HMGB1
炎症
信号转导
免疫印迹
NF-κB
角膜上皮
体外
TLR2型
化学
细胞生物学
TLR4型
生物
免疫学
角膜
医学
基因
生物化学
眼科
作者
X. Chen,Xiaoxiao Zheng,Ting Shen,Ting He,YangQi Zhao,Yi Dong
标识
DOI:10.1016/j.acthis.2023.152111
摘要
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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