Journal ArticleDOI
Interaction between NO and COX pathways in retinal cells exposed to elevated glucose and retina of diabetic rats
TLDR
In vitro results suggest that the hyperglycemia-induced increase in NO in retinal Müller cells and endothelial cells increases production of cytotoxic prostaglandins via COX-2 and that inhibition of retinopathy by aminoguanidine or aspirin is due at least in part to inhibition of this NO/COX- 2 axis.Abstract:
A nonselective inhibitor of cyclooxygenase (COX; high-dose aspirin) and a relatively selective inhibitor of inducible nitric oxide synthase (iNOS; aminoguanidine) have been found to inhibit develop...read more
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Book
Müller Cells in the Healthy and Diseased Retina
Andreas Bringmann,Thomas Pannicke,Jens Grosche,Mike Francke,Peter Wiedemann,Serguei N. Skatchkov,Neville N. Osborne,Andreas Reichenbach +7 more
TL;DR: A proper understanding of the gliotic responses of Müller cells in the diseased retina, and of their protective vs. detrimental effects, is essential for the development of efficient therapeutic strategies that use and stimulate the neuron-supportive/protective-and prevent the destructive-mechanisms of gliosis.
Journal ArticleDOI
Inflammation in diabetic retinopathy.
TL;DR: The inflammatory mediators and their relationship to early and late DR are reviewed, and the potential of anti-inflammatory approaches to inhibit development of different stages of the retinopathy is discussed.
Journal ArticleDOI
Contributions of Inflammatory Processes to the Development of the Early Stages of Diabetic Retinopathy
TL;DR: This new hypothesis offers new insight into the pathogenesis of diabetic retinopathy, and offers novel targets to inhibit the ocular disease.
ReviewArticle Contributions of Inflammatory Processes to the Development of the Early Stages of Diabetic Retinopathy
TL;DR: The concept that localized inflammatory processes play a role in the development of diabetic retinopathy is relatively new, but evidence that supports the hypothesis is accumulating rapidly as mentioned in this paper, and offers novel targets to inhibit the ocular disease.
Journal ArticleDOI
Role of Inflammation in Diabetic Retinopathy
TL;DR: This review focuses on the involvement of inflammation in the pathophysiology of diabetic retinopathy with special emphasis on the functional relationships between glial cells and neurons, and summarizes recent advances using novel targets to inhibit inflammation.
References
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Journal ArticleDOI
Inhibition of NF-kappa B by sodium salicylate and aspirin
Elizabeth Kopp,Sankar Ghosh +1 more
TL;DR: The anti-inflammatory drugs sodium salicylate and aspirin inhibited the activation of NF-kappa B, which further explains the mechanism of action of these drugs.
Journal ArticleDOI
Nitric oxide activates cyclooxygenase enzymes
Daniela Salvemini,Thomas P. Misko,Jaime L. Masferrer,Karen Seibert,Mark G. Currie,Philip Needleman +5 more
TL;DR: It is demonstrated that NO enhances COX activity through a mechanism independent of cGMP and suggested that, in conditions in which both the NOS and COX systems are present, there is an NO-mediated increase in the production of proinflammatory prostaglandins that may result in an exacerbated inflammatory response.
Journal ArticleDOI
A Fluorometric Assay for the Measurement of Nitrite in Biological Samples
TL;DR: This fluorometric method combines speed and sensitivity with the handling of a large number of samples for the quantification of nitrite generated from in vivo and in vitro sources.
Journal ArticleDOI
Selective inhibition of the inducible nitric oxide synthase by aminoguanidine.
Thomas P. Misko,William M. Moore,Thomas P. Kasten,G. Allen Nickols,John A. Corbett,Ronald G. Tilton,Michael L. McDaniel,Joseph R. Williamson,Mark G. Currie +8 more
TL;DR: It is demonstrated that aminoguanidine selectively inhibits the cytokine-inducible isoform of NO synthase which appears to be responsible for the excess production of NO linked to these disease states.
Journal ArticleDOI
Accelerated death of retinal microvascular cells in human and experimental diabetic retinopathy.
TL;DR: Findings indicate that diabetes and galactosemia lead to accelerated death in situ of both retinal pericytes and endothelial cells; the event is specific for vascular cells; it precedes histological evidence of retinopathy; and it can be induced by isolated hyperhexosemia.