The present study was aimed to reveal the function of extracellular RNAs (exRNAs) in retinal ischemia reperfusion (I/R) injury, and evaluate whether RNase administration can effectively reduce I/R injury. A retinal I/R injury C57BL/6J wild-type mice model was established by elevating intraocular pressure for 1 h. All mice received 3 doses of RNase or the same dose of normal saline at different time points. After 7 days of reperfusion, retinal damage was quantified by counting retinal ganglion cells and measuring retinal layer thickness. The apoptotic retinal cells were detected by the TUNEL experiment, and the expressions of caspase-3, proinflammatory cytokines in retinal tissues, and glial fibrillary acidic protein (GFAP) protein and mRNA were detected to determine the underlying mechanism. It was found that RNase administration (1) reduced the significant loss of retinal morphology caused by I/R injury; (2) down-regulated the expression of NF-κBp65, IL-6 and GFAP relative to the I/R mice; (3) decreased the apoptosis of retinal cells and the levels of caspase-3; (4) attenuated exRNAs levels in retinal tissues on day 7 after retinal I/R. In short, increased exRNAs may contribute to retinal I/R damages in mice, and RNase therapy can effectively attenuate retinal damage by reducing inflammatory response and apoptosis.

本研究旨在揭示细胞外RNA（exRNA）在视网膜缺血再灌注（I / R）损伤中的功能，并评估是否施用RNase可以有效减轻I / R损伤。通过升高眼内压1 h建立视网膜I / R损伤C57BL / 6J野生型小鼠模型。所有小鼠在不同时间点接受3剂量的RNase或相同剂量的生理盐水。再灌注7天后，通过计数视网膜神经节细胞并测量视网膜层厚度来量化视网膜损伤。通过TUNEL实验检测凋亡的视网膜细胞，检测视网膜组织中caspase-3，促炎细胞因子的表达以及神经胶质纤维酸性蛋白（GFAP）和mRNA的表达，以确定其潜在的机制。研究发现，RNase的使用（1）减少了I / R损伤引起的视网膜形态的显着丧失；（2）相对于I / R小鼠下调NF-κBp65，IL-6和GFAP的表达；（3）降低视网膜细胞凋亡和caspase-3水平；（4）视网膜I / R后第7天，视网膜组织中的exRNAs水平降低。简而言之，增加的exRNA可能会导致小鼠视网膜I / R损伤，而RNase治疗可以通过减少炎症反应和凋亡来有效减轻视网膜损伤。