Shao Yi-Ching, Liou Jyh-Cheng, Kuo Chan-Yen, Tsai Yun-Shan, Lin En-Chieh, Hsieh Ching-Ju, Lin Si-Ping, Chen Bo-Yie
Department of Ophthalmology, Chung Shan Medical University Hospital, Taichung, Taiwan.
Department of Optometry, Chung Shan Medical University, Taichung, Taiwan.
Mol Vis. 2017 Apr 12;23:219-227. eCollection 2017.
Uveitic inflammatory injury can cause irreversible visual loss; however, no single animal model recapitulates all the characteristics of human uveitis. Ultraviolet radiation (UVR) is one of the risk factors for uveitis, but the role of UVR in the pathogenesis of uveitic injury is unclear. The aim of this study was to elucidate whether UVB promotes the initiation of, and subsequently contributes to, uveitic inflammatory injury.
Mice were assigned to either a blank control group or one of three UVB treatment groups: no protection, protection with Nelfilcon A contact lens (Food and Drug Administration [FDA] class II, about 46.8% UVB transmittance), or protection with Etafilcon A contact lens (FDA class IV, about 0.55% UVB transmittance). The contact lenses acted as blocking barriers against UVR. After the application of UVR, pathologic injuries were determined with slit-lamp microscopy and histologic examination.
Compared with the intact status of the controls, the anterior eyes of the UVB groups showed pathologic alterations in physiologic properties and tissue integrity. UVR promoted anterior uveitic inflammatory injury, with expansion of the hyperemic iris vessels, over-production of aqueous humor protein, disruption of the blood-aqueous barrier, and embedding of infiltrative leukocytes inside the iridocorneal angle. However, blockage of UVR in vivo retarded the progression of uveitic inflammatory injury. The highest level of UV protection in the Etafilcon A group resulted in greater inhibition of uveitic inflammatory injury than that in the Nelfilcon A group.
This study demonstrates that UVB initiated and promoted uveitic inflammatory injury. UV protection is needed for the clinical management of anterior uveitis. The Etafilcon A lenses provide better protection of the anterior segment of the eye against UVB damage compared with the Nelfilcon A lenses.
葡萄膜炎性损伤可导致不可逆的视力丧失；然而，没有单一的动物模型能概括人类葡萄膜炎的所有特征。紫外线辐射（UVR）是葡萄膜炎的危险因素之一，但UVR在葡萄膜炎性损伤发病机制中的作用尚不清楚。本研究的目的是阐明UVB是否促进葡萄膜炎性损伤的起始并随后导致该损伤。
将小鼠分为空白对照组或三个UVB治疗组之一：无保护组、用奈非那酮A隐形眼镜保护组（食品药品监督管理局[FDA] II类，约46.8%的UVB透过率）或用依他菲康A隐形眼镜保护组（FDA IV类，约0.55%的UVB透过率）。隐形眼镜作为阻挡UVR的屏障。在施加UVR后，通过裂隙灯显微镜检查和组织学检查确定病理损伤。
与对照组的完整状态相比，UVB组的眼前部在生理特性和组织完整性方面出现了病理改变。UVR促进了前葡萄膜炎性损伤，表现为虹膜血管充血扩张、房水蛋白过度产生、血-房水屏障破坏以及浸润性白细胞嵌入虹膜角膜角。然而，体内UVR的阻断延缓了葡萄膜炎性损伤的进展。依他菲康A组的最高水平的紫外线防护比奈非那酮A组对葡萄膜炎性损伤的抑制作用更强。
本研究表明UVB引发并促进了葡萄膜炎性损伤。前葡萄膜炎的临床管理需要紫外线防护。与奈非那酮A镜片相比，依他菲康A镜片能更好地保护眼球前部免受UVB损伤。
