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Kenji Nagata, Kazuichi Maruyama, Hiroshi Keino, Shigeru Kinoshita; Effect of Cyclooxygenase 2 Inhibitor on Experimental Autoimmune Uveoretinitis in Rats. Invest. Ophthalmol. Vis. Sci. 2011;52(14):2951.
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© ARVO (1962-2015); The Authors (2016-present)
Celecoxib, a nonsteroidal anti-inflammatory drug, selectively inhibits cyclooxygenase-2 (COX-2), which is known to suppress tumor growth, angiogenesis, and lymphogenesis. The purpose of this study was to investigate the anti-inflammatory effect of celecoxib on an experimental autoimmune uveitis (EAU).
Lewis rats were immunized with bovine interphotoreceptor retinoid-binding protein (IRBP) peptide (R14) and given 500ppm of celecoxib daily by oral administration. Intraocular inflammation was assessed by slit-lamp biomicroscopy and histopathological examination on Day 14 after the injection of IRBP. The animals were then sacrificed at Day 14. The expression levels of tumor necrosis factor (TNF)-α, interferon (INF)-γ, and prostaglandin E (PGE) in the retina and lymph node were analyzed by real-time PCR.
The average of the clinical score (2.6 in celecoxib group, 5.0 in control group) and histopathological score (2.6 in celecoxib group, 3.4 in control group) showed that the clinical and histopathological inflammatory change was significantly reduced (p<0.01, p<0.05) in the celecoxib group compared with the control group. The levels of TNF-α, IFN-γ, and PGE in the retina were 1.68±0.14, 1.00±0.13, and 0.35±0.08, respectively, in the celecoxib group, and were 2.97±0.49, 1.20±0.19, and 0.39±0.07, respectively, in the control group. The level of TNF-α was significantly lower in the celecoxib group. The levels of IFN-γ and PGE showed no significant difference between the two groups. Real-time PCR analysis of these three cytokines in the lymph node showed no significant difference between the two groups.
The results of this study show that systemic administration of celecoxib suppresses IRBP-induced EAU in rats.
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