ArticleFrontiers in pharmacology2022
Targeting HMGB1-NFκb Axis and miR-21 by Glycyrrhizin: Role in Amelioration of Corneal Injury in a Mouse Model of Alkali Burn.
Article in Frontiers in pharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Therapeutic Efficacy of Rapamycin in an Experimental Mouse Model of Corneal Alkali Burn.International journal of molecular sciences · 2026Article
- Functionalized metal-organic framework-based photosensitive hydrogel eye drops for inhibition of corneal neovascularization and promotion of epithelial repair.Journal of nanobiotechnology · 2026Article
- Targeting lactylation in a novel metabolic-epigenetic-inflammatory axis mitigates inflammation and promotes healing following corneal injury.Journal of translational medicine · 2026Article
- Glycyrrhizin (GLY) and glycyrrhetinic acid (GA) as potential multi-target antimicrobials: mechanisms, biofilm disruption, and synergy against drug-resistant pathogens.Frontiers in microbiology · 2026Review
- Transforming corneal alkali burn treatment: unveiling mechanisms and pioneering therapies from bench to bedside.Journal of translational medicine · 2025Review
- KGF-2 Alleviates Dry Eye Disease by Regulating the HMGB1/TLR4 Pathway.Investigative ophthalmology & visual science · 2025Article
- Review
- Trimebutine prevents corneal inflammation in a rat alkali burn model.Scientific reports · 2024Article
- Bone morphogenetic protein 4 thermosensitive hydrogel inhibits corneal neovascularization by repairing corneal epithelial apical junctional complexes.Materials today. Bio · 2024Article
- HMGB1, a potential regulator of tumor microenvironment in KSHV-infected endothelial cells.Frontiers in microbiology · 2023Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Corneal neovascularization (CNV) is a sight-threatening condition usually associated with various inflammatory settings including chemical injury. High mobility group box 1 (HMGB1) is identified as an inflammatory alarmin in diverse tissue damage. Here, we evaluate the expression of HMGB1 and the consequences of its inhibition through its selective inhibitor glycyrrhizin (GLY) in alkali burn-induced corneal inflammation and neovascularization. GLY effectively attenuated alkali burn-induced HMGB1 expression at both mRNA and protein levels. Furthermore, slit-lamp analysis, ink perfusion, H&E staining, and CD31 histochemical staining showed that GLY relieved corneal neovascularization, while GLY attenuated VEGF expression via inhibiting HMGB1/NF-κB/HIF-1α signal pathway. In addition, GLY treatment decreased the cytokine expression of CCL2 and CXCL5, accompanied by the reduction of their receptors of CCR2 and CXCR2. GLY diminished the inflammatory cell infiltration of the cornea, as well as reduced the expression of IL-1β, IL-6, and TNF-α. Moreover, treatment with GLY reduced the degree of cornea opacity through inactivating extracellular HMGB1 function, which otherwise induces TGF-β1 release and myofibroblast differentiation. Furthermore, we found that GLY treatment attenuated the upregulation of miR-21 levels in alkali burned cornea; while inhibition of miR-21in keratocytes
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