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作 者:胡冬华[1] 李雅兰[1] 梁赵佳[1] 钟曌 唐杰柯 廖婧 田和 汪梦霞[1] 佘高明 刘誉[2] 邢会杰 唐福星[4] Hu Donghua;Li Yalan;Liang Zhaojia;Zhong Zhao;Tang Jieke;Liao Jing;Tian He;Wang Mengxia;She Gaoming;Liu Yu;Xing Huijie;Tang Fuxing(Department of Anesthesia, First Affiliated Hospital, Jinan University, Guangzhou 510630, China;Department of Biochemistry ,Medical College, Jinan University, Guangzhou 510630, Chin;Institute of Laboratory Animal Science, Jinan University, Guangzhou 510630 , China;Analysis and Testing Center, Jinan University, Guangzhou 510630 , Chin)
机构地区:[1]暨南大学附属第一院麻醉科,510630 [2]暨南大学医学院生化教研室 [3]暨南大学实验动物中心 [4]暨南大学测试中心
出 处:《中华老年医学杂志》2018年第4期451-455,共5页Chinese Journal of Geriatrics
基 金:广东省科技计划项目(2009030801032)
摘 要:目的探讨长期髙脂饮食对肥胖SD大鼠认知功能和海马超微结构的影响。方法40只SD大鼠随机分为髙脂饮食(HFD)组和普通饮食(CD)组。建立高脂饮食诱发的肥胖SD大鼠模型,用水迷宫测试不同时期肥胖SD大鼠空间学习和记忆功能,应用透射电镜观察相应时期大鼠海马超微结构变化。结果高脂饲料喂养到12周、16周、20周的肥胖SD大鼠比普通饮食组大鼠平均重25%、28%和22%,Lee's指数比普通饮食组大鼠大6%、4%和8%。游泳平均潜伏期比普通饮食组大鼠长52%、44%和40%,平均游泳距离比普通饮食组长85%、45%和51%,平均游泳速度比普通饮食组大鼠快57%、34%和18%,其在平台所在象限停留的时间比普通饮食组短32%、54%和63%,穿越平台的次数比普通饮食组大鼠少30%、34%和34%(均P〈0.001)。而相应时期肥胖SD大鼠大脑海马CA1区退化、变性的神经元数量比普通饮食组多,畸形、空泡变性的线粒体数量比普通饮食组大鼠多,粗面内质网也是同样的变化趋势。结论长期髙脂饮食破坏肥胖SD大鼠海马的超微结构,损害SD肥胖大鼠的空间学习和记忆功能,加速认知老化。Objective To investigate the effect of long-term high-fat diet on cognitive function and hippocampus neurons ultrastructure in obese rats.MethodsForty SD rats were randomly assigned to a high-fat diet (HFD) group and a common diet (CD) group.Meanwhile, HFD-induced obese rat model were established.The spatial learning and memory were measured by the Morris water maze, and the neurons ultrastructural changes in rat hippocampus CA1 region at the corresponding period were observed by transmission electron microscopy.ResultsThe average weight of rats was 25%, 28%, and 22% higher in the HFD group than in the CD group at the 12, 16, and 20 weeks, respectively; the Lee's indexes were 6%, 4%, and 8% higher; the average swimming latency were 52%, 44%, and 40% longer; the average swimming distance were 85%, 45%, and 51% longer; the average swimming speed were 57%, 34%, and 18% higher; the duration of staying in the target quadrant were 32%, 54%, and 63% shorter; and the average times of crossing the plate-form were 30%, 34%, and 34% shorter, respectively (all P〈0.001). In comparison of ultrastructure in hippocampus CA1 region of rats at corresponding time points, the amounts of degenerated and necrosis neurons, of the deformed and vacuolar mitochondria, and of the less rough endoplasmic reticulum were significantly more at 12, 16, and 20 weeks in the HFD group than in the CD group.ConclusionsLong-term HFD-induced obesity damages the structure of neurons in the hippocampus, impairs spatial learning and memory function, and accelerates cognitive aging in rats.
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