Neuroprotective effect of 1-Deoxynojirimycin on cognitive impairment, β-amyloid deposition, and neuroinflammation in the SAMP8 mice

被引：30
作者：
Chen, Weike [1 ]
Liang, Tingting [1 ]
Zuo, Wenwen [1 ]
Wu, Xin [1 ]
Shen, Zibo [1 ]
Wang, Fang [3 ]
Li, Cunyu [1 ,2 ]
Zheng, Yunfeng [1 ,2 ]
Peng, Guoping [1 ,2 ]
机构：
[1] Nanjing Univ Chinese Med, Pharm Coll, Room 526,Zhongying Tang Sci & Tech Bldg, Nanjing 210023, Jiangsu, Peoples R China
[2] Jiangsu Collaborat Innovat Ctr Chinese Med Resour, Nanjing 210023, Jiangsu, Peoples R China
[3] Nanjing Univ Finance & Econ, Coll Food Sci & Engn, Nanjing 210023, Jiangsu, Peoples R China
来源：
BIOMEDICINE & PHARMACOTHERAPY | 2018年 / 106卷
基金：
中国国家自然科学基金;
关键词：
1-Deoxynojirimycin; SAMP8; mice; A beta deposition; Neuroinflammation; Microglia; BDNF/TrkB; ALZHEIMERS-DISEASE; MEMORY; MOUSE; ACTIVATION; MICROGLIA; PATHWAYS; BRAIN; MODEL; RATS;
D O I：
10.1016/j.biopha.2018.06.106
中图分类号：
R-3 [医学研究方法]; R3 [基础医学];
学科分类号：
1001 ;
摘要：
beta-amyloid deposition and neuroinflammation play a crucial part in Alzheimer's disease. Therefore, this study was designed to find the effects of 1-deoxynojirimycin (DNJ) purified from mulberry leaves on pathological deposition of A beta peptides and neuroinflammation in senescence-accelerated-prone mouse 8 (SAMP8) mice. Compared to senescence-accelerated-resistant mouse 1 (SAMR1) mice, SAMP8 mice exhibited conspicuous declines in spatial memory abilities and brain-derived neurotrophic factor (BDNF) and tyrosine kinase receptors (TrkB) level in hippocampus; increased A beta deposition, beta-secretase (BACE1) level, microglia activation and inflammatory factors, including interleukin-1 beta (IL-1 beta), interleukin-6 (IL-6) and tumor necrosis factor alpha(TNF-alpha) in the brain. The SAMP8 mice were treated with DNJ (40 or 160 mg/kg/day) by oral administration for two months. Our results indicated that DNJ treatment improved these changes, and the 160-mg/kg/day DNJ group revealed more significant alleviation. Therefore, DNJ potentially has the neuroprotective effect by inhibiting BACE1 expression, attenuating A beta deposition, remitting neuroinflammation, and up-regulating the BDNF/TrkB signal pathway in the brain.
引用
收藏
页码：92 / 97
页数：6
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