Graphene quantum dots conjugated neuroprotective peptide improve learning and memory capability

被引:126
|
作者
Xiao, Songhua [1 ]
Zhou, Daoyou [2 ,3 ]
Luan, Ping [4 ]
Gu, Beibei [5 ]
Feng, Longbao [6 ]
Fan, Shengnuo [1 ]
Liao, Wang [1 ]
Fang, Wenli [1 ]
Yang, Lianhong [1 ]
Tao, Enxiang [1 ]
Guo, Rui [6 ]
Liu, Jun [1 ,7 ,8 ]
机构
[1] Sun Yat Sen Univ, Sun Yat Sen Mem Hosp, Dept Neurol, 107 Yanjiang West Rd, Guangzhou 510120, Peoples R China
[2] Guangdong Prov Hosp Tradit Chinese Med, Dept Neurol, Guangzhou 510120, Peoples R China
[3] Guangdong Prov Hosp Tradit Chinese Med, Outpatient Dept Internal Med, Guangzhou 510120, Peoples R China
[4] Shenzhen Univ, Sch Med, 3688 Nanhai Ave, Shenzhen 518060, Peoples R China
[5] Sun Yat Sen Univ, Sun Yat Sen Mem Hosp, Dept Anesthesiol, Guangzhou 510120, Peoples R China
[6] Jinan Univ, Dept Biomed Engn, Key Lab Biomat, Guangdong Higher Educ Inst, Guangzhou 510632, Guangdong, Peoples R China
[7] Sun Yat Sen Univ, Sun Yat Sen Mem Hosp, Lab RNA & Major Dis Brain & Heart, Guangzhou 510120, Peoples R China
[8] Sun Yat Sen Univ, Zhongshan Sch Med, Guangdong Prov Key Lab Brain Funct & Dis, Guangzhou 510080, Guangdong, Peoples R China
基金
中国国家自然科学基金;
关键词
Graphene quantum dots; Neuroprotective peptide; Amyloid-beta (A beta); Dendritic spine; Alzheimer disease (AD); INDUCED SOMATOSTATIN DEPLETION; ALZHEIMERS-DISEASE MICE; CENTRAL-NERVOUS-SYSTEM; N-TERMINAL TRIPEPTIDE; GROWTH-FACTOR-I; AMYLOID AGGREGATION; NEUROTROPHIC FACTOR; DRUG-DELIVERY; MESSENGER-RNA; BETA;
D O I
10.1016/j.biomaterials.2016.08.021
中图分类号
R318 [生物医学工程];
学科分类号
0831 ;
摘要
Alzheimer disease (AD) is a neurodegenerative disorder and the most common form of dementia. Histopathologically is characterized by the presence extracellular neuritic plaques and with a large number of neurons lost. In this paper, we design a new nanomaterial, graphene quantum dots (GQDs) conjugated neuroprotective peptide glycine-proline-glutamate (GQDG) and administer it to APP/PS1 transgenic mice. The in vitro assays including ThT and CD proved that GQDs and GQDG could inhibit the aggregation of A beta(1-42) fibrils. Morris water maze was performed to exanimate learning and memory capacity of APP/PS1 transgenic mice. The surface area of A beta plaque deposits reduced in the GQDG group compared to the Tg Ctrl groups. Furthermore, newly generated neuronal precursor cell and neuron were test by immunohistochemical. Besides, neurons were impregnated by Dil using gene gun to show dendritic spine. Results indicated enhancement of learning and memory capacity and increased amounts of dendritic spine were observed. Inflammation factors and amyloid-beta (A beta) were tested with suspension array and ELISA, respectively. Several pro-inflammatory cytokines (IL-1 alpha, IL-1 beta, IL-6, IL-33, IL-17 alpha, MIP-1 beta and TNF-alpha) had decreased in GQDG group compared with Control group. Reversely, anti-inflammatory cytokines (IL-4, IL-10) had increased in GQDG group compared with Control group. Thus, we demonstrate that the GQDG is a promising drug in treatment of neurodegenerative diseases such as AD. (C) 2016 Elsevier Ltd. All rights reserved.
引用
收藏
页码:98 / 110
页数:13
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