AIM: To test whether subconjunctival injection of avastin could suppress corneal neovascularization induced by alkali injury and study its mechanisms.

METHODS: Alkali injury was induced by application of 1mol/L NaOH to right eyes of New Zealand white rabbits for 30 seconds(n=20). All animals were randomly assigned to A, B groups, each consisting of 10 eyes. Group A received subjunctival injection of avastin after alkali injury immediately in 2.5mg dosage. Group B received subconjuctival injection of normal salt. Biomicroscopic neovascularization was observed on 3, 7, 14, 21 and 28 days. The average length, area and inhibitory rate of corneal neovascularization(CNV)were calculated respectively. Five rabbits were randomly killed in each group on 7 and 28 days and the corneas were taken for histopathological examination.Immunohistochemical studies on the expression of VEGF in corneal paraffin sections were also carried out.

RESULTS:The vessel meshworks of corneal limb were dilated and congested on the 1^st day, then neovascularization(NV)began to invade cornea on 3^rd day, and reached to its developmental peaks between 7 and 14 days, lastly, NV started to regress on 14-21 days after alkali injury. Significant difference(P<0.05)in the area of NV, average length of NV and corneal edema were found respectively between group A and B(P<0.05); the inhibitory rate of CNV ranges from 44.2% to 55% in group A. There were slight epithelium and fiber edema in group A,and disappeared in the late, the fiber arranged straightly and less NV intruded into the central cornea. Immunohistochemical studies indicated that the expression of vascular endothelial growth factor(VEGF)in group A was obvious lower compared to group B on 7 and 28 days.

CONCLUSION:Avastin suppresses corneal neovascu- larization induced by alkali injury on rabbit eyes with subconjunctival injection through decreasing expression of VEGF.