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R.N. Aravalli, S.P. Ayalasomayajula, A.C. Amrite, U.B. Kompella; Celecoxib, a selective COX–2 inhibitor, inhibits diabetes–induced retinal PGE2 secretion . Invest. Ophthalmol. Vis. Sci. 2004;45(13):3580.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: Previously we have demonstrated that celecoxib, a selective inhibitor of cyclooxygenase–2 (COX–2) enzyme, inhibits diabetes–induced retinal vascular endothelial growth factor (VEGF) expression and vascular leakage. The objective of this study was to determine whether COX–2 is responsible for diabetes–induced PGE2 secretion from isolated rat retinas. Methods: All the animals were treated according to the ARVO statement for animal care. Diabetes was induced in Sprague Dawley rats by single intraperitoneal injection of streptozotocin (60 mg/kg) following 24 hours of fasting. The blood glucose levels were determined using onetouch ultra® and animals with blood glucose levels > 250 mg/dL were deemed diabetic. On day 14, the animals were euthanized with single intraperitoneal injection of pentobarbital sodium (250 mg/Kg). The retinas (both nondiabetic and diabetic rats) were isolated and immersed in 100 µL of assay buffer (pH: 7.4) and incubated in the presence or absence of 1 µM celecoxib (a selective COX–2 inhibitor) or SC560 (a selective COX–1 inhibitor). The secreted PGE2 levels at the end of 2 hours in the supernatants were determined using EIA (Cayman chemicals). Results: The secreted PGE2 levels from isolated diabetic retinas were significantly higher compared to nondiabetic controls (32.1 ± 4.7 vs 11.1 ± 1.6 pg/mg, p<0.05). Co–incubation with celecoxib (11.76 ± 4.5 pg/mg, p<0.05) but not SC560 (30 ± 1.2 pg/mg) significantly reduced diabetes–induced retinal PGE2 secretion. However, both celecoxib and SC560 had no affect on basal PGE2 secretion from the isolated non–diabetic rat retinas Conclusion: The PGE2 secretion is significantly induced in diabetic rat retinas. Celecoxib but not SC560 inhibited diabetes–induced PGE2 secretion from isolated retinas, suggesting that the activity of COX–2 but not COX–1 might be responsible for the diabetes induced PGE2 secretion. Financial Support: Supported by NIH grant DK064172. Disclosures/Conflicts: None
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