Zhao Ting Ting, Shin Keon Sung, Park Hyun Jin, Kim Kyung Sook, Lee Kung Eun, Cho Yoon Jeong, Lee Myung Koo
Department of Pharmacy, College of Pharmacy, Chungbuk National University, 1, Chungdae-ro, Seowon-gu, Cheongju 28644, Republic of Korea; Research Center for Bioresource and Health, College of Pharmacy, Chungbuk National University, 1, Chungdae-ro, Seowon-gu, Cheongju 28644, Republic of Korea.
Department of Pharmacy, College of Pharmacy, Chungbuk National University, 1, Chungdae-ro, Seowon-gu, Cheongju 28644, Republic of Korea.
Neurosci Lett. 2016 Nov 10;634:114-118. doi: 10.1016/j.neulet.2016.09.055. Epub 2016 Oct 4.
This study investigated the effects of (-)-sesamin on memory deficits induced by chronic electric footshock (EF)-induced stress in mice. Mice were treated with (-)-sesamin (25 and 50mg/kg, p.o., daily for 21day) prior to chronic EF stress (0.6mA, 1s every 5s for 3min, daily for 21day). Transfer retention latencies in the elevated plus maze test and N-methyl-d-aspartate (NMDA) receptor (type 1) phosphorylation in the hippocampus increased with chronic EF stress, and they were reduced by treatment with (-)-sesamin at both doses. Phosphorylation of extracellular signal-regulated kinase (ERK1/2) and cyclic AMP-responsive element binding protein (CREB), which were reduced by chronic EF stress, were increased by treatment with (-)-sesamin. Retention latencies in the passive avoidance test and dopamine levels in the substantia nigra-striatum were also reduced by chronic EF stress, and similarly recovered with (-)-sesamin treatment. These results suggest that (-)-sesamin ameliorates the effects of chronic EF stress-induced spatial and habit learning memory deficits by modulating both NMDA receptor and dopaminergic neuronal systems.
本研究调查了（-）-芝麻素对慢性电足部电击（EF）诱导的小鼠应激所致记忆缺陷的影响。在慢性EF应激（0.6mA，每5秒1次，每次1秒，共3分钟，每天进行，持续21天）之前，给小鼠灌胃（-）-芝麻素（25和50mg/kg，每天1次，持续21天）。在高架十字迷宫试验中，转移潜伏期以及海马中N-甲基-D-天冬氨酸（NMDA）受体（1型）磷酸化水平随慢性EF应激而增加，而两种剂量的（-）-芝麻素处理均可使其降低。细胞外信号调节激酶（ERK1/2）和环磷腺苷反应元件结合蛋白（CREB）的磷酸化水平因慢性EF应激而降低，（-）-芝麻素处理可使其增加。慢性EF应激还降低了被动回避试验中的潜伏期以及黑质-纹状体中的多巴胺水平，（-）-芝麻素处理同样可使其恢复。这些结果表明，（-）-芝麻素通过调节NMDA受体和多巴胺能神经元系统，改善慢性EF应激诱导的空间和习惯学习记忆缺陷。
