Influence Of Topical Carbonic Anhydrase Inhibitor On The Expression Of Aquaporin-1in Rat Cornea With Neovascularization

Background Researches showed that aquaporin-1(AQP1) is closelyassociated with corneal neovescularization (CNV). Carbonic anhydraseinhibitor has the inhibitory effect on the AQP1and further suppresses theCNV. However, the systemic adverse effect of Carbonic anhydraseinhibitor limit its clinical application. Therefore, the influence of topicalcarbonic anhydrase inhibitor on CNV is concerned. Objective Presentstudy was to investigate the effects of topical carbonic anhydrase inhibitorson the expression of AQP1in rat cornea after alkali burn and explore itsrole in corneal neovascularization (CNV).Methods The alkali-burn animal models were established in60eyesof30clean Sprague Dawley rats by putting the filter paper soaked1mol/LNaOH solution at the central cornea for40seconds.1%Brinzolamide wastopically administered in the30eyes of15models (Brinzolamide group),and the normal saline solution was used at the same way in other30eyes of15rats (model group). The10eyes of5normal Sprague Dawley receivedthe eye drops of normal saline solution as the normal control group. Thecorneal burning degree was graded on the Mahoney’s criteria in the thirdday, and Ee’s method was used to score the opacification of cornea and theCNV area was analyzed in3,5,7,10days under the slit lamp microscope.The cornea tissue was obtained in the tenth day after burning for theobservation of the pathology under the light microscope and the ultrastructure under the transmission electron microscope(TEM). Theexpressions of AQP1and vascular endothelial growth factor (VEGF) incornea tissue were detected using immunohistochemistry. The use ofanimals complied with the Statement of ARVO.Results No significant difference was seen in the scores of ratcorneal alkali burn between the model group and brinzolamide group(t=0.97, P>0.05). The scores of corneal edema and opacification andneovascular area were lower in brinzolamide group compared with modelgroup (t=2.18, P<0.05; t=6.58, P<0.01). The pathological andultrastructural examinations showed less CNV and inflammatory cells inrat corneal tissue of the brinzolamide group in comparison with modelgroup. The grey values of AQP1were88.01±11.03and58.10±12.14, and’those of VEGF were84.92±9.49and78.18±11.41in the model group andbrinzolamide group respectively, showing statistically significantdifferences (AQP1: t=9.99, P=0.00; VEGF: t=2.48, P=0.02).Conclusions1%Brinzolamide suppresses alkali burn-inducedCNV by downregulating the expressions of AQP1and VEGF in cornea inrat.