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reseatch for the neuro-protection ofretina and optic nerve by trans-corneal electrical stimulation

经角膜电刺激对视网膜和视神经神经保护的研究

基本信息

批准号：
18591918
负责人：
FUJIKADO Takashi
金额：
$ 2.49万
依托单位：
Osaka University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2006
资助国家：
日本
起止时间：
2006 至 2007
项目状态：
已结题

项目摘要

(1). Molecular mechanism of neroprotection for the retina and optic nerve by trans-corneal electrical stimulation.Based on our previous report that trans-corneal electrical stimulation to the retina prevented neuronal death of retinal ganglion cells with up-regulation of Insulin-like growth factor 1(IGF1), we studied if IGF-1 was up-regulated by electrical stimulation to the cultured Mueller cells using RT-PCR. The result was that the mRNA of IGF-1 significantly increased if the mRNA was extracted just after the cessation of 30 minutes electrical stimulation. The Ca++ imaging showed that intracellular Ca++ concentration increased just after the start of electrical stimulation, reached 1.5 fold at 30minutes. The increase of Ca++ concentration was completely blocked by the application of Nifedipine, an L-type Ca++ channel blocker. These results indicated that the electrical stimulation promotes the transcription of IGF-1 gene and this phenomenon is related to the increase of intracellular concentration of Ca++ through the L-type Ca++ channel.(2). Clinical investigation of trans-corneal electrical stimulation to the optic neuropathyWe investigated the effect of trans-corneal electrical stimulation (TcES) to the eye with ischemic optic neumpathy (ION) or traumatic optic neumpathy (TON). Consecutive chromic patients with ION (20 eyes) and TON (10 eyes) who visited Osaka University hospital between June 2003 and May 2006 in which TcES was applied with an interval of 6 to 8 weeks were examined. The increase of visual acuity greater than 0.3 Log MAR unit were observed in 6 eyes (30%) of ION and 5 eyes (50%) of TON. No patient decreased vision more than 0.3 Log MAR unit. These data suggests that TcES is effecive in some patients with ION and TON.

（一）.经角膜电刺激对视网膜和视神经保护作用的分子机制基于我们先前的报道，即经角膜电刺激视网膜通过上调胰岛素样生长因子1（IGF-1）来防止视网膜神经节细胞的神经元死亡，我们使用RT-PCR研究了电刺激是否上调培养的Mueller细胞的IGF-1。结果表明，如果在停止30分钟电刺激后立即提取IGF-1的mRNA，则IGF-1的mRNA显著增加。Ca ~（++）显像显示，电刺激开始后，细胞内Ca ~（++）浓度迅速升高，30 min时达1.5倍。应用L型Ca++通道阻滞剂硝苯地平可完全阻断Ca++浓度的升高。结果表明，电刺激可促进IGF-1基因的转录，这一现象与L-型Ca ~（++）通道增加细胞内Ca ~（++）浓度有关。（二）、经角膜电刺激治疗视神经病变的临床研究我们观察了经角膜电刺激（trans-corneal electrical stimulation，TcES）对缺血性视神经病变（ischemic optic nephropathy，ION）和外伤性视神经病变（traumatic optic nephropathy，TON）的治疗效果。对2003年6月至2006年5月期间在大坂大学医院就诊的患有ION（20只眼）和TON（10只眼）的先天性色素沉着患者进行了检查，其中TcES应用间隔6至8周。术后视力提高> 0.3LogMAR单位者，ION组6眼（30%），TON组5眼（50%）。没有患者视力下降超过0.3 Log MAR单位。提示TcES对部分ION和TON患者有一定疗效。