Age-related expression of STUB1 in senescence-accelerated mice and its response to anti-Alzheimer's disease traditional Chinese medicine

被引:25
作者
Zhang, Gui-Rong [1 ]
Cheng, Xiao-Rui [1 ]
Zhou, Wen-Xia [1 ]
Zhang, Yong-Xiang [1 ]
机构
[1] Beijing Inst Pharmacol & Toxicol, Dept Neuroimmunopharmacol, Beijing 100850, Peoples R China
基金
中国国家自然科学基金;
关键词
Alzheimer's disease; STIP1 homology and U-box-containing protein 1; senescence-accelerated mouse; traditional chinese medicine;
D O I
10.1016/j.neulet.2008.04.075
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Increasing evidences have indicated that STUB1 may be closely linked to Alzheimer's disease (AD). Senescence-accelerated mice (SAM) prone/8 (SAMP8) is a generally acknowledged animal model for senescence and AD, and SAM resistant/1 (SAMR1) is its control. in this study, we investigated the detailed expression of STUB1 in the brain of SAMP8 with aging and its responses to five anti-AD traditional Chinese medicinal (TCM), using real-time fluorescence quantitative PCR and Western blot technique. Results showed that with the aging process, both mRNA and protein expression of STUB1 in the cerebral cortex and hippocampus from SAMR1 increased after 2 months, while they decreased in brain tissues from SAMP8 after 6 months. Compared with SAMR1, the mRNA and protein expression of STUB1 decreased after 10 months in SAMP8 but could be up-regulated by the five anti-AD TCM used in this study. These results indicated that the expression of STUB1 in the brain of SAMP8 was abnormal and this abnormality could be reversed by anti-AD TCM. The data suggested that a deficiency in STUB1 may lead to a reduction in aberrant protein scavenging, causing abnormal protein accumulation in the brain of SAMP8. Thus, STUB1 might be a potential target for anti-AD TCM. (c) 2008 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:371 / 375
页数:5
相关论文
共 37 条
[31]  
Qiao Hai-fa, 2005, Zhongguo Zhong Xi Yi Jie He Za Zhi, V25, P429
[32]   In vivo evidence of CHIP up-regulation attenuating tau aggregation [J].
Sahara, N ;
Murayama, M ;
Mizoroki, T ;
Urushitani, M ;
Imai, Y ;
Takahashi, R ;
Murata, S ;
Tanaka, K ;
Takashima, A .
JOURNAL OF NEUROCHEMISTRY, 2005, 94 (05) :1254-1263
[33]   CHIP-Hsc70 complex ubiquitinates phosphorylated tau and enhances cell survival [J].
Shimura, H ;
Schwartz, D ;
Gygi, SP ;
Kosik, KS .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2004, 279 (06) :4869-4876
[34]   The co-chaperone carboxyl terminus of Hsp70-interacting protein (CHIP) mediates α-synuclein degradation decisions between proteasomal and lysosomal pathways [J].
Shin, YG ;
Klucken, J ;
Patterson, C ;
Hyman, BT ;
McLean, PJ .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2005, 280 (25) :23727-23734
[35]   Senescence-accelerated mouse (SAM): A novel murine model of senescence [J].
Takeda, T ;
Hosokawa, M ;
Higuchi, K .
EXPERIMENTAL GERONTOLOGY, 1997, 32 (1-2) :105-109
[36]   Stepwise proteolysis liberates tau fragments that nucleate the Alzheimer-like aggregation of full-length tau in a neuronal cell model [J].
Wang, Y. P. ;
Biernat, J. ;
Pickhardt, M. ;
Mandelkow, E. ;
Mandelkow, E.-M. .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2007, 104 (24) :10252-10257
[37]   Alzheimer's disease-related gene expression in the brain of senescence accelerated mouse [J].
Wei, XL ;
Zhang, YZ ;
Zhou, JH .
NEUROSCIENCE LETTERS, 1999, 268 (03) :139-142