Wallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, Atlanta, GA, USA.
George W. Woodruff School of Mechanical Engineering, Georgia Institute of Technology, Atlanta, GA, USA.
Transl Vis Sci Technol. 2022 May 2;11(5):7. doi: 10.1167/tvst.11.5.7.
Scleral stiffening may protect against glaucomatous retinal ganglion cell (RGC) loss or dysfunction associated with ocular hypertension. Here, we assess the potential neuroprotective effects of two treatments designed to stiffen either the entire posterior sclera or only the sclera adjacent to the peripapillary sclera in an experimental model of glaucoma.
Rat sclerae were stiffened in vivo using either genipin (crosslinking the entire posterior sclera) or a regionally selective photosensitizer, methylene blue (stiffening only the juxtaperipapillary region surrounding the optic nerve). Ocular hypertension was induced using magnetic microbeads delivered to the anterior chamber. Morphological and functional outcomes, including optic nerve axon count and appearance, retinal thickness measured by optical coherence tomography, optomotor response, and electroretinography traces, were assessed.
Both local (juxtaperipapillary) and global (whole posterior) scleral stiffening treatments were successful at increasing scleral stiffness, but neither provided demonstrable neuroprotection in hypertensive eyes as assessed by RGC axon counts and appearance, optomotor response, or electroretinography. There was a weak indication that scleral crosslinking protected against retinal thinning as assessed by optical coherence tomography.
Scleral stiffening was not demonstrated to be neuroprotective in ocular hypertensive rats. We hypothesize that the absence of benefit may in part be due to RGC loss associated with the scleral stiffening agents themselves (mild in the case of genipin, and moderate in the case of methylene blue), negating any potential benefit of scleral stiffening.
The development of scleral stiffening as a neuroprotective treatment will require the identification of better tolerated stiffening protocols and further preclinical testing.
巩膜变硬可能有助于预防与眼高压相关的青光眼性视网膜神经节细胞（RGC）损失或功能障碍。在这里，我们评估了两种治疗方法的潜在神经保护作用，这两种方法旨在使整个后巩膜变硬或仅使视盘周围巩膜变硬，以建立青光眼的实验模型。
通过使用京尼平（交联整个后巩膜）或局部选择的光敏剂亚甲蓝（仅使视神经周围的视盘周围区域变硬），使大鼠巩膜在体内变硬。通过将磁性微珠递送至前房来诱导眼高压。评估形态和功能结果，包括视神经轴突计数和外观，通过光学相干断层扫描测量视网膜厚度，光动反应和视网膜电图轨迹。
局部（视盘周围）和全局（整个后巩膜）巩膜变硬治疗均成功地增加了巩膜硬度，但两种治疗方法均未通过 RGC 轴突计数和外观，光动反应或视网膜电图评估在高血压眼中显示出明显的神经保护作用。有微弱的迹象表明，通过光学相干断层扫描评估，巩膜交联可防止视网膜变薄。
在患有眼高压的大鼠中，巩膜变硬并未显示出神经保护作用。我们假设，缺乏益处的部分原因可能是巩膜变硬剂本身引起的 RGC 损失（京尼平的情况下较轻，亚甲蓝的情况下较严重），从而否定了巩膜变硬的任何潜在益处。
医学科学
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