中国神经再生研究(英文版) ›› 2016, Vol. 11 ›› Issue (8): 1278-1284.doi: 10.4103/1673-5374.189193

• 原著:脑损伤修复保护与再生 • 上一篇    下一篇

蛛网膜下腔出血后脑组织神经生长因子及其受体TrkA的动态表达

  

  • 出版日期:2016-08-31 发布日期:2016-08-31
  • 基金资助:
    国家自然科学基金(30870844)

Dynamic expression of nerve growth factor and its receptor TrkA after subarachnoid hemorrhage in rat brain

Jin-ning Song1, *, Zun-wei Liu1, Long Sui1, 2, Bin-fei Zhang1, Yong-lin Zhao1, Xu-dong Ma1, Hua Gu1   

  1. 1 Department of Neurosurgery, the First Affliated Hospital of Xi’an Jiaotong University, Xi’an, Shaanxi Province, China 2 Department of Neurosurgery, the 521 Hospital of China North Industries Group, Xi’an, Shaanxi Province, China
  • Online:2016-08-31 Published:2016-08-31
  • Contact: Jin-ning Song, M.D., jinningsong@126.com.
  • Supported by:
    This study was funded by the National Natural Science Foundation of China, No. 30870844; and the New Century Supporting Program to Excellent Talents in China, No. NCET-05-0831.

摘要:

蛛网膜下腔出血后发生的迟发性神经功能缺损,与脑内神经细胞丢失有关,神经生长因子及其受体TrkA可以促进神经细胞的再生,但其在蛛网膜下腔出血后的动态表达变化尚不清楚。实验采用枕大池二次注血法制作蛛网膜下腔出血大鼠模型,应用免疫组织化学染色发现,(1)蛛网膜下腔出血模型大鼠大脑皮质和脑干神经生长因子及TrkA表达在建模后6 h开始升高,12 h达到高峰,1 d后下降;(2)海马区神经生长因子和TrkA表达在建模后6 h开始升高,1 d达到高峰,3 d后下降;(3)建模后12 h和3 d,蛛网膜下腔出血模型大鼠神经功能出现明显障碍。(4)结果说明,蛛网膜下腔出血后,神经生长因子及其受体TrkA在脑组织中表达先增加后下降,呈明显的动态变化,发挥这一变化特点可为临床神经保护提供参考。 

orcid: 0000-0002-0620-8983 (Jin-ning Song)

关键词: 神经再生, 蛛网膜下腔出血, 神经生长因子, TrkA受体, 内源性, 动态表达, 神经再生, 皮质, 海马, 脑干, 急性期, 保护作用, 国家自然科学基金

Abstract: Delayed ischemic neurologic defcit after subarachnoid hemorrhage results from loss of neural cells. Nerve growth factor and its receptor TrkA may promote regeneration of neural cells, but their expression after subarachnoid hemorrhage remains unclear. In the present study, a rat model of subarachnoid hemorrhage was established using two injections of autologous blood into the cistern magna. Immunohistochemical staining suggested that the expression of nerve growth factor and TrkA in the cerebral cortex and brainstem increased at 6 hours, peaked at 12 hours and decreased 1 day after induction of subarachnoid hemorrhage, whereas the expression in the hippocampus increased at 6 hours, peaked on day 1, and decreased 3 days later. Compared with those for the rats in the sham and saline groups, neurobehavioral scores decreased signifcantly 12 hours and 3 days after subarachnoid hemorrhage (P < 0.05). These results suggest that the expression of nerve growth factor and its receptor TrkA is dynamically changed in the rat brain and may thus participate in neuronal survival and nerve regeneration after subarachnoid hemorrhage.

Key words: nerve regeneration, subarachnoid hemorrhage, nerve growth factor, TrkA, intrinsic, dynamic expression, cortex, hippocampus; brainstem, acute phase, neural regeneration