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Peer-reviewedCC BY-NC-ND 4.0Molecular Medicine Reports

Glycyrrhizic acid attenuates corneal inflammation and pathological angiogenesis through FAK/PI3K/AKT signaling

  • Jinjin Yu1,2
  • Huiheng Qu3,4
  • Yinming Fang2
  • Weicheng Xu2
  • Nannan Ding5
  • Jie Ji1
  • Nan Wang4,6
  • Wei Shi2
6 affiliations
  1. 1Department of Ophthalmology, Wuxi Affiliated Hospital of Nanjing University of Chinese Medicine, Wuxi, Jiangsu 214000, P.R. China
  2. 2Department of Ophthalmology, Nanjing Hospital Affiliated to Nanjing University of Chinese Medicine, The First Clinical Medical College of Nanjing University of Chinese Medicine, Nanjing, Jiangsu 210003, P.R. China
  3. 3Department of General Surgery, Jiangnan University Medical Center, Jiangnan University, Wuxi, Jiangsu 214002, P.R. China
  4. 4Department of Cancer Biology, Atrium Health Wake Forest Baptist Comprehensive Cancer Center, Winston-Salem, NC 27157, USA
  5. 5Department of Ophthalmology, Jiangnan University Medical Center, Jiangnan University, Wuxi, Jiangsu 214002, P.R. China
  6. 6Department of Breast Surgery, Tianjin Medical University Cancer Institute and Hospital, Key Laboratory of Cancer Prevention and Therapy, National Clinical Research Center for Cancer, Tianjin 300060, P.R. China
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Abstract

Corneal alkali burns lead to severe inflammation and corneal neovascularization (CNV), both of which are major causes of visual impairment. The suppression of inflammation, promotion of epithelial repair and inhibition of CNV formation are promising therapeutic strategies for restoring corneal transparency. This study investigated the effects and underlying mechanisms of glycyrrhizic acid (GA) on inflammation, epithelial wound healing and CNV in a murine model of alkali burn. GA markedly alleviated corneal opacity, enhanced epithelial wound closure and reduced CNV formation in alkali-burned mice. Mechanistically, GA markedly downregulated tumor necrosis factor-α, interleukin (IL)-6, IL-17 and vascular endothelial growth factor A (VEGF-A) expression in injured corneas. In human umbilical vein endothelial cells, GA attenuated VEGF-A-induced proliferation and angiogenic activity. In human corneal epithelial cells, GA activated the focal adhesion kinase (FAK)/PI3K/AKT signaling pathway, upregulated Bcl-2 and cyclin D1 expression and suppressed Bax and caspase-3 expression, thereby promoting cell proliferation and reducing apoptosis. Overall, GA exerts protective effects against alkali burn-induced corneal injury by suppressing inflammation and neovascularization while promoting epithelial repair through activation of the FAK/PI3K/AKT signaling pathway.

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Cite

BibTeXRIS
BibTeX
@article{yu2026glycyrrhizic,
  title = {{Glycyrrhizic acid attenuates corneal inflammation and pathological angiogenesis through FAK/PI3K/AKT signaling}},
  author = {Jinjin Yu and Huiheng Qu and Yinming Fang and Weicheng Xu and Nannan Ding and Jie Ji and Nan Wang and Wei Shi},
  journal = {Molecular Medicine Reports},
  year = {2026},
  month = oct,
  doi = {10.3892/mmr.2026.14046},
  url = {https://doi.org/10.3892/mmr.2026.14046},
  note = {CC BY-NC-ND 4.0},
}
RIS
TY  - JOUR
TI  - Glycyrrhizic acid attenuates corneal inflammation and pathological angiogenesis through FAK/PI3K/AKT signaling
AU  - Jinjin Yu
AU  - Huiheng Qu
AU  - Yinming Fang
AU  - Weicheng Xu
AU  - Nannan Ding
AU  - Jie Ji
AU  - Nan Wang
AU  - Wei Shi
PY  - 2026
DA  - 2026/10/15
JO  - Molecular Medicine Reports
DO  - 10.3892/mmr.2026.14046
UR  - https://doi.org/10.3892/mmr.2026.14046
AB  - Corneal alkali burns lead to severe inflammation and corneal neovascularization (CNV), both of which are major causes of visual impairment. The suppression of inflammation, promotion of epithelial repair and inhibition of CNV formation are promising therapeutic strategies for restoring corneal transparency. This study investigated the effects and underlying mechanisms of glycyrrhizic acid (GA) on inflammation, epithelial wound healing and CNV in a murine model of alkali burn. GA markedly alleviated corneal opacity, enhanced epithelial wound closure and reduced CNV formation in alkali-burned mice. Mechanistically, GA markedly downregulated tumor necrosis factor-α, interleukin (IL)-6, IL-17 and vascular endothelial growth factor A (VEGF-A) expression in injured corneas. In human umbilical vein endothelial cells, GA attenuated VEGF-A-induced proliferation and angiogenic activity. In human corneal epithelial cells, GA activated the focal adhesion kinase (FAK)/PI3K/AKT signaling pathway, upregulated Bcl-2 and cyclin D1 expression and suppressed Bax and caspase-3 expression, thereby promoting cell proliferation and reducing apoptosis. Overall, GA exerts protective effects against alkali burn-induced corneal injury by suppressing inflammation and neovascularization while promoting epithelial repair through activation of the FAK/PI3K/AKT signaling pathway.
SN  - 1791-2997
SN  - 1791-3004
ER  -