Effect of ERK inhibitor on corneal neovascularization induced by alkali burn in mice and its mechanism

The objective of this study is to explore the effect of extracellular signal–regulated kinase (ERK) inhibitors on corneal neovascularization induced by alkali burn in mice and its mechanism. A total of 30 standard diet (SD) healthy mice were divided into normal group, alkali burn group, and inhibitor group. Normal group was not treated. Alkali burn group and inhibitor group were used to establish corneal neovascularization model induced by alkali burn. After successful modeling, ERK inhibitor was used to intervene in inhibitor group, and saline of equal volume was used in normal group and alkali burn group. The area of corneal neovascularization was calculated and the expression of vascular endothelial growth factor (VEGF), c-Fos, c-Jun, ERK1/2, and p-ERK1/2 protein in cornea tissue of three groups of mice was detected. The relative expression of vascular area, length, VEGF, c-Fos, c-Jun, ERK1/2, and p-ERK1/2 protein in cornea tissue of mice in alkali burn group was significantly higher than that in normal group and inhibitor group. The relative expression of vascular area, length, VEGF, c-Fos, c-Jun, ERK1/2, and p-ERK1/2 protein in cornea tissue of mice in inhibitor group was higher than that in normal group, and the expression level of PEDF was lower than that in normal group ( P  < 0.05). ERK inhibitors inhibit the formation of corneal neovascularization by inhibiting the expression of VEGF, c-Fos, and c-Jun proteins through the action of ERK signaling pathway.