Intravitreal Nilotinib Reduces Fibroblast Growth Factor-2 Levels in a Rat Model of Dispase-Induced Intraocular Inflammation.

Purpose: To evaluate the effect of nilotinib, a tyrosine kinase inhibitor, on cytokine levels in a dispase-induced rat model of intraocular inflammation. Methods: Twenty-one Sprague-Dawley rats were randomized into 3 groups, with 7 rats in each group. Group 1 (control) received no intervention. Groups 2 (sham) and 3 (treatment) received 0.07 IU/0.1 mL dispase at baseline. At week 8, Group 2 received dimethyl sulfoxide, while Group 3 received intravitreal nilotinib (2 ng/µL). All animals were euthanized at week 8, and an enzyme-linked immunosorbent assay was used to analyze enucleated eyes for levels of transforming growth factor-β, platelet-derived growth factor, fibroblast growth factor-2, vascular endothelial growth factor (VEGF), and interleukin-1β. Results: Compared with controls, Group 2 showed significant increases in all cytokines (P < .05). In Group 3, transforming growth factor-β, platelet-derived growth factor, VEGF, and interleukin-1β were reduced compared with Group 2, but these decreases were not statistically significant. In contrast, fibroblast growth factor-2 levels were significantly lower in Group 3 (P < .01). Conclusions: The biochemical findings of the current study indicate the potential of nilotinib in modulating fibrotic processes. Further investigations incorporating anatomic endpoints may help to more clearly define nilotinib's possible role in the treatment of ocular diseases associated with fibrosis.