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 (23): 2198-2203.doi: 10.3969/j.issn.1673-5374.2013.23.010

• 原著:脑损伤修复保护与再生 • 上一篇    下一篇

细胞红蛋白基因过表达抑制细胞的缺氧损伤

  

  • 收稿日期:2013-04-14 修回日期:2013-07-21 出版日期:2013-08-15 发布日期:2013-08-15

Overexpression of cytoglobin gene inhibits hypoxic injury to SH-SY5Y neuroblastoma cells

Overexpression of cytoglobin gene inhibits hypoxic injury to SH-SY5Y neuroblastoma cells   

  • Received:2013-04-14 Revised:2013-07-21 Online:2013-08-15 Published:2013-08-15
  • Contact: Dianwen Gao, Chief physician, Professor, Doctoral supervisor, Department of Ophthalmology, Shengjing Hospital, China Medical University, Shenyang 110004, Liaoning Province, China, drgaodianwen@ 163.com.
  • About author:Xiuling Yu, M.D., Chief physician.

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摘要：

实验用pAcGFP1-C1-Cygb质粒转染SH-SY5Y细胞后，加入氯化钴诱导建立缺氧模型。Western blot检测显示，转染后SH-SY5Y细胞中细胞红蛋白呈过表达，而缺氧诱导因子1α微量表达；氯化钴诱导缺氧后，SH-SY5Y细胞中细胞红蛋白和缺氧诱导因子1α表达逐步增加。流式细胞仪结果显示，随着缺氧时间的延长，2组SH-SY5Y细胞正常细胞所占比例均显著减少，早期凋亡细胞比例增加，但转染组凋亡细胞比例明显低于未转染组。实验结果还说明，在细胞红蛋白减少缺氧诱导细胞死亡的同时，缺氧诱导因子1α蛋白表达水平增加，提示细胞红蛋白表达的氧依赖性与缺氧诱导因子1有关。

关键词: 神经再生, 细胞红蛋白, 绿色荧光蛋白, 缺氧, 转染, SH-SY5Y细胞, 氯化钴, 重组质粒, 神经保护

Abstract:

A plasmid for cytoglobin expression, pAcGFP1-C1-cytoglobin, was transfected into SH-SY5Y cells. Cobalt chloride was used to establish a model of hypoxia. Western blotting indicated that cytoglobin was overexpressed and there was low expression of hypoxia-inducible factor-1α in SH-SY5Y cells after transfection. Following cobalt chloride-induced hypoxia, cytoglobin and hypoxia-inducible fac-tor-1α expression gradually increased in SH-SY5Y cells. Flow cytometry showed that with increas-ing duration of hypoxia, the proportion of normal cells significantly diminished in the transfected and non-transfected groups. The proportion of cells in the early stages of apoptosis increased. However, the proportion of apoptotic cells was significantly lower in the transfected group compared with the non-transfected group. These results demonstrate that cytoglobin and hypoxia-inducible factor-1α are strongly up-regulated by hypoxia, and that there is a strong relationship between hypox-ia-inducible factor-1α and cytoglobin during hypoxic injury.