中国神经再生研究(英文版)

中国神经再生研究(英文版) ›› 2016, Vol. 11 ›› Issue (7): 1081-1089.doi: 10.4103/1673-5374.187039

• 原著:脑损伤修复保护与再生 • 上一篇    下一篇

缺血预处理对短暂性前脑缺血沙鼠海马CA1区氧化应激状态的影响

  

  • 出版日期:2016-07-30 发布日期:2016-07-30
  • 基金资助:
    韩国科学，ICT和未来计划部国家研究基金优先研究中心课题(NRF-2009-0093812)；韩国教育部国家基础科学研究基金(NRF-2014R1A1A2057013)

Effect of ischemic preconditioning on antioxidant status in the gerbil hippocampal CA1 region after transient forebrain ischemia

Seung Min Park1, 2, #, Chan Woo Park2, #, Tae-Kyeong Lee3, Jeong Hwi Cho3, Joon Ha Park3, Jae-Chul Lee3, Bai Hui Chen4, Bich-Na Shin4, Ji Hyeon Ahn5, Hyun-Jin Tae5, Myoung Cheol Shin2, Taek Geun Ohk2, Jun Hwi Cho2, Moo-Ho Won3, Soo Young Choi 5, *, In Hye Kim3, *   

  1. 1 Department of Emergency Medicine, Sacred Heart Hospital, College of Medicine, Hallym University, Anyang, South Korea 2 Department of Emergency Medicine, School of Medicine, Kangwon National University, Chuncheon, South Korea 3 Department of Neurobiology, School of Medicine, Kangwon National University, Chuncheon, South Korea 4 Department of Physiology, College of Medicine, Hallym University, Chuncheon, South Korea 5 Department of Biomedical Science, Research Institute of Bioscience and Biotechnology, Hallym University, Chuncheon, South Korea
  • Online:2016-07-30 Published:2016-07-30
  • Contact: In Hye Kim, Ph.D. or Soo Young Choi, Ph.D., inhye1987@naver.com or sychoi@hallym.ac.kr.
  • Supported by:
    This work was supported by a Priority Research Center Program grant (No. NRF-2009-0093812) through the National Research Foundation of Korea funded by the Ministry of Science, ICT and Future Planning; by 2015 Research Grant from Kangwon National University; and by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education (No.NRF-2014R1A1A2057013).

PDF

615

摘要：

缺血预处理可诱导脑组织产生内源性保护机制，提高脑组织对缺血的耐受性，但其作用机制尚不十分明确。实验旨在探讨缺血预处理对短暂性前脑缺血沙鼠海马CA1区抗氧化酶免疫反应的影响。沙鼠短暂性脑缺血后5d海马CA1区锥体细胞层大部分锥体神经元死亡，而缺血预处理则预防性抑制了锥体神经元的死亡。作者应用免疫组化和免疫印迹法检测发现假手术组沙鼠海马CA1区锥体神经元超氧化物歧化酶、过氧化氢酶和谷胱甘肽过氧化物酶免疫阳性反应很强、蛋白表达水平较高，但其在短暂性脑缺血后5d沙鼠海马CA1区锥体神经元中的免疫反应则很弱、蛋白表达水平较低，其免疫反应和蛋白表达在缺血预处理干预的缺血沙鼠海马CA1区中则维持在一个较高水平。说明缺血预处理可以维持或提高短暂性前脑缺血沙鼠海马CA1区抗氧化酶的活性，从而起到神经保护作用。 

orcid: 0000-0001-9216-6208 (In Hye Kim) 0000-0001-5541-4479 (Soo Young Choi)

关键词: 神经再生, 缺血预处理, 神经保护, 短暂性前脑缺血, 海马, 锥体神经元, 抗氧化酶

Abstract: Ischemic preconditioning (IPC) is a condition of sublethal transient global ischemia and exhibits neuroprotective effects against subsequent lethal ischemic insult. We, in this study, examined the neuroprotective effects of IPC and its effects on immunoreactive changes of antioxidant enzymes including superoxide dismutase (SOD) 1 and SOD2, catalase (CAT) and glutathione peroxidase (GPX) in the gerbil hippocampal CA1 region after transient forebrain ischemia. Pyramidal neurons of the stratum pyramidale (SP) in the hippocampal CA1 region of animals died 5 days after lethal transient ischemia without IPC (8.6% (ratio of remanent neurons) of the sham-operated group); however, IPC prevented the pyramidal neurons from subsequent lethal ischemic injury (92.3% (ratio of remanent neurons) of the sham-operated group). SOD1, SOD2, CAT and GPX immunoreactivities in the sham-operated animals were easily detected in pyramidal neurons in the stratum pyramidale (SP) of the hippocampal CA1 region, while all of these immunoreactivities were rarely detected in the stratum pyramidale at 5 days after lethal transient ischemia without IPC. Meanwhile, their immunoreactivities in the sham-operated animals with IPC were similar to (SOD1, SOD2 and CAT) or higher (GPX) than those in the sham-operated animals without IPC. Furthermore, their immunoreactivities in the stratum pyramidale of the ischemia-operated animals with IPC were steadily maintained after lethal ischemia/reperfusion. Results of western blot analysis for SOD1, SOD2, CAT and GPX were similar to immunohistochemical data. In conclusion, IPC maintained or increased the expression of antioxidant enzymes in the stratum pyramidale of the hippocampal CA1 region after subsequent lethal transient forebrain ischemia and IPC exhibited neuroprotective effects in the hippocampal CA1 region against transient forebrain ischemia.

Key words: nerve regeneration, ischemic preconditioning, neuroprotection, transient forebrain ischemia, pyramidal neurons, hippocampus, antioxidant enzymes, neural regeneration