Abstract
The pathophysiological processes of inflammation can lead to a host of diseases, such as periodontitis, atherosclerosis, rheumatoid arthritis, and even cancer. The dysregulated inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) activation play important roles in the development of certain inflammatory diseases. Here, we investigated the effects of CDr10b which is originally developed for a microglia staining probe on inflammation, by modulating NF-κB activation and iNOS and COX-2 expression induced by lipopolysaccharide (LPS) in murine macrophages. The CDr10b suppressed NF-κB activation and iNOS and COX-2 expression induced by LPS. All the results suggest that CDr10b is a promising novel agent for the treatment of inflammatory diseases.
Keywords:
CDr10b; Cyclooxygenase-2; Inducible nitric oxide synthase; Inflammation; Nuclear factor-κB.
Copyright © 2014 Elsevier B.V. All rights reserved.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Anti-Inflammatory Agents / pharmacology
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Boron Compounds / pharmacology*
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Cell Line
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Cyclooxygenase 2 / genetics
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Cyclooxygenase 2 / metabolism*
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Enzyme Activation / drug effects
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Gene Expression / drug effects
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Immunologic Factors / pharmacology
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Inflammation / drug therapy
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Inflammation / metabolism
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Lipopolysaccharides / pharmacology*
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Macrophages / drug effects
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Macrophages / metabolism
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Mice
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Myeloid Differentiation Factor 88 / metabolism
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NF-kappa B / metabolism
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Nitric Oxide Synthase Type II / genetics
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Nitric Oxide Synthase Type II / metabolism*
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Signal Transduction / drug effects
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Toll-Like Receptor 4 / metabolism
Substances
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Anti-Inflammatory Agents
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Boron Compounds
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CDr10b compound
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Immunologic Factors
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Lipopolysaccharides
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Myd88 protein, mouse
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Myeloid Differentiation Factor 88
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NF-kappa B
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Tlr4 protein, mouse
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Toll-Like Receptor 4
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Nitric Oxide Synthase Type II
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Nos2 protein, mouse
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Ptgs2 protein, mouse
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Cyclooxygenase 2