体外验证:GLY通过HMGB1-TLR/MyD88 NF-κB信号通路减轻紫外线诱导的角膜上皮损伤。

IF 4.6 Q2 MATERIALS SCIENCE, BIOMATERIALS ACS Applied Bio Materials Pub Date : 2023-11-06 DOI:10.1016/j.acthis.2023.152111
XinYi Chen , XiaoXiao Zheng , Ting Shen , Ting He , YangQi Zhao , Yi Dong
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引用次数: 0

摘要

紫外线诱导的角膜损伤是一种常见的眼表损伤,通常会导致角膜损伤,引起持续的炎症。高迁移率组盒1(HMGB1)被确定为各种组织损伤中的炎症警报。在此,本研究首先评估了HMGB1选择性抑制剂GLY对紫外线诱导的角膜损伤的修复作用;其次,研究了GLY对紫外线诱导的角膜损伤诱导的炎症的抑制作用及其潜在的治疗机制。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,敲低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的炎症反应。
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In vitro validation: GLY alleviates UV-induced corneal epithelial damage through the HMGB1-TLR/MyD88-NF-κB signaling pathway

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.

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来源期刊
ACS Applied Bio Materials
ACS Applied Bio Materials Chemistry-Chemistry (all)
CiteScore
9.40
自引率
2.10%
发文量
464
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