中国神经再生研究(英文版)

中国神经再生研究(英文版) ›› 2017, Vol. 12 ›› Issue (4): 596-602.doi: 10.4103/1673-5374.205099

• 原著:脑损伤修复保护与再生 • 上一篇    下一篇

有氧运动联合虎纹蜘蛛毒素1可减轻慢性脑缺血损伤

  

  • 收稿日期:2017-02-28 出版日期:2017-04-15 发布日期:2017-04-15
  • 基金资助:

    江西省教育厅科技计划项目（GJJ14705）；江西省卫计委科技计划项目（20175563）

Aerobic exercise combined with huwentoxin-I mitigates chronic cerebral ischemia injury

Hai-feng Mao1, 2, Jun Xie2, Jia-qin Chen1, Chang-fa Tang1, Wei Chen1, Bo-cun Zhou1, Rui Chen1, Hong-lin Qu1, 2, Chu-zu Wu2   

  1. 1 Key Laboratory of Physical Fitness and Exercise Rehabilitation of Hunan Province, Hunan Normal University, Changsha, Hunan Province, China; 2 College of Physical Education, Yichun University, Yichun, Jiangxi Province, China)
  • Received:2017-02-28 Online:2017-04-15 Published:2017-04-15
  • Contact: Jia-qin Chen, M.D., chenjiaqin2010@sina.com.
  • Supported by:

    This work was supported by a grant from the Science and Technology Plans of Jiangxi Province Education Department of China, No. GJJ14705; a grant from the Science and Technology Plans of Health and Family Planning Commission of Jiangxi Province of China, No. 20175563.

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摘要：

Ca2+通道阻滞剂被认为可以保护神经元免受缺血损伤，同时研究显示有氧运动也对多种慢性疾病具有显著的保护作用。为此，我们对慢性脑缺血模型小鼠以0.05 μg/g的剂量尾静脉注射新型钙离子通道阻滞剂虎纹蜘蛛毒素1，每2d注射一次，共注射15次，同时接受/不接受跑台运动5周。发现慢性脑缺血小鼠大脑皮质损伤明显减轻，神经功能明显改善，且联合治疗的效果优于单独虎纹蜘蛛毒素1注射或有氧运动治疗；虎纹蜘蛛毒素1能有效激活慢性脑缺血小鼠脑组织及血液中Notch信号转导通路，有氧运动则能上调慢性脑缺血小鼠脑组织及血液中突触素mRNA的表达。结果显示有氧运动联合虎纹蜘蛛毒素1可通过Notch信号转导通路有效减轻慢性脑缺血导致的神经元损伤。

ORCID:0000-0002-2968-9193(Jia-qin Chen)

关键词: 神经再生, 慢性脑缺血损伤, 有氧运动, 虎纹蜘蛛毒素1, Notch信号通路, 钙超载

Abstract:

Ca2+ channel blockers have been shown to protect neurons from ischemia, and aerobic exercise has significant protective effects on a variety of chronic diseases. The present study injected huwentoxin-I (HWTX-I), a spider peptide toxin that blocks Ca2+ channels, into the caudal vein of a chronic cerebral ischemia mouse model, once every 2 days, for a total of 15 injections. During this time, a subgroup of mice was subjected to treadmill exercise for 5 weeks. Results showed amelioration of cortical injury and improved neurological function in mice with chronic cerebral ischemia in the HWTX-I + aerobic exercise group. The combined effects of HWTX-I and exercise were superior to HWTX-I or aerobic exercise alone. HWTX-I effectively activated the Notch signal transduction pathway in brain tissue. Aerobic exercise up-regulated synaptophysin mRNA expression. These results demonstrated that aerobic exercise, in combination with HWTX-I, effectively relieved neuronal injury induced by chronic cerebral ischemia via the Notch signaling pathway and promoting synaptic regeneration.

Key words: nerve regeneration, chronic cerebral ischemia, aerobic exercise, huwentoxin-I, Notch signaling pathway, calcium overload, neural regeneration