Abstract
Purpose: Resveratrol (RSV), an antioxidant polyphenol, has demonstrated beneficial effects in various ocular diseases including glaucoma. Our study was designed to evaluate the effects of RSV on nitric oxide synthase (NOS) enzymes, nitric oxide (NO) and interleukin-1 alpha (IL-1 α), in human glaucomatous trabecular meshwork (TM) cells. Methods: Western blot was utilized to determine endothelial and inducible NOS (eNOS, iNOS) expression. The concentration-related effects of RSV on IL-1 α and NO levels were assessed using the respective ELISA kits. Results: Densitometry data showed concentration-related increases in eNOS, and reduction in iNOS expression at high RSV concentrations. RSV treatment (0.1, 1, 10 and 100 µM) resulted in increased NO levels (6 ± 0.7, 7 ± 0.8, 7.3 ± 0.7 and 9.5 ± 1 nM/mg protein, respectively). The average value obtained for control was 4.8 ± 0.6 nM/mg protein. Significant increases in IL-1α levels were observed with lower concentrations of RSV. However, at higher RSV concentrations (10–100 μM), IL-1 levels decreased. Conclusions: Resveratrol increased NO in glaucomatous TM cells, possibly by increasing eNOS expression. Thus, RSV-induced NO production supports the beneficial effects of this antioxidant in glaucoma. Furthermore, our results showing a reduction in iNOS, a contributor to oxidative stress expression, further support RSV’s antioxidant capabilities in vision.
Highlights
Glaucoma is a neurodegenerative disease often associated with age progression
We examined the changes in iNOS protein expression following treatment with resveratrol at the highest concentration used in the other studies
Our results demonstrate that resveratrol produced a concentration-dependent increase in eNOS expression in glaucomatous trabecular meshwork (TM) cells
Summary
Glaucoma is a neurodegenerative disease often associated with age progression. Progressive visual field loss and possible irreversible blindness accompany this ocular disease [1]. Our laboratory is interested in the oxidative stress-induced degeneration of the ocular epithelium in the trabecular meshwork (TM) endothelial cells, which is a characteristic of primary open-angle glaucoma (POAG). In POAG patients, the number of TM endothelial cells is significantly decreased when compared to age-matched controls [2]. Oxidative stress and inflammation are believed to be primary factors in the loss of these TM cells [2,3]. The oxidative stress can cause DNA damage, which is a significant factor inducing elevated IOP in POAG [1]
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