晶状体损伤对RCS大鼠光感受器的保护作用

ISRN ophthalmology Pub Date : 2013-09-19 eCollection Date: 2013-01-01 DOI:10.1155/2013/814814
Peter Heiduschka, Daniel Renninger, Dietmar Fischer, Adrienne Müller, Sabine Hofmeister, Ulrich Schraermeyer
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引用次数: 9

摘要

晶状体损伤诱导视网膜胶质细胞活化,随后释放睫状体神经营养因子(CNTF)和白血病抑制因子(LIF),有效地保护被轴突切除的视网膜神经节细胞免于凋亡,促进受损视神经轴突再生。本研究的目的是研究是否类似的效果也适用于视网膜色素变性模型的光感受器的恢复。在皇家外科学院(RCS)大鼠1月龄时进行晶状体损伤。用组织学方法评估光感受器的存活,用视网膜电图(ERG)分析视网膜功能。同时分析CNTF的表达。与未治疗的对照组相比,晶状体损伤显著提高了术后1个月光感受器的存活率,这与增强的ERG反应有关。此外,晶状体损伤显著保护对侧眼的光感受器免受变性,尽管程度要小得多。我们可以证明晶状体损伤足以暂时延缓RCS大鼠光感受器的退化。观察到的神经保护作用可能至少部分是由晶状体损伤后CNTF表达上调介导的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Lens Injury Has a Protective Effect on Photoreceptors in the RCS Rat.

Lens Injury Has a Protective Effect on Photoreceptors in the RCS Rat.

Lens Injury Has a Protective Effect on Photoreceptors in the RCS Rat.

Lens Injury Has a Protective Effect on Photoreceptors in the RCS Rat.

Lens injury induced activation of retinal glia, and subsequent release of ciliary neurotrophic factor (CNTF) and leukaemia inhibitory factor (LIF) potently protect axotomised retinal ganglion cells from apoptosis and promotes axon regeneration in the injured optic nerve. The goal of the current study was to investigate if similar effects may also be applicable to rescue photoreceptors from degeneration in a model of retinitis pigmentosa. Lens injury was performed in the Royal College of Surgeons (RCS) rats at the age of one month. The survival of photoreceptors was evaluated histologically, and retinal function was analysed by electroretinography (ERG). Expression of CNTF was also analysed. Lens injury significantly enhanced the survival of photoreceptors 1 month after surgery compared to untreated controls, which was associated with an enhanced ERG response. In addition, lens injury significantly protected photoreceptors from degeneration in the contralateral eye, although to a much lesser extent. We could show that lens injury is sufficient to transiently delay the degeneration of photoreceptors in the RCS rat. The observed neuroprotective effects may be at least partially mediated by an upregulation of CNTF expression seen after lens injury.

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