J Korean Ophthalmol Soc > Volume 50(8); 2009 > Article
Journal of the Korean Ophthalmological Society 2009;50(8):1254-1258.
DOI: https://doi.org/10.3341/jkos.2009.50.8.1254    Published online August 15, 2009.
Effect of Dexamethasone on the Production of Nitric Oxide in Trabecular Meshwork Cells.
Soo Yoon Lee, Jae Woo Kim
Department of Ophthalmology, Catholic University of Daegu College of Medicine, Daegu, Korea. jwkim@cu.ac.kr
섬유주세포에서 덱사메타존이 산화질소의 생성에 미치는 영향
이수윤ㆍ김재우
Department of Ophthalmology, Catholic University of Daegu College of Medicine, Daegu, Korea
Abstract
PURPOSE
To investigate the effects of dexamethasone (DEX) on the production of nitric oxide (NO) and its enzymatic synthetic pathway in cultured human trabecular meshwork (HTM) cells. METHODS: Primarily cultured HTM cells were exposed to 0, 10, 100, 1000 nM of DEX for 3 days. In addition, 100 micrometer sepiapterin, 100 micrometer ascorbic acid, and 10 micrometer methotrexate were co-exposed to DEX. The cellular survival and nitrite production rates were assessed by MTT assay and Griess assay, respectively. RESULTS: DEX did not significantly affect the survival of cultured HTM cells. DEX decreased the NO production in a dose-dependent manner. With co-exposure of DEX, ascorbic acid nullified the DEX-induced decrease of NO production. Sepiapterin and methotrexate did not affect DEX-induced decrease of NO production. CONCLUSIONS: DEX decreased NO production in HTM cells and the de novo pathway of tetrahydrobiopterin may be involved. This decrease may raise intraocular pressure by decreasing trabecular outflow.
Key Words: Dexamethasone;Nitric oxide;Tetrahydrobiopterin;Trabecular meshwork cells


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