中国神经再生研究(英文版) ›› 2014, Vol. 9 ›› Issue (16): 1502-1505.doi: 10.4103/1673-5374.139472

• 观点:视神经损伤修复保护与再生 • 上一篇    下一篇

粒细胞集落刺激因子对大鼠前部缺血性视神经病变的神经保护效应

  

  • 收稿日期:2014-06-24 出版日期:2014-08-22 发布日期:2014-08-22

Efficacy of granulocyte-colony stimulating factor treatment in a rat model of anterior ischemic optic neuropathy

Shun-Ping Huang 1, Rong-Kung Tsai 2, 3   

  1. 1 Department of Molecular Biology and Human Genetics, Tzu Chi University, Hualien 97002, Taiwan, China
    2 Institute of Eye Research, Buddhist Tzu Chi General Hospital, Hualien 97002, Taiwan, China
    3 Institute of Medical Sciences, Tzu Chi University, Hualien 97002, Taiwan, China
  • Received:2014-06-24 Online:2014-08-22 Published:2014-08-22
  • Contact: Rong-Kung Tsai, M.D., Ph.D., Institute of Eye Research, Buddhist Tzu Chi General Hospital, Tzu Chi University, No. 707, Sec. 3, Chung-Yang Rd, Hualien, 97002, Taiwan, China, rktsai@tzuchi.com.tw.

摘要:

前部缺血性视神经病变是55岁以上老年人视觉损伤的主要原因,目前还缺乏有效的治疗方法。以往研究发现,粒细胞集落刺激因子及其受体广存在于成体中枢及视网膜系统。来自中国台湾慈济大学眼科研究所蔡荣坤教授所在研究小组的最新研究结果表明,粒细胞集落刺激因子对前部缺血性视神经病变大鼠有神经保护作用,其机制可能同时涉及抗凋亡和抗炎两个过程。他们未来研究的目标是评估粒细胞集落刺激因子和其他抗炎药物在前部缺血性视神经病变的作用途径,以便增加视网膜神经节细胞的存活量。这些研究可能为缺血性视神经病变的治疗开辟新的治疗途径。

Abstract:

Non-arteritic anterior ischemic optic neuropathy (NA-AION) is the most common cause of acute ischemic damage to the optic nerve (ON), and the leading cause of seriously impaired vision in people over 55 years of age. It demonstrated that subcutaneous administration of Granulocyte colony-stimulating factor (G-CSF) reduces RGC death in an ON crush model in rats, and that the neuroprotective effects may involve both anti-apoptotic and anti-inflammatory processes. Our recent work shows that the protective actions of G-CSF in rAION models may involve both anti-apoptotic and anti-inflammatory processes. However, the exact rescuing mechanisms involved in the administration of G-CSF in rAION models need further investigation. In addition, further studies on the administration of G-CSF at different time intervals after the induction of rAION may be able to illustrate whether treatment given at a later time is still neuroprotective. Further, it is unknown whether treatment using G-CSF combined with other drugs will result in a synergistic effect in a rAION model. Inflammation induced by ischemia plays an essential role on the ON head in NA-AION, which can result in disc edema and compartment changes. Therefore, it is reasonable that adding an anti-inflammatory drug may enhance the therapeutic effects of G-CSF. An ongoing goal is to evaluate the novel sites of action of both G-CSF and other anti-inflammatory drugs, and to identify the functionally protective pathways to enhance RGC survival. These investigations may open up new therapeutic avenues for the treatment of ischemic optic neuropathy.

Key words: optic nerve, anterior ischemic optic neuropathy, retinal damage, granulocyte colony-stimulating factor, inflammatory response