中国神经再生研究(英文版) ›› 2016, Vol. 11 ›› Issue (5): 752-757.doi: 10.4103/1673-5374.182701

• 原著:脑损伤修复保护与再生 • 上一篇    下一篇

752-757

  

  • 收稿日期:2016-01-06 出版日期:2016-05-20 发布日期:2016-05-20
  • 基金资助:

    国家自然科学基金(81001541);福建省自然科学基金(2013J01331)

Inhibition of TYRO3/Akt signaling participates in hypoxic injury in hippocampal neurons

Yan-zhen Zhu, Wei Wang, Na Xian, Bing Wu   

  1. School of Basic Medical Sciences, Fujian Medical University, Fuzhou, Fujian Province, China
  • Received:2016-01-06 Online:2016-05-20 Published:2016-05-20
  • Contact: Yan-zhen Zhu, zhuyanzhen1976@126.com.
  • Supported by:

    "This study was supported by the National Natural Science Foundation of China, No. 81001541; the Natural Science Foundation of Fujian Province of China, No. 2013J01331."

摘要:

实验旨在通过缺氧海马神经元原代培养模型,揭示Tyro 3/Akt信号在缺氧导致海马神经元损伤中的作用。以MTT 法显示缺氧抑制神经元增殖活力,TUNEL 法证实缺氧导致神经元凋亡,并呈时间依赖性。以免疫荧光法显示缺氧抑制细胞Tyro 3蛋白表达,Western blot法表明缺氧降低Akt的磷酸化水平,并随缺氧时间的延长呈加重的趋势。结局说明缺氧具有抑制海马神经元增殖,促进细胞凋亡的作用,并且Tyro 3/Akt信号受抑制在缺氧导致海马神经元损伤过程中是起到重要作用的2个事件。

orcid: 0000-0001-6090-7497(Yan-zhen Zhu)

关键词: 神经再生, Tyro 3, Akt, 凋亡, 海马神经元, 原代培养, 缺氧, 增殖

Abstract:

"In this study, we investigated the role of the TYRO3/Akt signaling pathway in hypoxic injury to hippocampal neurons. 3-(4,5-Dimethylthiazol- 2-yl)-2,5-diphenyltetrazolium bromide assay showed that hypoxia inhibited the proliferation and viability of hippocampal neurons. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling assay demonstrated that hypoxia induced neuronal apoptosis in a time-dependent manner, with a greater number of apoptotic cells with longer hypoxic exposure. Immunofluorescence labeling revealed that hypoxia suppressed TYRO3 expression. Western blot assay showed that hypoxia decreased Akt phosphorylation levels in a time-dependent manner. Taken together, these findings suggest that hypoxia inhibits the proliferation of hippocampal neurons and promotes apoptosis, and that the inhibition of the TYRO3/Akt signaling pathway plays an important role in hypoxia-induced neuronal injury."

Key words: nerve regeneration, TYRO3, Akt, apoptosis, hippocampal neurons, primary culture, hypoxia, proliferation, neural regeneration