（mitogen-activated protein kinase,MAPK）家族相关蛋白：细胞外信号调节蛋白激酶（extra-cellular signal-regulated protein kinase,ERK）、p38、c-Jun氨基末端激酶（c-Jun N-terminal kinase,JNK）的磷酸化水平。结果：模型组与假手术组比较：大鼠的逃避潜伏期明显延长（P〈0.05）,在第Ш象限逗留的时间明显减少（P〈0.05）,跨越平台次数明显减少（P〈0.05）;大脑皮质MDA含量增加（P〈0.05）,GR、GSH-PX的含量降低（P〈0.05）;p38、JNK磷酸化增强,ERK磷酸化水平降低。而枫叶黄酮治疗后：大鼠逃避潜伏期明显缩短（P〈0.05）,在第Ⅲ象限逗留的时间明显增加（P〈0.05）,跨越平台次数明显增加（P〈0.05）;大脑皮质MDA含量降低（P〈0.05）,GR、GSH-PX的含量升高（P〈0.05）;p38、JNK磷酸化被抑制,ERK的磷酸化增加。结论：枫叶黄酮能改善学习记忆能力,对抗大鼠神经系统衰老。其作用可能是通过上调痴呆模型大鼠大脑皮质内源性巯醇抗氧化物（酶）GR和GSH-PX的含量,抑制p38、JNK磷酸化并增强ERK磷酸化而实现的。

英文摘要：

Objective： To explore the anti-oxidative effects and relative molecular mechanism of the flavonoid,the Aβ1-42 plus D-galactose induced AD rat model was established.Methods： Male SD rats were randomly divided into three groups： sham group,model group and treatment group.AD rat models were established by lateral ventricle injection of Aβ1-42 and abdominal cavity injection of D-galactose.Meantime,the rats were treated by intragastric administration of the flavonoid.The spatial learning and memory capacity of experimental rats was examined by the morris water maze（MWM）.The concentration of the MDA and endogenous thiol antioxidants（including GR,GSH,GSH-PX,SOD） were examined by colorimetric method in the cerebral cortex.The concentration of the ERK,p38 and JNK,p-ERK,p-p38,p-JNK were examined by Western blotting methods.Results：When compared with control group,rats in model group exhibited a significant increase in escape latencies（P0.05）,while a decrease in the time of staying at the third quadrants of platform and the number of crossing over a platform;The concentration of MDA was increased（P0.05）,while the concentration of GR,GSH-PX were decreased in cerebral cortex（P0.05）;The expression of p-p38,p-JNK were increased,while the expression of p-ERK was decreased（P0.05）.After treatment of the Flavonoid,the AD model rats exhibited a significant decrease in escape latencies（P0.05）,an increase in the time of staying the third quadrants of platform（P0.05）,and the number of crossing over a platform compared with the model group（P0.05）.The concentration of MDA was decreased,while the concentration of GR,GSH-PX were increased（P0.05）.The expression of p-p38,p-JNK were decreased,while p-ERK was increased（P0.05）.Conclusion： The Flavonoid could improve the spatial learning and memory capacity and prevent the aging of central nervous systems in AD model rats by up-regulating the expression of the endogenous thiol antioxidants（including GR and GSH-PX） and p-ERK,down-regulat