中国神经再生研究(英文版)

中国神经再生研究(英文版) ›› 2013, Vol. 8 ›› Issue (16): 1491-1499.doi: 10.3969/j.issn.2095-4344.2012.33.027

• 原著:脑损伤修复保护与再生 • 上一篇    下一篇

脑损伤后JNK3基因参与神经细胞凋亡及神经功能恢复

  

  • 收稿日期:2012-12-07 修回日期:2013-03-08 出版日期:2013-06-05 发布日期:2013-06-05

JNK3 involvement in nerve cell apoptosis and neurofunctional recovery after traumatic brain injury

Jiang Long1, Li Cai1, Jintao Li2, Lei Zhang1, Haiyang Yang1, Tinghua Wang2   

  1. 1 Department of Neurosurgery, First Affiliated Hospital of Kunming Medical University, Kunming 650032, Yunnan Province, China
    2 Neuroscience Institute of Kunming Medical University, Kunming 650500, Yunnan Province, China
  • Received:2012-12-07 Revised:2013-03-08 Online:2013-06-05 Published:2013-06-05
  • Contact: Jiang Long☆, M.D., Associate chief physician, Department of Neurosurgery, First Affiliated Hospital of Kunming Medical University, Kunming 650032, Yunnan Province, China, longjiang69@163.com. Tinghua Wang, M.D., Professor, Neuroscience Institute of Kunming Medical University, Kunming 650500, Yunnan Province, China, tinghua_neuron@263.net.
  • About author:Jiang Long and Li Cai contributed equally to this work

PDF

996

摘要：

越来越多的证据表明,脑损伤后c-Jun氨基末端激酶(c-Jun amino-terminal kinase，JNK)通路的激活参与神经细胞凋亡及神经功能恢复。然而，通过激活JNK家族中哪些基因在发挥作用呢？目前并不十分明确。因此，实验采取原位末端标记法、反转录-聚合酶链反应、神经功能缺损评分方法，探讨脑损伤大鼠JNK1，JNK2，JNK3基因的表达变化，以及与神经元凋亡和神经功能改变的关系。发现大鼠脑组织JNK3表达在脑损伤后1h、6h、1d和7d下降，JNK1和JNK2的表达无明显变化，脑损伤皮质周边区凋亡神经细胞逐渐减少。大鼠神经功能缺损评分在脑损伤后1，3，5，7，14，28 d逐渐降低。说明JNK3在脑损伤后早期表达下调，可能与神经细胞凋亡有关，JNK3的下调可能促进脑损伤后神经功能的恢复。

关键词: 神经再生, 脑损伤, JNK1, JNK2, JNK3, 原位末端标记, 细胞凋亡, 神经功能恢复

Abstract:

Increasing evidence has revealed that the activation of the JNK pathway participates in apoptosis of nerve cells and neurological function recovery after traumatic brain injury. However, which genes in the JNK family are activated and their role in traumatic brain injury remain unclear. Therefore, in this study, in situ end labeling, reverse transcription-PCR and neurological function assessment were adopted to investigate the alteration of JNK1, JNK2 and JNK3 gene expression in cerebral injured rats, and their role in cell apoptosis and neurological function restoration. Results showed that JNK3 expression significantly decreased at 1 and 6 hours and 1 and 7 days post injury, but that JNK1 and JNK2 expression remained unchanged. In addition, the number of apoptotic nerve cells surrounding the injured cerebral cortex gradually reduced over time post injury. The Neurological Severity Scores gradually decreased over 1, 3, 5, 14 and 28 days post injury. These findings suggested that JNK3 expression was downregulated at early stages of brain injury, which may be associated with apoptosis of nerve cells. Downregulation of JNK3 expression may promote the recovery of neurological function following traumatic brain injury.

Key words: neural regeneration, JNK1, JNK2, JNK3, traumatic brain injury, TdT-mediated dUTP nick end labeling, reverse transcription-PCR, cell apoptosis, neurological function recovery, neuroregeneration