Antiangiogenic Effect of a Novel Fusion Protein PF-MC inhibiting NF­κB pathway in a Corneal Alkali Injury Rat Model

SALICA, JP; ORTIZ, G; GUERRIERI, D; CHULUYAN, E; GALLO, JE

Seattle

Congreso; ARVO Annual Meeting; 2016

ASSOCIATION FOR RESEARCH IN VISION AND OPHTHALMOLOGY

Antiangiogenic Effect of a Novel Fusion Protein PF-MC inhibiting NF­κB pathway in a Corneal Alkali Injury Rat ModelPurpose: To investigate the effect of the Fusion Protein FP-MC (SLPI and Cementoin) on the NF­κB (nuclear factor kappa­light­chain­enhancer of activated B cells) pathway during the acute inflammation process on a rat corneal alkali injury model. Methods: An alkali injury was produced with a filter paper of 3 mm with 1 N NaOH during 40 seconds in the right cornea of 27 Sprague­Dowley rats under isoflurane anesthesia. They were treated with 10 ul of FP­MC (0,2 ug/ul; n=9), SLPI (0,2 ug/ul; n=9) or vehicle (n=9) topically, four times a day. Three rats of each group were sacrificed at 6 hours, 4 days and 10 days after injury. Corneas were examined with a slit lamp and digital photographs were taken before euthanasia. Corneal Neovascularization (CNV) area was quantified. NF­kB was studied by Western Blot and RT-PCR using a primary antibody anti NF-KB 65/100 and corresponding primer, respectively. Results: The alkali injury induced CNV area was reduced in PF-MC treated group at 10 days. The NF-kB curve (from 6 hours to 10 days) was significantly reduced by FP-MC in comparison to the SLPI and Buffer treatment NF-kB mRNA levels were lower in the Fusion Protein treated group. Conclusions: The Fusion Protein FP-MC reduced corneal neovascularization. The inhibition of NF­kB pathway is one of the proven mechanisms of action of this novel protein.