三七皂苷R1通过与TRIB1结合并抑制TRIB1来减轻蓝光诱导的角膜损伤和伤口愈合延迟。
Notoginsenoside R1 alleviates blue light-induced corneal injury and wound healing delay by binding to and inhibiting TRIB1.
作者信息
Chen Kuangqi, Li Jiafeng, Chen Zhitong, Shen Chang, Li Xiang, Li Yuanyuan, Song Dongjie, Li Xiuyi, Wang Xinglin, Xia Yutong, Yu Xin, Wang Yinhao, Shen Ye, Tong Jianping
机构信息
Department of Ophthalmology, The First Affiliated Hospital of Zhejiang University, Hangzhou, Zhejiang, China; State Key Laboratory Cultivation Base, Shandong Provincial Key Laboratory of Ophthalmology, School of Ophthalmology, Eye Hospital of Shandong First Medical University (Shandong Eye Hospital), Eye Institute of Shandong First Medical University, Shandong First Medical University, Jinan, Shandong, China.
Department of Orthopedic Surgery, The First Affiliated Hospital of Zhejiang University, Hangzhou, Zhejiang, China.
出版信息
Phytomedicine. 2025 Mar;138:156399. doi: 10.1016/j.phymed.2025.156399. Epub 2025 Jan 17.
BACKGROUND
With the escalating use of digital devices, blue light (BL) exposure has emerged as a critical concern due to its potential to cause ocular damage. This study explores the protective effects of notoginsenoside R1 (NR1), a bioactive compound from Panax notoginseng (Burkill) F.H. Chen (Sanqi), against BL-induced corneal epithelial injury.
PURPOSE
This research aims to investigate the protective effects of NR1 on BL-induced corneal injury and wound healing delay.
METHODS
Human corneal epithelial cells (hCECs) were pretreated with NR1 (0-50 μM) or N-acetylcysteine (NAC, 10 mM), then exposed to BL (570 μW/cm²) for 24 h. Cell viability, proliferation, migration, and ROS levels were assessed using various techniques. In mice, NR1 (25 μM and 50 μM) and NAC (0.3 %) eye drops were administered during BL exposure. Corneal injury, healing rates, cell proliferation, migration, ROS, and inflammation were evaluated. RNA-sequencing, bioinformatics, and molecular binding validation identified tribbles homolog 1 (TRIB1) as a key molecule mitigating BL damage with NR1. Functional studies via gene silencing, overexpression, and pharmacological modulation further explored TRIB1's role in BL exposure.
RESULTS
NR1 significantly reduced BL-induced inflammation, ROS production, and inhibited migration and proliferation in hCECs and murine corneas. It also alleviated BL-induced corneal injury and delayed healing in mice. NR1 inhibited TRIB1 upregulation, a marker of BL-induced injury and healing delay. Overexpression of TRIB1 negated NR1's therapeutic effects on hCECs, while TRIB1 silencing mitigated functional impairment. In mice, increased Trib1 expression caused corneal injury and delayed healing, reversed by NR1 treatment.
CONCLUSION
NR1 shows potential as a therapeutic agent by inhibiting TRIB1 elevation in response to BL exposure, providing a novel promising target for corneal injury and wound healing delay induced by BL, and offering a comprehensive strategy for clinical pharmacological intervention.
背景
随着数字设备使用的不断增加，蓝光（BL）暴露因其可能导致眼部损伤而成为一个关键问题。本研究探讨三七生物活性化合物三七皂苷R1（NR1）对蓝光诱导的角膜上皮损伤的保护作用。
目的
本研究旨在探讨NR1对蓝光诱导的角膜损伤和伤口愈合延迟的保护作用。
方法
用人角膜上皮细胞（hCEC）分别用NR1（0 - 50 μM）或N - 乙酰半胱氨酸（NAC，10 mM）预处理，然后暴露于蓝光（570 μW/cm²）24小时。使用各种技术评估细胞活力、增殖、迁移和活性氧水平。在小鼠中，蓝光暴露期间给予NR1（25 μM和50 μM）和NAC（0.3%）眼药水。评估角膜损伤、愈合率、细胞增殖、迁移、活性氧和炎症。通过RNA测序、生物信息学和分子结合验证确定TRIB1是减轻蓝光损伤的关键分子，NR1可调节该分子。通过基因沉默、过表达和药理学调节的功能研究进一步探讨TRIB1在蓝光暴露中的作用。
结果
NR1显著减轻蓝光诱导的hCEC和小鼠角膜中的炎症、活性氧产生，并抑制迁移和增殖。它还减轻了蓝光诱导的小鼠角膜损伤和愈合延迟。NR1抑制TRIB1上调，TRIB1是蓝光诱导损伤和愈合延迟的标志物。TRIB1过表达消除了NR1对hCEC的治疗作用，而TRIB1沉默减轻了功能障碍。在小鼠中，Trib1表达增加导致角膜损伤和愈合延迟，NR1治疗可逆转这一现象。
结论
NR1通过抑制蓝光暴露引起的TRIB1升高显示出作为治疗剂的潜力，为蓝光诱导的角膜损伤和伤口愈合延迟提供了一个新的有前景的靶点，并为临床药理干预提供了一个全面的策略。
Zotero 插件