UV-induced corneal damage is a common ocular surface injury that usually leads to corneal lesions causing persistent inflammation. High mobility group box 1 (HMGB1) is identified as an inflammatory alarm in various tissue injuries. Here, this study first evaluates the repair effect of the HMGB1-selective inhibitor GLY in UV-induced corneal damage; Secondly, the inhibitory effect of GLY on UV-induced corneal damage induced inflammation and the potential therapeutic mechanism of GLY were studied. GLY effectively attenuates the expression of UV-induced inflammatory factors and HMGB1, TLR/MyD88, NF-κB signaling pathway genes at the mRNA and protein levels. In addition, RT-PCR and Western Blot experiments after knocking down HMGB1 and TLR2/9 genes showed that GLY alleviated corneal inflammation by inhibiting the HMGB1-TLR/MyD88 signaling pathway. The results of this study show that targeting HMGB1-NF-κB by GLY can alleviate the inflammatory response induced by UV induction.

紫外线引起的角膜损伤是一种常见的眼表损伤，通常会导致角膜病变，从而引起持续性炎症。高迁移率族蛋白 1 (HMGB1) 被认为是各种组织损伤中的炎症警报。在这里，本研究首先评估了HMGB1选择性抑制剂GLY对紫外线引起的角膜损伤的修复效果；其次，研究了GLY对紫外线引起的角膜损伤引起的炎症的抑制作用以及GLY的潜在治疗机制。GLY 在 mRNA 和蛋白质水平上有效减弱紫外线诱导的炎症因子和 HMGB1、TLR/MyD88、NF-κB 信号通路基因的表达。此外，敲除HMGB1和TLR2/9基因后的RT-PCR和Western Blot实验表明，GLY通过抑制HMGB1-TLR/MyD88信号通路来减轻角膜炎症。本研究结果表明，GLY靶向HMGB1-NF-κB可以减轻紫外线诱导引起的炎症反应。