| Background and ObjectiveCorneal alkali burn can result in corneal edema and then corneal neovascularization (CRNV) in advanced cases. Because of its exudation, hemorrhage and secondary fibrosis, the corneal transparence was impared. Published data indicate the involvement of Nitric oxide (NO) in neovascularization. Inducible nitric oxide synthase (iNOS) is the primary NO provider in inflammation. However, the role of iNOS on neovascularization is still not well known. Present study focused on the role of NO and iNOS on alkali injury induced CRNV.Material and Methods1. CRNV was induced by alkali injury and compared in NOS inhibitor -treated or vehicle treated mice from 1 week before injury. NOS expression at 2 and 4 days after injury was quantified by RT-PCR. CRNV was observed and compared by ophthalmic microscope and CD31-immunostaining 14 days after injury.2. CRNV was induced by alkali injury and compared in iNOS inhibitor -treated or vehicle treated mice. iNOS was inhibited by AG in 0.2% sodium hyaluronate(HA) local administration 3 times per day after alkali injury. Vehicle mice were treated with 0.2%HA. iNOS and VEGF expression at 2 and 4 days after injury was quantified by RT-PCR. CRNV was observed and compared by ophthalmic microscope and CD31-immunostaining 2 weeks after injury.Results1. Compared with vehicle treated mice, NOS inhibitor-treated mice exhibited decreased intra-corneal NOS mRNA expression in the early phase (day 2, day 4) after alkali injury and enhanced CRNV 2 weeks after injury, as evidenced by enlarged CD31-positive areas. 2. Compared with vehicle treated mice, iNOS inhibitor-treated mice exhibited decreased intra-corneal iNOS mRNA expression and enhanced intra-corneal VEGF mRNA expression in the early phase (day 2, day 4) after alkali injury. However, no significant CRNV change was found 2 weeks after injury, as evidenced by enlarged CD31-positive areas.ConclusionOur results suggest NOS (NO) but not iNOS promote the alkali injury induced CRNV. |
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