Abstract
Abstract: :
Purpose: It has been reported that intravitreal triamcinolone inhibits choroidal neovasculization (CNV) in exudative age-related macular degeneration (AMD) and in laser-induced CNV animal model. The mechanism of inhibition of angiogenesis by triamcinolone remains unknown. Since vascular endothelial growth factor (VEGF) is a major stimulator of CNV, we examined whether triamcinolone can regulate VEGF expression in rat retina. Methods: Triamcinolone acetonide of 320 µg in 8 µl was injected intravitreally into eyes of normal adult Sprague-Dawley rats, and saline of equal volume was injected into fellow eyes of each animal as controls. Animals were sacrificed at 3 days, 1 week, and 2 weeks after injection (N = 3 for each stage), and eyes were processed for in situ hybridization using radio-labeled rat VEGF riboprobes. Results: VEGF mRNA expression signals are localized in choroid, retinal pigment epithelium (RPE), cells in the inner nuclear layer, and ganglion cells, as reported in previous studies. High levels of hybridization signals are present in choroid and cells in the INL. Image analyses show no significant difference in VEGF expression levels in these cells between triamcinolone- and saline-injected eyes from 3 days to 2 weeks following injection. Conclusion: Our studies show that intravitreal triamcinolone does not change VEGF mRNA expression 2 weeks after injection in normal adult rats. It remains to be determined whether triamcinolone regulates VEGF expression in CNV caused by exudative AMD or induced by laser treatment in animal models.
Keywords: 308 age-related macular degeneration • 346 choroid: neovascularization • 423 growth factors/growth factor receptors