短期高脂饮食缓解冈田酸诱导的大鼠认知功能损伤  

Short term high-fat diet feeding alleviates the cognitive impairment induced by okada acid injection in rats

作　　者：朱天碧 张钊[2] 罗飘[1,2] 楚世峰 陈乃宏[1,2] 

机构地区：[1]湖南中医药大学药学院,湖南长沙410208 [2]中国医学科学院,北京协和医学院药物研究所神经科学中心,北京100050

出　　处：《药学学报》2018年第3期383-387,共5页Acta Pharmaceutica Sinica

基　　金：国家自然科学基金资助项目(81603316); 2017年湖南省中药饮片标准化及功能工程技术研究中心开放基金资助项目(BG201701); 中国医学科学院医学与健康科技创新工程经费资助项目(2016-I2M-1-004)

摘　　要：观察短期高脂饮食对阿尔茨海默病模型鼠认知功能损伤的影响及相关机制。建立阿尔茨海默病模型并给予高脂饮食喂养后,对大鼠进行水迷宫(Morris water maze,MWM)行为学实验检测动物的学习记忆能力。取材后对海马切片进行尼氏染色检测神经元损伤,Western blot检测NLRP3(NOD-like receptor family,pyrin domain containing 3)和caspase-1通路的表达。水迷宫结果表明短期高脂饮食能缓解冈田酸造成认知功能损伤,海马病理检测表明短期高脂饮食可能通过调节NLRP3及caspase-1信号通路缓解对神经元的损伤,发挥了神经保护功能。This study was designed to test the effect of short-term high-fat diet feeding on the cognitive impairment in a rat model of Alzheimer＇s disease. After establishment of Alzheimer＇s disease model, the rats were fed on a high-fat diet, and subjected to water maze（Morris water maze, MWM） behavioral test for learning and memory ability. Western blot was used to detect the expression of caspase-1 pathway. The results showed that short-term high-fat diet could alleviate the damage of okada acid in Morris water maze. The mechanism may be mediated by the regulation of the NLRP3/caspase-1 signaling pathway, which alleviates neuronal damage, resulting in a protective effect.

关 键 词：阿尔茨海默病 冈田酸 高脂饮食 神经保护 炎性小体 

分 类 号：R966[医药卫生—药理学]