中国神经再生研究(英文版) ›› 2017, Vol. 12 ›› Issue (6): 918-924.doi: 10.4103/1673-5374.208573

• 原著:退行性病与再生 • 上一篇    下一篇

缺血预处理维持钙结合蛋白D28k表达保护海马CA1区缺血性锥体神经元损伤

  

  • 收稿日期:2017-05-15 出版日期:2017-06-15 发布日期:2017-06-15
  • 基金资助:

     

    韩国Hallym大学研究项目(HRF-201605-012);韩国教育部国家研究基金基础科学研究项目(NRF-2016R1A6A3A01011698).

Neuroprotective effects of ischemic preconditioning on hippocampal CA1 pyramidal neurons through maintaining calbindin D28k immunoreactivity following subsequent transient cerebral ischemia

 In Hye Kim1, Yong Hwan Jeon2, Tae-Kyeong Lee1, Jeong Hwi Cho1, Jae-Chul Lee1, Joon Ha Park3, Ji Hyeon Ahn3, Bich-Na Shin4, Yang Hee Kim5, Seongkweon Hong5, Bing Chun Yan6, Moo-Ho Won1, Yun Lyul Lee4   

  1. 1 Department of Neurobiology, School of Medicine, Kangwon National University, Chuncheon, South Korea; 2 Department of Radiology, School of Medicine, Kangwon National University, Chuncheon, South Korea; 3 Department of Biomedical Science, Research Institute of Bioscience and Biotechnology, Hallym University, Chuncheon, South Korea; 4 Department of Physiology, College of Medicine, Hallym University, Chuncheon, South Korea; 5 Department of Surgery, School of Medicine, Kangwon National University, Chuncheon, South Korea; 6 Institute of Integrative Traditional & Western Medicine, Medical College, Yangzhou University, Yangzhou, Jiangsu Province, China
  • Received:2017-05-15 Online:2017-06-15 Published:2017-06-15
  • Contact: Moo-Ho Won, D.V.M., Ph.D., or Yun Lyul Lee, D.V.M., Ph.D., mhwon@kangwon.ac.kr or yylee@hallym.ac.kr.
  • Supported by:

    This research was supported by Hallym University Research Fund, 2016 (HRF-201605-012), and by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education (NRF-2016R1A6A3A01011698).

摘要:

 

实验观察了2min的缺血预处理对5min的短暂性脑缺血致海马CA1区锥体神经元损伤的保护作用,以及钙结合蛋白D28k免疫反应的影响。发现5min的短暂性脑缺血后4d,海马CA1区锥体神经元出现大量死亡,而缺血预处理可以减少CA1区锥体神经元的死亡。同时还发现5min的短暂性脑缺血后2d,钙结合蛋白D28k免疫反应明显减弱,在缺血后5d几乎检测不到,缺血预处理则可维持短暂性脑缺血后的钙结合蛋白D28k免疫反应。这些结果说明缺血预处理可减轻短暂性脑缺血对海马CA1区锥体神经元的损伤,该作用是通过维持钙结合蛋白D28k的表达实现的。

ORCID:0000-0002-7178-6501(Moo-Ho Won);0000-0003-0504-5825(Yun Lyul Lee)

关键词: 神经再生, 神经保护, 短暂性脑缺血, 缺血耐受, 钙结合蛋白, 海马, 锥体神经元

Abstract:

Ischemic preconditioning elicited by a non-fatal brief occlusion of blood flow has been applied for an experimental therapeutic strategy against a subsequent fatal ischemic insult. In this study, we investigated the neuroprotective effects of ischemic preconditioning (2-minute transient cerebral ischemia) on calbindin D28k immunoreactivity in the gerbil hippocampal CA1 area following a subsequent fatal transient ischemic insult (5-minute transient cerebral ischemia). A large number of pyramidal neurons in the hippocampal CA1 area died 4 days after 5-minute transient cerebral ischemia. Ischemic preconditioning reduced the death of pyramidal neurons in the hippocampal CA1 area. Calbindin D28k immunoreactivity was greatly attenuated at 2 days after 5-minute transient cerebral ischemia and it was hardly detected at 5 days post-ischemia. Ischemic preconditioning maintained calbindin D28k immunoreactivity after transient cerebral ischemia. These findings suggest that ischemic preconditioning can attenuate transient cerebral ischemia-caused damage to the pyramidal neurons in the hippocampal CA1 area through maintaining calbindin D28k immunoreactivity.

Key words: nerve regeneration, transient cerebral ischemia, ischemic tolerance, neuroprotection, hippocampus, pyramidal neurons, calcium binding protein, neural regeneration