莫里斯水上航行任务
丙二醛
超氧化物歧化酶
认知缺陷
认知功能衰退
树突棘
海马体
海马结构
谷胱甘肽过氧化物酶
突触可塑性
突触素
神经科学
化学
心理学
药理学
氧化应激
认知
医学
内科学
生物化学
痴呆
认知障碍
免疫组织化学
受体
疾病
作者
Jianxin Jia,Xu-Sheng Yan,Zhiping Cai,Wei Song,Dong-Sheng Huo,Bai-feng Zhang,He Wang,Zhan-Jun Yang
标识
DOI:10.1080/15287394.2017.1367097
摘要
Cognitive deficits are closely associated with hippocampal synaptic changes. Phenylethanoid glycosides (PhG), derived from Herba cistanche, are known to exert protective effects on cognitive deficits in Alzheimer's disease (AD); however, the underlying mechanisms of this herbal extract on cognitive performance remain unclear. The aim of this study was thus to examine the protective mechanism attributed to PhG on cognitive deficits in an AD senescence accelerated mouse prone 8 (SAMP8) model. Cognitive deficit parameters examined included (1) Morris water maze (MWM) assessing cognitive performance and (2) quantification of dendritic spine density in hippocampal CA1 region by Golgi staining, a molecular biomarker of synaptic function. In addition, levels of malondialdehyde (MDA) and activities of superoxide dismutase (SOD) and gluthathione peroxidase (GSH-Px) were determined to examine the potential role of oxidant processes in cognitive dysfunction. Data showed that PhG significantly decreased escape latency and path length, associated with a rise in the percentage of time spent in the target quadrant and number of platform crossings. In addition, PhG significantly increased dendritic spine density in the hippocampal CA1 region accompanied by elevated expression levels of synaptophysin (SYN) and post synaptic density 95 (PSD-95), reduced MDA content, and elevated the activities of SOD and GSH-Px. Data suggest that the ability of PhG to ameliorate cognitive deficits in SAMP8 mice may be related to promotion in synaptic plasticity involving antioxidant processes.
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