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
XinYi Chen , XiaoXiao Zheng , Ting Shen , Ting He , YangQi Zhao , Yi Dong
{"title":"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。","authors":"XinYi Chen ,&nbsp;XiaoXiao Zheng ,&nbsp;Ting Shen ,&nbsp;Ting He ,&nbsp;YangQi Zhao ,&nbsp;Yi Dong","doi":"10.1016/j.acthis.2023.152111","DOIUrl":null,"url":null,"abstract":"<div><p>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.</p></div>","PeriodicalId":2,"journal":{"name":"ACS Applied Bio Materials","volume":null,"pages":null},"PeriodicalIF":4.6000,"publicationDate":"2023-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"In vitro validation: GLY alleviates UV-induced corneal epithelial damage through the HMGB1-TLR/MyD88-NF-κB signaling pathway\",\"authors\":\"XinYi Chen ,&nbsp;XiaoXiao Zheng ,&nbsp;Ting Shen ,&nbsp;Ting He ,&nbsp;YangQi Zhao ,&nbsp;Yi Dong\",\"doi\":\"10.1016/j.acthis.2023.152111\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><p>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.</p></div>\",\"PeriodicalId\":2,\"journal\":{\"name\":\"ACS Applied Bio Materials\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":4.6000,\"publicationDate\":\"2023-11-06\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"ACS Applied Bio Materials\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S0065128123001186\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"MATERIALS SCIENCE, BIOMATERIALS\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"ACS Applied Bio Materials","FirstCategoryId":"99","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0065128123001186","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"MATERIALS SCIENCE, BIOMATERIALS","Score":null,"Total":0}
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。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
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
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信