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

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.