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Juan Pablo Salica, Alejandro Fichetti, Eduardo Chuluyan, Diego Guerrieri, Juan E Gallo; Antiangiogenic Effect of a Novel Fusion Protein PFMC inhibiting NFKB pathway on Corneal Alkali Injury Rat Model. Invest. Ophthalmol. Vis. Sci. 2016;57(12):3514.
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© ARVO (1962-2015); The Authors (2016-present)
To investigate the effect of the Fusion Protein FPMC (SLPI and Cementoin) on the NFkB (nuclear factor kappa light chain enhancer of activated B cells) pathway during the acute inflammation process on a rat corneal alkali injury model.
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 Sprague Dawley 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 studied by slit lamp and pictured before euthanasia. Corneal Neovascularization (CNV) area was quantified. NFkB was assayed by Western Blot. Vascular endothelial growth factor (VEGF) protein was evaluated by immunohistochemistry. VEGF and NF-kB mRNA levels were determined by reverse transcription-polymerase chain reaction (RT-PCR).
The alkali injury induced CNV area was reduced in PFMC treated group. The NFkB curve on the acute inflammation process was significantly reduced by FPMC in comparison to the SLPI and Buffer treatment. VEGF and NFkB mRNA levels were lower on the Fusion Protein treated group.
The fusion protein FPMC demonstrated to reduce corneal neovascularization. The inhibition of NFkB pathway is one of the proven mechanisms of action of this novel protein.
This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.
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