ORIGINAL RESEARCH article
Front. Med.
Sec. Ophthalmology
Volume 12 - 2025 | doi: 10.3389/fmed.2025.1664376
This article is part of the Research TopicMolecular Mechanisms and Pathophysiology of Dry Eye Disease and Meibomian Gland DysfunctionView all 5 articles
Electroacupuncture Improves Scopolamine Hydrobromide induced Dry Eye in Mice via Inhibiting Ocular Surface Inflammation and Regulating the HMGB1-Related Signaling Pathways
Provisionally accepted
- Nanjing University of Chinese Medicine, Nanjing, China
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Objective: This study aims to observe the effect of Electroacupuncture (EA) on improving ocular surface inflammation and HMGB1-related signaling pathways in dry eye disease (DED). Methods: Healthy male C57BL/6J mice were treated with scopolamine hydrobromide for 21 consecutive days to establish the animal models for DED. After 21 days, fluorometholone (Flu), EA, and sham EA (Sham) treatments were performed. The effect of EA on DED surface inflammation was evaluated by corneal fluorescence staining, phenol red thread test, in vivo confocal microscopy (IVCM), and corneal histopathology. The influence of EA on high-mobility group box 1(HMGB1), receptor for advanced glycation end products (RAGE), toll-like receptor 2(TLR2) and toll-like receptor 4 (TLR4) was assessed by immunohistochemistry, real-time quantitative polymerase chain reaction (RT-qPCR), and western blot. The influence of EA on interleukin-6 (IL-6) and interleukin-10 (IL-10) were measured by enzyme-linked immunosorbent assay (ELISA). Results: EA can significantly increase tear flow and reduce corneal staining and corneal stromal inflammation, while also improving the morphologic structure of the cornea and lacrimal glands. The levels of HMGB1, RAGE, TLR2, TLR4 and IL-6 were significantly decreased while IL-10 level was significantly in-creased after EA treatment, indicating that EA may improve dry eye surface inflammation by inhib-iting HMGB1-related signaling pathways. Conclusion: The findings presented in our study demonstrate that EA may improve ocular surface inflammation in mice with DED by inhibiting the HMGB1-related signaling pathways. Therefore, EA may be a potential therapeutic target for DED.
Keywords: Dry eye disease (DED), electroacupuncture (EA), High mobility group proteinB1(HMGB1), Receptor for advanced glycation end products (RAGE), ocular surface inflammation
Received: 11 Jul 2025; Accepted: 13 Oct 2025.
Copyright: © 2025 Wu, Ding, Liang, Han, Fan, Wu and Wei. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Yunchuan Wu, 270847@njucm.edu.cn
Qingbo Wei, 270762@njucm.edu.cn
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