ArticleScientific reports2024
Trimebutine prevents corneal inflammation in a rat alkali burn model.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed.
- Terahertz Photons Promote Corneal Injury Repair via Epithelial Proliferation, Migration, and Inflammation Reduction.Investigative ophthalmology & visual science · 2026Article
- Esomeprazole plus trimebutine maleate improves symptoms, esophageal function, and acid control without increasing risks in elderly GERD: a real-world retrospective study.American journal of translational research · 2026Article
- Single-Cell Transcriptomics Shows Cellular Heterogeneity, Intercellular Communication, and Extracellular Matrix Remodeling in Corneal Fibrosis In Vivo.Investigative ophthalmology & visual science · 2025Article
- Rapamycin Mitigates Corneal Damage in a Mouse Model of Alkali Burn Injury.Bioengineering (Basel, Switzerland) · 2025Article
- Efficacy and safety of Fe-curcumin coordination polymer nanodots to prevent corneal neovascularization in alkali burn models.Journal of nanobiotechnology · 2025Article
- Supersaturated Oxygen Emulsion Mitigates Hypoxia-Driven Corneal Neovascularization after Alkali Burn.Ophthalmology scienceArticle
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alkaline burns to the cornea lead to loss of corneal transparency, which is essential for normal vision. We used a rat corneal alkaline burn model to investigate the effect of ophthalmic trimebutine solution on healing wounds caused by alkaline burns. Trimebutine, an inhibitor of the high-mobility group box 1-receptor for advanced glycation end products, when topically applied to the burned cornea, suppressed macrophage infiltration in the early phase and neutrophil infiltration in the late phase at the wound site. It also inhibited neovascularization and myofibroblast development in the late phase. Furthermore, trimebutine effectively inhibited interleukin-1β expression in the injured cornea. It reduced scar formation by decreasing the expression of type III collagen. These findings suggest that trimebutine may represent a novel therapeutic strategy for corneal wounds, not only through its anti-inflammatory effects but also by preventing neovascularization.
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Registered trials
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