Increased expression of ferritin in cerebral cortex after human traumatic brain injury

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• 作者：Huan-Dong Liu (1)
  Wei Li (2)
  Zhen-Rui Chen (1)
  Meng-Liang Zhou (2)
  Zong Zhuang (2)
  Ding-Ding Zhang (2)
  Lin Zhu (2)
  Chun-Hua Hang (1) (2)
  
• 关键词：Ferritin ; Iron ; Traumatic brain injury ; Inflammation
• 刊名：Neurological Sciences
• 出版年：2013
• 出版时间：July 2013
• 年：2013
• 卷：34
• 期：7
• 页码：1173-1180
• 全文大小：522KB
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• 作者单位：Huan-Dong Liu (1)
  Wei Li (2)
  Zhen-Rui Chen (1)
  Meng-Liang Zhou (2)
  Zong Zhuang (2)
  Ding-Ding Zhang (2)
  Lin Zhu (2)
  Chun-Hua Hang (1) (2)
  
  1. Department of Neurosurgery, School of Medicine, Southern Medical University (Guangzhou), Jinling Hospital, 305 East Zhongshan Road, Nanjing, 210002, Jiangsu Province, People’s Republic of China
  2. Department of Neurosurgery, Jinling Hospital, School of Medicine, Nanjing University, 305 East Zhongshan Road, Nanjing, 210002, Jiangsu Province, People’s Republic of China
  

文摘

Despite numerous researches and improvements in the past few years, the precise mechanisms underlying secondary brain injury after trauma remain obscure. Iron is essential for almost all types of cells, including nerve cells. However, excess of iron has been proved to contribute to the brain injury following trauma in animal models. As a key iron-handling protein in the brain, ferritin might be involved in iron-induced pathophysiological process of various brain disorders. Therefore, the current study was aimed to investigate the expression of ferritin in the human contused brain. Nineteen contused brain samples were obtained from 19 patients undergoing surgery for brain contusions 3?h-7?d after trauma, and three normal temporal pole samples from 3 patients with petroclival meningioma were collected as controls. Expression of ferritin-H-chain was measured by quantitative real-time polymerase chain reaction (PCR), western blot and immunohistochemistry, respectively. Perl’s reaction was taken for iron staining. The results showed that human traumatic brain injury (TBI) could up-regulate ferritin-H-chain in pericontusional cortex. A marked increase of ferritin was detected in the early group (?2?h), and remained elevated for a long time till after 48?h post-injury. The location of ferritin-H-chain was found mainly at the neuron-like cells and seldom at glia-like cells. Perl’s reaction showed that most of the iron-positive cells were glia-like cells. These findings suggested that iron and ferritin might be involved in the secondary brain injury and could be therapeutic targets for patients with TBI.