中国神经再生研究(英文版) ›› 2014, Vol. 9 ›› Issue (6): 630-636.doi: 10.4103/1673-5374.130108

• 原著:脑损伤修复保护与再生 • 上一篇    下一篇

黄芩苷抑制黑质损伤后铁积聚的机制:铁浓度变化与相关转铁蛋白的表达有关吗?

  

  • 收稿日期:2014-02-26 出版日期:2014-03-22 发布日期:2014-03-22
  • 基金资助:

    北京市教育委员会科技计划面上项目(KM20110025010)

Baicalin suppresses iron accumulation after substantia nigra injury: relationship between iron concentration and transferrin expression

Chunyan Guo, Xin Chen, Pei Xiong   

  1. Traditional Chinese Medicine School, Capital Medical University, Beijing, China
  • Received:2014-02-26 Online:2014-03-22 Published:2014-03-22
  • Contact: Xin Chen, Traditional Chinese Medicine School, Capital Medical University, Beijing 100069, China, chenxin4283@126.com.
  • Supported by:

    This work was supported by the Scientific Research Common Program of Beijing Municipal Commission of Education, No. KM20110025010.

摘要:

课题组以往研究表明,黄芩苷能够阻止脑黑质损伤后铁的积聚,并能降低鱼藤酮致帕金森病大鼠黑质内转铁蛋白二价金属离子转运体1的表达,同时升高膜铁转运蛋白1的表达,但铁浓度与这两个蛋白的表达是否具有相关性呢?鉴于此,实验同时封闭二价金属离子转运蛋白1和膜铁转运蛋白1受体,使C6细胞内转出铁含量减少41%。以噻唑蓝法及免疫组织化学法检测,显示不同浓度柠檬酸铁铵(10,50,100,400 µg/mL)负载C6细胞后,细胞存活率和膜铁转运蛋白1的表达与铁负载浓度呈负相关,而二价金属离子转运蛋白1的表达与铁负载浓度呈正相关。黄芩苷或去铁胺给药能使柠檬酸铁铵(100 µg/mL)负载的C6细胞内二价金属离子转运蛋白1表达减少,而膜铁转运蛋白1表达升高,结果表明,黄芩苷可下调细胞微环境铁离子浓度,铁离子浓度可正性调节转铁蛋白二价金属离子转运蛋白1的表达,负性调节膜铁转运蛋白1的表达,以此黑质损伤后的铁积聚。

关键词: 神经再生, 神经退行性变, 帕金森病, 铁, 黄芩苷, 二价金属离子转运蛋白1, 膜铁转运蛋白1, 去铁胺, C6细胞

Abstract:

Previous studies have shown that baicalin prevented iron accumulation after substantia nigra injury, reduced divalent metal transporter 1 expression, and increased ferroportin 1 expression in the substantia nigra of rotenone-induced Parkinson’s disease rats. In the current study, we investigated the relationship between iron accumulation and transferrin expression in C6 cells, to explore the mechanisms of the inhibitory effect of baicalin on iron accumulation observed in Parkinson’s disease rats. Iron content was detected using inductively coupled plasma-atomic emission spectroscopy. Results showed that iron content decreased 41% after blocking divalent metal transporter 1 and ferroportin 1 proteins. After treatment with ferric ammonium citrate of differing concentrations (10, 50, 100, 400 µg/mL) in C6 glioma cells, cell survival rate and ferroportin 1 expression were negatively correlated with ferric ammonium citrate concentration, but divalent metal transporter 1 expression positively correlated with ferric ammonium citrate concentration. Baicalin or deferoxamine reduced divalent metal transporter 1 expression, but increased ferroportin 1 expression in the 100 µg/mL ferric ammonium citrate-loaded C6 cells. These results indicate that baicalin down-regulated iron concentration, which positively regulated divalent metal transporter 1 expression and negatively regulated ferroportin 1 expression, and decreased iron accumulation in the substantia nigra.

Key words: nerve regeneration, Parkinson’s disease, iron, baicalin, divalent metal transporter 1, ferroportin 1, deferoxamine, C6 cells, the Scientific Research Common Program of Beijing Municipal Commission of Education, neural regeneration