Investigative ophthalmology & visual science · 2026
Temporally Resolved Characterization of 254-nm UV Radiation-Induced Photokeratitis in a Rabbit Model.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Zhu Litong, Nie Zukang, Cui Mengdi, Yang Ying, Guan Yaxin, Qiu Mengqi, Xing Jiahao, Liang Chao, Wang Jiarui, Yang Zaifu, Jiao Luguang
Аннотация
PURPOSE: This study systematically characterized the dynamic progression of corneal injury and the subsequent repair following suprathreshold exposure to 254-nm UV-C radiation.
METHODS: A pulsed laser system was used to investigate pathological alterations in rabbit corneas over 3 months following acute 254-nm UV exposure. Four laser exposure doses (265, 530, 1150, and 2125 mJ/cm2) were selected to induce varying severities of corneal injury. Corneal changes were assessed using slit-lamp biomicroscopy, optical coherence tomography, histopathology, and immunohistochemical analyses of cyclobutane pyrimidine dimers and caspase-3.
RESULTS: Following acute 254-nm UV-C exposure, photokeratitis exhibited delayed onset characterized by conjunctival hyperemia, photophobia, and corneal epithelial defects. The extent of epithelial defects and stromal edema correlated positively with the radiant exposure dose. Linear mixed-effects modeling demonstrated significant effects of dose and time, as well as their interaction on corneal thickness (all P < 0.001). Corneal thickness showed a strong dose-dependent correlation during the edematous phase, peaking at 36 hours (r = 0.866; P < 0.001), and the highest-dose group (2125 mJ/cm2) exhibited a 61.5% increase relative to baseline (600.50 ± 40.85 µm vs. 371.75 ± 30.91 µm). Although the ocular surface findings resolved within 7 days, histological restoration required at least 14 days. Cyclobutane pyrimidine dimer immunostaining revealed pan-epithelial DNA photodamage.
CONCLUSIONS: Acute 254-nm UV-C exposure induces a temporally ordered sequence of corneal injury characterized by epithelial thinning, epithelial denudation, re-epithelialization, cellular proliferation, and epithelial restratification, highlighting a dissociation between clinical recovery and histological repair.
METHODS: A pulsed laser system was used to investigate pathological alterations in rabbit corneas over 3 months following acute 254-nm UV exposure. Four laser exposure doses (265, 530, 1150, and 2125 mJ/cm2) were selected to induce varying severities of corneal injury. Corneal changes were assessed using slit-lamp biomicroscopy, optical coherence tomography, histopathology, and immunohistochemical analyses of cyclobutane pyrimidine dimers and caspase-3.
RESULTS: Following acute 254-nm UV-C exposure, photokeratitis exhibited delayed onset characterized by conjunctival hyperemia, photophobia, and corneal epithelial defects. The extent of epithelial defects and stromal edema correlated positively with the radiant exposure dose. Linear mixed-effects modeling demonstrated significant effects of dose and time, as well as their interaction on corneal thickness (all P < 0.001). Corneal thickness showed a strong dose-dependent correlation during the edematous phase, peaking at 36 hours (r = 0.866; P < 0.001), and the highest-dose group (2125 mJ/cm2) exhibited a 61.5% increase relative to baseline (600.50 ± 40.85 µm vs. 371.75 ± 30.91 µm). Although the ocular surface findings resolved within 7 days, histological restoration required at least 14 days. Cyclobutane pyrimidine dimer immunostaining revealed pan-epithelial DNA photodamage.
CONCLUSIONS: Acute 254-nm UV-C exposure induces a temporally ordered sequence of corneal injury characterized by epithelial thinning, epithelial denudation, re-epithelialization, cellular proliferation, and epithelial restratification, highlighting a dissociation between clinical recovery and histological repair.