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 (6): 945-952.doi: 10.4103/1673-5374.208589

• 原著:神经损伤修复保护与再生 • 上一篇    下一篇

单唾液酸神经节苷酯1可能缓解丙泊酚联合瑞芬太尼对神经干细胞的毒性作用

  

  • 收稿日期:2017-03-05 出版日期:2017-06-15 发布日期:2017-06-15
  • 基金资助:

    湖北省自然科学基金项目（2012FFC060）; 湖北医药学院自然科学基金项目（2011QDZR-2）; 十堰市科技项目（14Y13）; 教育部大学生创新创业训练计划项目（201610929005，201210929004）;湖北医药学院2016年教学研究项目（2016027）; 湖北医药学院2015年学科建设项目（2015）; 湖北医药学院附属太和医院2016年科技项目（2016JJXM001）

Monosialoganglioside 1 may alleviate neurotoxicity induced by propofol combined with remifentanil in neural stem cells

Jiang Lu1, 2, Xue-qin Yao1, 2, Xin Luo3, 5, Yu Wang2, Sookja Kim Chung4, He-xin Tang1, Chi Wai Cheung1, 3, 5, Xian-yu Wang1, 2, Chen Meng1, 2, Qing Li1, 2   

  1. 1 Anesthesiology Research Institute of Hubei University of Medicine, Shiyan, Hubei Province, China; 2 Department of Anesthesiology, Taihe Hospital, Hubei University of Medicine, Shiyan, Hubei Province, China; 3 Department of Anesthesiology, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong Special Administrative Region, China; 4 Department of Anatomy, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong Special Administrative Region, China; 5 Laboratory and Clinical Research Institute for Pain, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong Special Administrative Region, China
  • Received:2017-03-05 Online:2017-06-15 Published:2017-06-15
  • Contact: Qing Li, M.D. or Jiang Lu, M.D., liqing8801@163.com or lulujiangjiang@hotmail.com.
  • Supported by:

    This study was supported by the Natural Science Foundation of Hubei Province of China, No. 2012FFC060; the Natural Science Foundation of Hubei University of Medicine of China, No. 2011QDZR-2; a grant from the Scientific and Technological Project of Shiyan City of Hubei Province of China, No. 14Y13; a grant from the National College Student Innovation and Entrepreneurship Training Program of Education Ministry of China, No. 201610929005 and No. 201210929004; the Educational Scientific Foundation of Hubei University of Medicine of China in 2016, No. 2016027; the Fund of Disciplines Construction of Hubei University of Medicine of China in 2015, No. 2015; the Scientific Foundation of Affiliated Taihe Hospital of Hubei University of Medicine of China in 2016, No. 2016JJXM001.

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摘要：

单唾液酸神经节苷酯1是神经节苷脂的主要亚型，对中枢神经系统中具有神经保护作用，是否会抑制丙泊酚和瑞芬太尼相互作用在麻醉中对神经发育方面存在的不利影响？从新生SD大鼠海马组织中分离的神经干细胞分别加入瑞芬太尼(5，10，20ng/mL)、丙泊酚(1.0，2.5，5.0μg/mL)和/或单唾液酸神经节苷酯1(12.5，25，50μg/mL)，见单唾液酸神经节苷酯1能逆转丙泊酚联合瑞芬太尼干预后BrdU阳性细胞数量的减少，神经干细胞增殖和分化过程中凋亡细胞比例的增加以及神经干细胞分化过程中细胞内钙离子浓度的降低，但不影响神经干细胞分化过程中β-tubulin阳性细胞和神经胶质酸性蛋白阳性细胞的比例。说明单唾液酸神经节苷酯1可能缓解丙泊酚联合瑞芬太尼对神经干细胞的破坏作用，对未成熟中枢神经系统具有保护作用。

ORCID:0000-0003-4557-5839(Qing Li)；0000-0001-7553-1277(Jiang Lu)

关键词: 神经再生, 单唾液酸神经节苷酯1, 异丙酚, 瑞芬太尼, 神经干细胞, 神经毒性, 神经保护, 增殖, 分化, 细胞凋亡, 细胞内钙浓度

Abstract:

Monosialoganglioside 1 (GM1) is the main ganglioside subtype and has neuroprotective properties in the central nervous system. In this study, we aimed to determine whether GM1 alleviates neurotoxicity induced by moderate and high concentrations of propofol combined with remifentanil in the immature central nervous system. Hippocampal neural stem cells were isolated from newborn Sprague-Dawley rats and treated with remifentanil (5, 10, 20 ng/mL) and propofol (1.0, 2.5, 5.0 μg/mL), and/or GM1 (12.5, 25, 50 μg/mL). GM1 reversed combined propofol and remifentanil-induced decreases in the percentage of 5-bromodeoxyuridine(+) cells and also reversed the increase in apoptotic cell percentage during neural stem cell proliferation and differentiation. However, GM1 with combined propofol and remifentanil did not affect β-tubulin(+) or glial fibrillary acidic protein(+) cell percentage during neural stem cell differentiation. In conclusion, we show that GM1 alleviates the damaging effects of propofol combined with remifentanil at moderate and high exposure concentrations in neural stem cells in vitro, and exerts protective effects on the immature central nervous system.

Key words: nerve regeneration, monosialoganglioside 1, propofol, remifentanil, neural stem cells, neurotoxicity, neuroprotection, proliferation, differentiation, apoptosis, [Ca2+]i, neural regeneration