Effects of Sesaminol Feeding on Brain Aβ Accumulation in a Senescence-Accelerated Mouse-Prone 8

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• 作者：Shigeru Katayama ; Haruka Sugiyama ; Shoko Kushimoto ; Yusuke Uchiyama ; Masato Hirano ; Soichiro Nakamura
• 刊名：Journal of Agricultural and Food Chemistry
• 出版年：2016
• 出版时间：June 22, 2016
• 年：2016
• 卷：64
• 期：24
• 页码：4908-4913
• 全文大小：367K
• 年卷期：0
• ISSN：1520-5118

文摘

Alzheimer’s disease (AD) is characterized by the progressive accumulation of extracellular β-amyloid (Aβ) aggregates. Recently, the senescence-accelerated mouse-prone 8 (SAMP8) model was highlighted as a useful model of age-related AD. Therefore, we used the SAMP8 mouse to investigate the preventive effects of sesame lignans on the onset of AD-like pathology. In preliminary in vitro studies, sesaminol showed the greatest inhibitory effect on Aβ oligomerization and fibril formation relative to sesamin, sesamolin, and sesaminol triglucoside. Hence, sesaminol was selected for further evaluation in vivo. In SAMP8 mice, feed-through sesaminol (0.05%, w/w, in standard chow) administered over a 16 week period reduced brain Aβ accumulation and decreased serum 8-hydroxydeoxyguanosine, an indicator of oxidative stress. Furthermore, sesaminol administration increased the gene and protein expression of ADAM10, which is a protease centrally involved in the non-amyloidogenic processing of amyloid precursor protein. Taken together, these data suggest that long-term consumption of sesaminol may inhibit the accumulation of pathogenic Aβ in the brain.