黄芪苷为何能抑制脑黑质损伤后的铁积聚异常

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黄芪苷为何能抑制脑黑质损伤后的铁积聚异常

帕金森病患者脑内黑质部位可出现铁沉积,可能是神经变性疾病神经元死亡的原因之一,脑黑质铁积聚的机制仍不明确。课题组以往研究表明,黄芩苷作为唇形科中药黄芩的主要有效成分之一,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,升高膜铁转运蛋白1的表达,能够阻止脑黑质损伤后铁的积聚

SICENCE新闻发布作者：郭春彦稿号：N201304033 黄芪苷为何能抑制脑黑质损伤后的铁积聚异常

帕金森病患者脑内黑质部位可出现铁沉积，可能是神经变性疾病神经元死亡的原因之一，脑黑质铁积聚的机制仍不明确。课题组以往研究表明，黄芩苷作为唇形科中药黄芩的主要有效成分之一，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，升高膜铁转运蛋白1的表达，能够阻止脑黑质损伤后铁的积聚，但铁浓度与这两个蛋白的表达是否具有相关性呢？来自中国首都医科大学郭春彦所在课题组在以往研究此基础上，进一步探讨黄芩苷抑制帕金森病动物黑质铁积聚的机制，结果发现，黄芩苷下调了细胞微环境中铁离子的浓度，铁离子浓度可正性调节了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，阻止了黑质损伤后的铁积聚。研究成果发表在《中国神经再生研究（英文版）》杂志2014年3月第6期。

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免疫组织化学染色显示，黄芩苷抑制甲磺酸去铁胺（400 µg/mL）负载C6细胞中二价金属离子转运蛋白1的表达（箭头所指）

Article: " Baicalin suppresses iron accumulation after substantia nigra injury: relationship between iron concentration and transferrin expression," by Chunyan Guo, Xin Chen, Pei Xiong (Traditional Chinese Medicine School, Capital Medical University, Beijing, China)

Guo CY, Chen X, Xiong P. Baicalin suppresses iron accumulation after substantia nigra injury: relationship between iron concentration and transferrin expression. Neural Regen Res. 2014;9(6):630-636

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Baicalin suppresses iron accumulation after substantia nigra injury

A growing number of studies have shown that excessive iron is closely associated with the pathogenesis of Parkinson’s disease. Previous studies from Chunyan Guo and co-workers from Capital Medical University in China 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. However, the relationship between iron concentration and transferrin expression is still unclear. Based on the previous findings, these scholars further explored the mechanisms of the inhibitory effect of baicalin on iron accumulation observed in Parkinson’s disease rats. Their findings published in the Neural Regeneration Research (Vol. 9, No. 6, 2014) indicate that baicalin

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