中国神经再生研究(英文版) ›› 2016, Vol. 11 ›› Issue (5): 807-815.doi: 10.4103/1673-5374.182709

• 原著:退行性病与再生 • 上一篇    下一篇

适度运动可减缓D-半乳糖诱导衰老小鼠的神经退变

  

  • 收稿日期:2015-09-19 出版日期:2016-05-20 发布日期:2016-05-20
  • 基金资助:

    国家自然科学基金项目(81373020);北京市自然科学基金项目(7112014);北京市教育局科技发展项目(KM201110025014);北京市科技项目(Z131107002213071)

Moderate exercise prevents neurodegeneration in D-galactose-induced aging mice

Li Li1, Meng Xu1, Bo Shen1, Man Li2, Qian Gao2, Shou-gang Wei2, *   

  1. "1 Department of Infectious Medicine, Beijing YouAn Hospital Affiliated to Capital Medical University, Beijing, China 2 Department of Children’s and Women’s Health, School of Public Health, Capital Medical University, Beijing, China"
  • Received:2015-09-19 Online:2016-05-20 Published:2016-05-20
  • Contact: Shou-gang Wei, Ph.D., lily690123@sina.com.
  • Supported by:

    "This work was supported by the National Natural Science Foundation of China, No. 81373020; Beijing Natural Science Foundation of China, No. 7112014; a grant from the Science and Technology Development Project of Beijing Municipal Education Commission of China, No. KM201110025014; and a grant from the Beijing Municipal Science and Technology Project of China, No. Z131107002213071."

摘要:

我们以D-半乳糖衰老小鼠为研究对象,观察运动对其神经退变和记忆能力及空间学习能力影响的机制。连续10周通过颈部皮下注射D-半乳糖建立小鼠衰老模型,同时每周6d进行跑台运动。观察显示小鼠水迷宫潜伏期缩短,海马中凋亡相关蛋白Fas和Bax阳性神经元数量减少,Bcl-2和神经营养因子阳性神经元数量增加,神经元凋亡率降低,突触数量增加,突触体膜流动性降低,脑内葡萄糖转运体1,4增加。多种数据表明适度运动可减缓或抑制D-半乳糖诱导的衰老小鼠神经退行性变的发生。

orcid: 0000-0002-4102-4792(Li Li)

关键词: 神经再生, D-半乳糖, 脑老化, 行为表现, 神经元凋亡, 葡萄糖转运体, 突触可塑性, 脑源性神经营养因子, 神经退行性变

Abstract:

"D-galactose has been widely used in aging research because of its efficacy in inducing senescence and accelerating aging in animal models. The present study investigated the benefits of exercise for preventing neurodegeneration, such as synaptic plasticity, spatial learning and memory abilities, in mouse models of aging. D-galactose-induced aging mice were administered daily subcutaneous injections of D-galactose at the base of the neck for 10 consecutive weeks. Then, the mice were subjected to exercise training by running on a treadmill for 6 days a week. Shortened escape latency in a Morris water maze test indicated that exercise improved learning and memory in aging mice. The ameliorative changes were likely induced by an upregulation of Bcl-2 and brain-derived neurotrophic factor, the repression of apoptosis factors such as Fas and Bax, and an increase in the activity of glucose transporters-1 and 4. The data suggest moderate exercise may retard or inhibit neurodegeneration in D-galactose-induced aging mice."

Key words: nerve regeneration, D-galactose, brain aging, behavioral performance, brain-derived neurotrophic factor, neuronal apoptosis, glucose transporters, synaptic plasticity, neurodegeneration, neural regeneration