Abstract
Inflammatory mediators are known to play a key role in tumorigenesis, therefore, it is a promising strategy to inhibit the inflammation for cancer prevention and/or treatment. Current study was performed to investigate the effects of chondroitin sulfate (CS) extracted from Styela clava tunic on TNF-alpha-induced inflammation and to elucidate the mechanism of CS on the regulation of inflammatory factors in JB6 cells. Our results showed that CS inhibited TNF-alpha-induced NF-kappaB activation and subsequent vascular cell adhesion molecule 1 and inducible nitric oxide synthase expressions by blocking Akt signals in JB6 cells. Our results suggest that CS may be developed as an effective anti-inflammatory agent in the future.
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 / isolation & purification
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Anti-Inflammatory Agents / pharmacology
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Blotting, Western
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Cell Line
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Cell Survival
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Chondroitin Sulfates / isolation & purification
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Chondroitin Sulfates / pharmacology*
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Down-Regulation / drug effects
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Epidermis / chemistry
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Inflammation / chemically induced
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Inflammation / metabolism
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Inflammation Mediators / metabolism*
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Mice
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NF-kappa B / metabolism*
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Nitric Oxide Synthase Type II / metabolism
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Proto-Oncogene Proteins c-akt / metabolism*
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Signal Transduction / drug effects
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Tumor Necrosis Factor-alpha / antagonists & inhibitors*
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Tumor Necrosis Factor-alpha / pharmacology
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Urochordata / chemistry*
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Vascular Cell Adhesion Molecule-1 / metabolism
Substances
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Anti-Inflammatory Agents
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Inflammation Mediators
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NF-kappa B
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Tumor Necrosis Factor-alpha
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Vascular Cell Adhesion Molecule-1
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Chondroitin Sulfates
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Nitric Oxide Synthase Type II
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Nos2 protein, mouse
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Proto-Oncogene Proteins c-akt