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 2.3 4区 生物学 Q4 CELL BIOLOGY
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。
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.

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来源期刊
Acta histochemica
Acta histochemica 生物-细胞生物学
CiteScore
4.60
自引率
4.00%
发文量
107
审稿时长
23 days
期刊介绍: Acta histochemica, a journal of structural biochemistry of cells and tissues, publishes original research articles, short communications, reviews, letters to the editor, meeting reports and abstracts of meetings. The aim of the journal is to provide a forum for the cytochemical and histochemical research community in the life sciences, including cell biology, biotechnology, neurobiology, immunobiology, pathology, pharmacology, botany, zoology and environmental and toxicological research. The journal focuses on new developments in cytochemistry and histochemistry and their applications. Manuscripts reporting on studies of living cells and tissues are particularly welcome. Understanding the complexity of cells and tissues, i.e. their biocomplexity and biodiversity, is a major goal of the journal and reports on this topic are especially encouraged. Original research articles, short communications and reviews that report on new developments in cytochemistry and histochemistry are welcomed, especially when molecular biology is combined with the use of advanced microscopical techniques including image analysis and cytometry. Letters to the editor should comment or interpret previously published articles in the journal to trigger scientific discussions. Meeting reports are considered to be very important publications in the journal because they are excellent opportunities to present state-of-the-art overviews of fields in research where the developments are fast and hard to follow. Authors of meeting reports should consult the editors before writing a report. The editorial policy of the editors and the editorial board is rapid publication. Once a manuscript is received by one of the editors, an editorial decision about acceptance, revision or rejection will be taken within a month. It is the aim of the publishers to have a manuscript published within three months after the manuscript has been accepted
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