Japanese journal of ophthalmology · 2005
Study of effects of antiglaucoma eye drops on N-methyl-D-aspartate-induced retinal damage.
Сравнительное исследованиеСтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Metoki Tomomi, Ohguro Hiroshi, Ohguro Ikuyo, Mamiya Kazuhisa, Ito Tadashi, Nakazawa Mitsuru
Аннотация
PURPOSE: To study the effects of antiglaucoma eye drops on N-methyl-D-aspartate (NMDA)-induced retinal damage.
METHODS: Several antiglaucoma eye drops, beta-blockers, alpha/beta-blockers, an alpha1-blocker, an alpha2-agonist, and a prostaglandin derivative, were topically administrated to NMDA-treated rat eyes daily for 2 weeks, and the retinal thickness, the number of retrograde-labeled retinal ganglion cells (RGCs), and the results of a cDNA microarray analysis were studied.
RESULTS: Intravitreal administration of NMDA caused a significant decrease in the thickness of the retinal layers and induced upregulation of glial fibrillary acidic protein (GFAP). Topical administration of beta-blockers (timolol, betaxolol, and carteolol) and a prostaglandin derivative (latanoprost) showed almost no significant effects on retinal thickness, the number of RGCs, or expression of GFAP. In contrast, the alpha/beta-blockers (nipradilol and levobunolol), the alpha1-blocker (bunazosin HCl), and the alpha2-agonist (brimonidine) showed preservation effects on retinal thickness and the number of RGCs, and marked suppression of NMDA-induced upregulation of GFAP. Among 1101 genes related to cellular regulatory mechanisms, the expression of two genes, both for insulin-like growth factors, (IGF-1) and ErbB3, was altered upon administration of the alpha/beta-blockers, the alpha1-blocker, and the alpha2-agonist.
CONCLUSION: Our present study suggests that modulations of the alpha-adrenergic receptor, alpha1-blocking and alpha2-stimulation, by antiglaucoma eye drops may cause beneficial effects on NMDA-induced retinal damage in the rat.
METHODS: Several antiglaucoma eye drops, beta-blockers, alpha/beta-blockers, an alpha1-blocker, an alpha2-agonist, and a prostaglandin derivative, were topically administrated to NMDA-treated rat eyes daily for 2 weeks, and the retinal thickness, the number of retrograde-labeled retinal ganglion cells (RGCs), and the results of a cDNA microarray analysis were studied.
RESULTS: Intravitreal administration of NMDA caused a significant decrease in the thickness of the retinal layers and induced upregulation of glial fibrillary acidic protein (GFAP). Topical administration of beta-blockers (timolol, betaxolol, and carteolol) and a prostaglandin derivative (latanoprost) showed almost no significant effects on retinal thickness, the number of RGCs, or expression of GFAP. In contrast, the alpha/beta-blockers (nipradilol and levobunolol), the alpha1-blocker (bunazosin HCl), and the alpha2-agonist (brimonidine) showed preservation effects on retinal thickness and the number of RGCs, and marked suppression of NMDA-induced upregulation of GFAP. Among 1101 genes related to cellular regulatory mechanisms, the expression of two genes, both for insulin-like growth factors, (IGF-1) and ErbB3, was altered upon administration of the alpha/beta-blockers, the alpha1-blocker, and the alpha2-agonist.
CONCLUSION: Our present study suggests that modulations of the alpha-adrenergic receptor, alpha1-blocking and alpha2-stimulation, by antiglaucoma eye drops may cause beneficial effects on NMDA-induced retinal damage in the rat.