Effect of Dexamethasone on the Production of Nitric Oxide in Trabecular Meshwork Cells.
10.3341/jkos.2009.50.8.1254
- Author:
Soo Yoon LEE
1
;
Jae Woo KIM
Author Information
1. Department of Ophthalmology, Catholic University of Daegu College of Medicine, Daegu, Korea. jwkim@cu.ac.kr
- Publication Type:Original Article
- Keywords:
Dexamethasone;
Nitric oxide;
Tetrahydrobiopterin;
Trabecular meshwork cells
- MeSH:
Ascorbic Acid;
Biopterin;
Dexamethasone;
Humans;
Intraocular Pressure;
Methotrexate;
Nitric Oxide;
Pterins;
Trabecular Meshwork
- From:Journal of the Korean Ophthalmological Society
2009;50(8):1254-1258
- CountryRepublic of Korea
- Language:Korean
-
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.
