Hannon Bailey G, Luna Coralia, Feola Andrew J, Ritch Matthew D, Read A Thomas, Stinnett Sandra S, Vo Harrison, Pardue Machelle T, Gonzalez Pedro, Ethier C Ross
George W. Woodruff School of Mechanical Engineering, Georgia Institute of Technology, Atlanta, GA, USA.
Duke Ophthalmology, Duke University School of Medicine, Durham, NC, USA.
Transl Vis Sci Technol. 2020 Sep 8;9(10):8. doi: 10.1167/tvst.9.10.8. eCollection 2020 Sep.
Genipin has been proposed as a possible neuroprotective therapy in myopia and glaucoma. Here, we aim to determine the effects of prolonged genipin-induced scleral stiffening on visual function.
Eyes from Brown Norway rats were treated in vivo with either a single 15 mM genipin retrobulbar injection or sham retrobulbar injection and were compared to naïve eyes. Intraocular pressure, optomotor response, and electroretinograms were repeatedly measured over 4 weeks following retrobulbar injections to determine visual and retinal function. At 4 weeks, we quantified retinal ganglion cell axon counts. Finally, molecular changes in gene and protein expression were analyzed via real-time polymerase chain reaction (RT-PCR) and proteomics.
Retrobulbar injection of genipin did not affect intraocular pressure (IOP) or retinal function, nor have a sustained impact on visual function. Although genipin-treated eyes had a small decrease in retinal ganglion cell axon counts compared to contralateral sham-treated eyes (-8,558 ± 18,646; mean ± SD), this was not statistically significant ( = 0.206, = 9). Last, we did not observe any changes in gene or protein expression due to genipin treatment.
Posterior scleral stiffening with a single retrobulbar injection of 15 mM genipin causes no sustained deficits in visual or retinal function or at the molecular level in the retina and sclera. Retinal ganglion cell axon morphology appeared normal.
These results support future in vivo studies to determine the efficacy of genipin-induced posterior scleral stiffening to help treat ocular diseases, like myopia and glaucoma.
京尼平已被提议作为一种可能用于治疗近视和青光眼的神经保护疗法。在此,我们旨在确定长期使用京尼平导致巩膜硬化对视觉功能的影响。
对来自挪威棕色大鼠的眼睛进行体内实验,一组进行单次15 mM京尼平球后注射,另一组进行假球后注射,同时设未处理的正常眼作为对照。在球后注射后的4周内,反复测量眼压、视动反应和视网膜电图,以确定视觉和视网膜功能。4周时,我们对视网膜神经节细胞轴突数量进行定量分析。最后,通过实时聚合酶链反应(RT-PCR)和蛋白质组学分析基因和蛋白质表达的分子变化。
球后注射京尼平不影响眼压(IOP)或视网膜功能,对视觉功能也没有持续影响。虽然与对侧假处理眼相比,经京尼平处理的眼睛视网膜神经节细胞轴突数量略有减少(-8,558 ± 18,646;平均值±标准差),但差异无统计学意义(P = 0.206,自由度 = 9)。最后,我们未观察到因京尼平处理导致的基因或蛋白质表达变化。
单次球后注射15 mM京尼平导致的后巩膜硬化在视觉或视网膜功能方面,以及在视网膜和巩膜的分子水平上均未造成持续损害。视网膜神经节细胞轴突形态看起来正常。
这些结果支持未来进行体内研究,以确定京尼平诱导后巩膜硬化在治疗近视和青光眼等眼部疾病方面的疗效。