Wang Xiao, Sun Yifan, Luan Changlin, Yang Shiqiao, Wang Kailei, Zhang Xiaoran, Hao Rui, Zhang Wei
Tianjin Eye Hospital, Tianjin Key Lab of Ophthalmology and Vision Science, Tianjin, P. R. China.
Clinical College of Ophthalmology, Tianjin Medical University, Tianjin, P. R. China.
Photochem Photobiol. 2025 Jan-Feb;101(1):106-115. doi: 10.1111/php.13952. Epub 2024 Apr 18.
Excessive exposure to blue light can cause retinal damage. Hydrogen-rich saline (HRS), one of the hydrogen therapies, has been demonstrated to be effective in eye photodamage, but the effect on the expression of melanopsin in intrinsically photosensitive retinal ganglion cells (ipRGCs) is unknown. In this study, we used a rat model of light-induced retinal injury to observe the expression of melanopsin after HRS treatment and to determine the effect of HRS on retinal ganglion cell protection. Adult SD rats were exposed to blue light (48 h) and treated with HRS for 0, 3, 7, and 14 days. Real-time polymerase chain reaction (qRT-PCR) and Western blotting (WB) were performed to find the expression of genes and proteins, respectively. The function of retinal ipRGCs was measured by pattern-evoked electroretinography (pERG). The number and morphological changes of melanopsin-positive ganglion cells in the retina were observed by immunofluorescence (IF). Acute blue light exposure caused a decrease in ipRGC function, decreased expression of melanopsin protein and the melanopsin-positive RGCs, and diminished immunoreactivity in dendrites. However, over time, melanopsin showed a tendency to self-recovery, with an increase in melanopsin protein expression and the number of melanopsin-positive RGCs, with incomplete recovery of function within two weeks. HRS treatment accelerated the recovery process, with a significant increase in melanopsin expression and the number of melanopsin-positive RGCs, and an improvement in the pERG waveform within two weeks.
过度暴露于蓝光会导致视网膜损伤。富氢盐水（HRS）作为氢疗法之一，已被证明对眼部光损伤有效，但对内在光敏视网膜神经节细胞（ipRGCs）中黑视蛋白表达的影响尚不清楚。在本研究中，我们使用光诱导视网膜损伤大鼠模型观察HRS治疗后黑视蛋白的表达，并确定HRS对视网膜神经节细胞保护的作用。成年SD大鼠暴露于蓝光（48小时），并分别在0、3、7和14天接受HRS治疗。分别通过实时聚合酶链反应（qRT-PCR）和蛋白质印迹法（WB）检测基因和蛋白质的表达。通过图形诱发视网膜电图（pERG）测量视网膜ipRGCs的功能。通过免疫荧光（IF）观察视网膜中黑视蛋白阳性神经节细胞的数量和形态变化。急性蓝光暴露导致ipRGC功能下降、黑视蛋白蛋白表达和黑视蛋白阳性RGCs减少，以及树突中的免疫反应性减弱。然而，随着时间的推移，黑视蛋白显示出自我恢复的趋势，黑视蛋白蛋白表达和黑视蛋白阳性RGCs数量增加，两周内功能未完全恢复。HRS治疗加速了恢复过程，黑视蛋白表达和黑视蛋白阳性RGCs数量显著增加，两周内pERG波形得到改善。
