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

Yu,Jinjin; Qu,Huiheng; Fang,Yinming; Xu,Weicheng; Ding,Nannan; Ji,Jie; Wang,Nan; Shi,Wei

doi:10.3892/mmr.2026.14046

December-2026 Volume 34 Issue 6

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December-2026 Volume 34 Issue 6

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

Authors:
- Jinjin Yu
- Huiheng Qu
- Yinming Fang
- Weicheng Xu
- Nannan Ding
- Jie Ji
- Nan Wang
- Wei Shi
View Affiliations / Copyright

Affiliations: Department of Ophthalmology, Wuxi Affiliated Hospital of Nanjing University of Chinese Medicine, Wuxi, Jiangsu 214000, P.R. China, Department of General Surgery, Jiangnan University Medical Center, Jiangnan University, Wuxi, Jiangsu 214002, P.R. China, Department 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, Department of Ophthalmology, Jiangnan University Medical Center, Jiangnan University, Wuxi, Jiangsu 214002, P.R. China

Copyright: © Yu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
Article Number: 335
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Published online on: October 15, 2026

https://doi.org/10.3892/mmr.2026.14046
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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.

Journals

International Journal of Molecular Medicine

International Journal of Oncology

Molecular Medicine Reports

Oncology Reports

Experimental and Therapeutic Medicine

Oncology Letters

Biomedical Reports

Molecular and Clinical Oncology

World Academy of Sciences Journal

International Journal of Functional Nutrition

International Journal of Epigenetics

Medicine International

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

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Abstract

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