Expression of Nemo-Like Kinase (NLK) in the Brain in a Rat Experimental Subarachnoid Hemorrhage Model

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• 作者：Gang Chen (1)
  Dongxia Feng (2)
  Li Zhang (1) (3)
  Baoqi Dang (1)
  Huixiang Liu (3)
  Zhong Wang (1)
  
• 关键词：NLK ; Subarachnoid hemorrhage ; Apoptosis
• 刊名：Cell Biochemistry and Biophysics
• 出版年：2013
• 出版时间：July 2013
• 年：2013
• 卷：66
• 期：3
• 页码：671-680
• 全文大小：740KB
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• 作者单位：Gang Chen (1)
  Dongxia Feng (2)
  Li Zhang (1) (3)
  Baoqi Dang (1)
  Huixiang Liu (3)
  Zhong Wang (1)
  
  1. Department of Neurosurgery, The First Affiliated Hospital of Soochow University, 188 Shizi Street, Suzhou, 215006, Jiangsu, China
  2. Department of Neurosurgery, University of Arkansas for Medical Sciences, Little Rock, AR, 72205, USA
  3. Department of Neurosurgery, Zhangjiagang Hospital, Soochow University, Suzhou, 215600, Jiangsu, China
  

文摘

This study aimed to investigate the expression of the Nemo-like kinase (NLK) in the brain after experimental subarachnoid hemorrhage (SAH) in rats. A total of 90 rats were randomly divided into six groups: control group, day 1, day 3, day 5, day 7, and day 14. Day 1, day 3, day 5, day 7, and day 14 groups were all SAH groups in which the rats were killed on days 1, 3, 5, 7, and 14, respectively. In SAH groups, autologous arterial blood was injected into cisterna magna once on day 0. Cross-sectional area of basilar artery was measured by H&E staining. Immunostaining and immunoblotting experiments were performed to detect the expression of NLK protein. Real-time polymerase chain reaction was used to analyze the presence and quantity of NLK mRNA. The level of oxidative stress in the artery was also measured. The basilar arteries exhibited vasospasm after SAH and became the most severe on day 3. The expressions of NLK protein and mRNA were decreased remarkably in SAH groups compared with the control group. The down-regulated expression of NLK was detected after SAH and the low ebb was on day 3, which was oppositely the peak time of oxidative stress. The expression of NLK was present mainly in the neurons in the brain and smooth muscle cells in the basilar artery. NLK is decreasingly expressed in an opposite time-course to the development of cerebral vasospasm (CVS) and SAH-induced brain injury in this rat experimental model of SAH and these findings might have important implications during the administration of specific NLK agonist to prevent or reduce CVS or neuronal apoptosis caused by SAH.