METHODS: Corneal neovascularization was established in mice by alkali burn. Sixty mice were then randomly distributed into normal group, Gly group and phosphate buffer solution(PBS)group. The mice were treated with subconjunctival injection of 2g/L Gly solution or vehicle alone every other day for 14d. Corneal inflammation and neovascularization were monitored with a slit lamp microscope. At the end of treatment, the corneas were harvested for hematoxylin-eosin(HE)staining as well as immunohistochemical of CD34 and myeloperoxidase(MPO)staining, microvessel density(MVD), neutrophils were then calculated.

RESULTS: At the 7 and 14d, the CNV area of Gly group were 4.16±0.00 and 7.33±0.13mm² respectively, which were lower than those in PBS group(7.58±0.20 and 9.24±0.08mm²; all P<0.05). The HE pathological staining showed that there were no changes in morphology as well as no neovascularization or inflammatory cell infiltration in the cornea of control group. In the Gly group, blood vessels and inflammatory cell infiltration nearly diminished with collagen in normal shape. While in the PBS group, extensive infiltration of inflammatory cells and neovascularization was examed in the corneal stroma. The immunohistochemical CD34 staining performed that the MVD in the Gly group was 11.13±1.46 bars per square millimeter, which was lower than that in PBS group(34.08±2.46)bars per square millimeter(P<0.001). Additionally, the immunohistochemical MPO staining showed that the number of neutrophils in Gly group was 17.50±1.98 cells per 200-fold field of view, lower than that in PBS group(59.56±4.79, P<0.001).

CONCLUSION: Gly can eliminate corneal inflammation and inhibit corneal neovascularization in mice with acute corneal alkali burn, which provides a new idea for clinical prevention and treatment of corneal neovascularization.