中国神经再生研究(英文版) ›› 2014, Vol. 9 ›› Issue (19): 1753-1762.doi: 10.4103/1673-5374.143419

• 原著:脑损伤修复保护与再生 • 上一篇    下一篇

脑缺血大鼠的炎症反应与神经元坏死

  

  • 收稿日期:2014-06-25 出版日期:2014-10-15 发布日期:2014-10-15
  • 基金资助:

    中国国家自然科学基金项目(81160148),江西省自然科学基金项目(2011033)

Inflammatory response and neuronal necrosis in rats with cerebral ischemia

Lingfeng Wu 1, 2, Kunnan Zhang 1, Guozhu Hu 3, Haiyu Yang 3, Chen Xie 3, Xiaomu Wu 1   

  1. 1 Nanchang University Medical College, Nanchang, Jiangxi Province, China
    2 Department of Neurology, People’s Hospital of Jiangxi Province, Nanchang, Jiangxi Province, China
    3 Institution of Neurology, People’s Hospital of Jiangxi Province, Nanchang, Jiangxi Province, China
  • Received:2014-06-25 Online:2014-10-15 Published:2014-10-15
  • Contact: Xiaomu Wu, M.D., Nanchang University Medical College, Nanchang 330006, Jiangxi Province, China, wu0709@hotmail.com.
  • Supported by:

    This project was supported by the National Natural Science Foundation of China, No. 81160148; the Natural Science Foundation of Jiangxi Province, No. 2011033.

摘要:

脑缺血后炎症反应主要发生于梗死区及其周围区域,且在损伤区域中神经元常出现坏死和凋亡,而此时会有小胶质细胞数量增加且被活化。为明确这一过程的变化途径,实验建立了大脑中动脉闭塞大鼠模型模拟脑缺血,发现在大脑中动脉闭塞12h后出现神经元凋亡,4-6d时达到峰值,炎症因子和小神经胶质细胞参与大脑中动脉闭塞损伤及修复过程,细胞间黏附分子1的表达与血脑屏障通透性呈正相关。提示细胞间黏附分子1可能参与破坏血脑屏障,激活小胶质细胞,参与大脑神经元凋亡过程。作者认为抑制其过程可产生对损伤神经元的保护效应。

关键词: 神经再生, 大脑中动脉闭塞, 炎症反应, 细胞间黏附分子1, 神经元, 血脑屏障, 小胶质细胞, NSFC grant

Abstract:

In the middle cerebral artery occlusion model of ischemic injury, inflammation primarily occurs in the infarct and peripheral zones. In the ischemic zone, neurons undergo necrosis and apoptosis, and a large number of reactive microglia are present. In the present study, we investigated the pathological changes in a rat model of middle cerebral artery occlusion. Neuronal necrosis appeared 12 hours after middle cerebral artery occlusion, and the peak of neuronal apoptosis appeared 4 to 6 days after middle cerebral artery occlusion. Inflammatory cytokines and microglia play a role in damage and repair after middle cerebral artery occlusion. Serum intercellular cell adhesion molecule-1 levels were positively correlated with the permeability of the blood-brain barrier. These findings indicate that intercellular cell adhesion molecule-1 may be involved in blood-brain barrier injury, microglial activation, and neuronal apoptosis. Inhibiting blood-brain barrier leakage may alleviate neuronal injury following ischemia.

Key words: nerve regeneration, middle cerebral artery occlusion, inflammatory reactions, intercellular cell adhesion molecule-1, neurons, blood-brain barrier, microglia, NSFC grant, neural regeneration