Abstract
Purpose:
To determine the effects of a novel Resolvin E1 analog, RX-10045, on lens epithelial cell (LEC) viability in vitro and in an ex vivo model of posterior capsule opacification (PCO).
Methods:
In vitro models using cultured human and canine LEC were used to determine if various RX-10045 concentrations (0.0, 0.1, or 0.5%) altered LEC migration and viability. A one-millimeter scratch was created in confluent cultures and cellular ingrowth was monitored over 24 hours. Concurrently, cultures were grown to 75% confluence prior to RX-10045 treatment; time to achieve confluence was evaluated at 8, 24, 30, and 48 hours. Cellular viability was assessed using an LDH assay on confluent LEC treated with RX-10045 for 2, 4, 8, or 24 hours. Ex vivo PCO formation was modeled by performing mock cataract surgery on canine cadaver eyes. Lens capsules were subsequently treated with 0.0, 0.1, or 0.5% RX-10045 for 7 days prior to histologic evaluation.
Results:
Both concentrations of RX-10045 (0.1 and 0.5%) inhibited restoration of the cellular monolayer following scratch formation and prevented sub-confluent LEC from obtaining confluence. Cellular viability was markedly reduced within 24 hours of RX-10045 treatment. Compared to controls, ex vivo PCO formation was delayed with 7 days of exposure to RX-10045.
Conclusions:
Seven days of intracapsular exposure to a novel Resolvin E1 analog, RX-10045, reduced PCO formation. Induction of cell death, rather than inhibition of cellular migration, is the likely mechanism of effect. These results warrant further evaluation of this promising drug for treatment of PCO.