中国神经再生研究(英文版) ›› 2013, Vol. 8 ›› Issue (15): 1360-1367.doi: 10.3969/j.issn.1673-5374.2013.15.002

• 原著:神经损伤修复保护与再生 • 上一篇    下一篇

大黄素对抗缺氧缺血性神经损伤的激活素A途径

  

  • 收稿日期:2012-08-13 修回日期:2013-03-18 出版日期:2013-05-25 发布日期:2013-05-25

Emodin prevents hypoxic-ischemic neuronal injury Involvement of the activin A pathway

Hongliang Guo1, 2, Xiaoran Shen3, Ye Xu4, Junliang Yuan1, Dongming Zhao2, Wenli Hu1   

  1. 1 Department of Neurology, Beijing Chaoyang Hospital Affiliated to Capital Medical University, Beijing 100020, China
    2 Beihua University, Jilin 132001, Jilin Province, China
    3 Jilin Municipal Central Hospital, Jilin 132001, Jilin Province, China
    4 Jilin Medical College, Jilin 132001, Jilin Province, China
  • Received:2012-08-13 Revised:2013-03-18 Online:2013-05-25 Published:2013-05-25
  • Contact: Wenli Hu, Doctoral supervisor, Professor, Department of Neurology, Beijing Chaoyang Hospital Affiliated to Capital Medical University, Beijing 100020, China, zz8898@ sina.com.
  • About author:Hongliang Guo☆, Ph.D., Associate chief physician. Hongliang Guo and Xiaoran Shen contributed equally to this study.

摘要:

从中药蓼科植物虎杖干燥根茎和根提取的大黄素被证明缺氧缺血性脑损伤神经元具有保护作用,实验旨在验证其作用途径。应用PC12细胞经小鼠神经生长因子刺激分化为神经元样细胞后,制备神经元细胞的氧糖剥夺模型,并在此基础上,给予大黄素干预。结果显示缺氧缺血环境培养的神经元样细胞的存活率下降,同时细胞中激活素A和caspase-3的表达水平增加;而大黄素则能提高氧糖剥夺神经元样细胞的生存率,进一步促进细胞中激活素A的表达,降低caspase-3表达水平。由此认为大黄素可通过激活素A途径抑制细胞凋亡,减轻氧糖剥夺神经细胞损伤。

关键词: 神经再生, 中医药, 大黄素, 氧糖剥夺, 激活素A, 凋亡, Caspase-3, 神经保护, 基金资助文章