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Pouya Pakneshan, Amy E. Birsner, Irit Adini, Christian M. Becker, Robert J. D'Amato; Differential Suppression of Vascular Permeability and Corneal Angiogenesis by Nonsteroidal Anti-inflammatory Drugs. Invest. Ophthalmol. Vis. Sci. 2008;49(9):3909-3913. doi: 10.1167/iovs.07-1527.
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purpose. Angiogenesis, the formation of new capillary blood vessels, is an essential biological process under physiological conditions, including embryonic development, reproduction, and wound repair. Under pathologic conditions, this process plays a critical role in a variety of diseases such as cancer, rheumatoid arthritis, atherosclerosis, endometriosis, diabetic retinopathy, and age-related macular degeneration. The purpose of this study was to examine the effects of cyclooxygenase inhibitors on basic fibroblast growth factor (bFGF)– and vascular endothelial growth factor (VEGF)–mediated ocular neovascularization and permeability.
methods. A modified Miles vascular permeability assay was used to examine VEGF-induced vascular hyperpermeability, and the mouse corneal model of angiogenesis was used to compare the efficacy of systemic treatment with different nonsteroidal anti-inflammatory drugs (NSAIDs) on bFGF- and VEGF-induced angiogenesis.
results. The authors demonstrated that systemic application of most NSAIDs, but not acetaminophen, blocked VEGF-induced permeability in mice. However, systemic treatment of mice with NSAIDs resulted in the differential inhibition of bFGF-induced (5%–57%) and VEGF-induced (3%–66%) corneal angiogenesis. The selective COX-2 inhibitors were more effective at suppressing bFGF-induced angiogenesis than VEGF-induced angiogenesis.
conclusions. Though most NSAIDS are effective at suppressing vascular leak, there exists a differential efficacy at suppressing the angiogenic response of specific cytokines such as bFGF and VEGF.
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