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精氨酸对非动脉炎性缺血性视神经病变啮齿动物模型眼解剖和电生理恶化的影响。

Effects of L-arginine on anatomical and electrophysiological deterioration of the eye in a rodent model of nonarteritic ischemic optic neuropathy.

机构信息

Department of Ophthalmology, Faculty of Medicine, University of Miyazaki, 5200 Kihara, Kiyotake, Miyazaki, Miyazaki Prefecture 889-1692, Japan.

出版信息

Jpn J Ophthalmol. 2013 Jul;57(4):402-9. doi: 10.1007/s10384-013-0250-z. Epub 2013 May 29.

DOI:10.1007/s10384-013-0250-z
PMID:23712653
Abstract

PURPOSE

The aims of this study were to clarify the effectiveness of L-arginine (1) for reducing the severity of anatomical changes in the eye and improving visual function in the acute stage of a rodent model of nonarteritic ischemic optic neuropathy (rNAION) and (2) in preventing those changes in anatomy and visual function.

METHODS

For the first aim, L-arginine was intravenously injected into rats 3 h after rNAION induction; for the second aim, rNAION was induced after the oral administration of L-arginine for 7 days. The inner retinal thickness was determined over time by optical coherence tomography, and the amplitude of the scotopic threshold response (STR) and the number of surviving retinal ganglion cells (RGCs) were measured. These data were compared with the baseline data from the control group.

RESULTS

Both intravenous infusion of L-arginine after rNAION induction and oral pretreatment with L-arginine significantly decreased optic disc edema in the acute stage and thinning of the inner retina, reduced the decrease in STR amplitude, and reduced the decrease in the number of RGCs during rNAION.

CONCLUSION

Based on these results, we conclude that L-arginine treatment is effective for reducing anatomical changes in the eye and improving visual function in the acute stage of rNAION and that pretreatment with L-arginine is an effective therapy to reduce the severity of the condition during recurrence in the other eye.

摘要

目的

本研究旨在阐明精氨酸(1)在减轻啮齿动物非动脉炎性缺血性视神经病变(rNAION)模型急性发作时眼部解剖结构变化的严重程度和改善视觉功能方面的有效性,以及(2)预防这些解剖结构和视觉功能变化的效果。

方法

为了达到第一个目的,在 rNAION 诱导后 3 小时,将精氨酸静脉内注射到大鼠体内;为了达到第二个目的,在 rNAION 诱导前,通过口服精氨酸进行 7 天的预处理。通过光学相干断层扫描随时间确定内视网膜厚度,测量暗适应阈值反应(STR)的幅度和存活的视网膜神经节细胞(RGC)的数量。将这些数据与对照组的基线数据进行比较。

结果

rNAION 诱导后静脉内输注精氨酸和口服精氨酸预处理均可显著减轻急性发作时视盘水肿和内视网膜变薄,减少 STR 幅度的下降,并减少 rNAION 期间 RGC 数量的减少。

结论

基于这些结果,我们得出结论,精氨酸治疗可有效减轻 rNAION 急性发作时眼部解剖结构的变化,改善视觉功能,而 rNAION 复发时进行精氨酸预处理可有效减轻病情的严重程度。

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Jpn J Ophthalmol. 2013 May;57(3):327-32. doi: 10.1007/s10384-012-0195-7. Epub 2012 Oct 10.
2
Rodent model of nonarteritic ischemic optic neuropathy and its electrophysiological evaluation.非动脉炎性缺血性视神经病变的啮齿动物模型及其电生理学评估。
Jpn J Ophthalmol. 2012 Sep;56(5):518-27. doi: 10.1007/s10384-012-0167-y. Epub 2012 Aug 3.
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Nonarteritic anterior ischemic optic neuropathy (NAION) and its experimental models.
非动脉炎性前部缺血性视神经病变(NAION)及其实验模型。
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The contribution of L-arginine to the neurotoxicity of recombinant tissue plasminogen activator following cerebral ischemia: a review of rtPA neurotoxicity.精氨酸对缺血性脑卒中后重组组织型纤溶酶原激活物神经毒性的作用:rtPA 神经毒性的综述。
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