中国神经再生研究(英文版)

中国神经再生研究(英文版) ›› 2013, Vol. 8 ›› Issue (11): 1016-1024.doi: 10.3969/j.issn.1673-5374.2013.11.007

• 原著:神经损伤修复保护与再生 • 上一篇    下一篇

激活素A干预氧糖剥夺神经元样细胞凋亡的过程

  

  • 收稿日期:2012-12-15 修回日期:2013-03-14 出版日期:2013-04-15 发布日期:2013-04-15

Activin A prevents neuron-like PC12 cell apoptosis after oxygen-glucose deprivation

Guihua Xu1, 2, Jinting He1, Hongliang Guo1, Chunli Mei1, Jiaoqi Wang1, Zhongshu Li1, Han Chen1, Jing Mang1, Hong Yang1, Zhongxin Xu1   

  1. 1 Department of Neurology, China-Japan Union Hospital, Jilin University, Changchun 130033, Jilin Province, China
    2 Department of Neurology, Changchun Central Hospital, Changchun 130051, Jilin Province, China
  • Received:2012-12-15 Revised:2013-03-14 Online:2013-04-15 Published:2013-04-15
  • Contact: Zhongxin Xu, Ph.D., Professor, Doctoral supervisor, Department of Neurology, China-Japan Union Hospital, Jilin University, Changchun 130031, Jilin Province, China, xuzhongxin999@ yahoo.com.cn. Jing Mang, Ph.D., Department of Neurology, China-Japan Union Hospital, Jilin University, Changchun 130031, Jilin Province, China, mangjing@jlu.edu.cn.
  • About author:Guihua Xu☆, Studying for doctorate.

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摘要：

实验以神经营养因子将PC12细胞诱导转化为神经元样细胞，建立氧糖剥夺模型，应用0，10，20，30，50，100ng/mL外源性激活素A进行干预。MTT染色和Hoechst33324染色显示氧糖剥夺后细胞存活率降低，凋亡率升高，而加入外源性激活素A可明显增加细胞的存活率，且效果呈剂量依赖性。反转录PCR检测结果显示，氧糖剥夺的神经元样细胞激活素A/smads信号转到通路关键位点激活素受体IIA，smad3和smad4 mRNA表达明显增加；而外源激活素A干预的细胞中激活素受体IIA ，smad3和smad4mRNA表达进一步增加，但凋亡关键调控基因caspase-3mRNA表达下降。提示外源性激活素A有对抗细胞凋亡保护神经元免受损伤的作用，其作用途径为激活素A/smads传导通路的激活进而发挥抗神经损伤的作用。 

关键词: 神经再生, 脑损伤, 生物因子, 氧糖剥夺, 激活素A, 激活素A/smads传导通路, caspase-3, 凋亡, 基金资助文章

Abstract:

In this study, PC12 cells were induced to differentiate into neuron-like cells using nerve growth factor, and were subjected to oxygen-glucose deprivation. Cells were treated with 0, 10, 20, 30, 50, 100 ng/mL exogenous Activin A. The 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl tetrazolium bromide assay and Hoechst 33324 staining showed that the survival percentage of PC12 cells significantly decreased and the rate of apoptosis significantly increased after oxygen-glucose deprivation. Exogenous Activin A significantly increased the survival percentage of PC12 cells in a dose-dependent manner. Reverse transcription-PCR results revealed a significant increase in Activin receptor IIA, Smad3 and Smad4 mRNA levels, which are key sites in the Activin A/Smads signaling pathway, in neuron-like cells subjected to oxygen-glucose deprivation, while mRNA expression of the apoptosis-regulation gene caspase-3 decreased. Our experimental findings indicate that exogenous Activin A plays an anti-apoptotic role and protects neurons by means of activating the Activin A/Smads signaling pathway.

Key words: neural regeneration, brain injury, biological factor, oxygen-glucose deprivation, Activin A, Activin A/Smads signaling pathway, caspase-3, apoptosis, grants-supported paper, neuroregeneration