Abstract
This study investigated the preventive effect of ribosomal protein S3 (rpS3) on 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced ear edema in mice. A cell permeable expression vector PEP-1-rpS3 was constructed. Topical application of the vector markedly inhibited TPA-induced expression levels of cyclooxygenase-2 (COX-2) and pro-inflammatory cytokines. Application of PEP-1-rpS3 also resulted in a significant reduction in the activation of nuclear factor-kappa B (NF-kB) and mitogen-activated protein kinase (MAPK) in TPA-treated ears. These results indicate that PEP-1-rpS3 inhibits inflammatory response cytokines and enzymes by blocking NF-kB and MAPK, prompting the suggestion that PEP-1-rpS3 can be used as a therapeutic agent against skin inflammation.
Copyright © 2010 Elsevier Ireland Ltd. All rights reserved.
Publication types
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Comparative Study
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Dermatitis / genetics
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Dermatitis / pathology
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Dermatitis / prevention & control*
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Edema / genetics
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Edema / pathology
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Edema / prevention & control
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Genetic Vectors / therapeutic use
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Humans
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Inflammation Mediators / metabolism
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Inflammation Mediators / physiology*
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Inflammation Mediators / therapeutic use
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Male
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Mice
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Mice, Inbred ICR
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Peptide Hydrolases / genetics*
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Peptide Hydrolases / therapeutic use
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Plant Proteins / genetics*
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Plant Proteins / therapeutic use
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Ribosomal Proteins / genetics*
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Ribosomal Proteins / therapeutic use
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Tetradecanoylphorbol Acetate / antagonists & inhibitors
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Tetradecanoylphorbol Acetate / toxicity*
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Transduction, Genetic / methods
Substances
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Inflammation Mediators
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Plant Proteins
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Ribosomal Proteins
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YRPS3 protein, Petunia hybrida
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ribosomal protein S3
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Peptide Hydrolases
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peptidase-1 (Pleurodeles)
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Tetradecanoylphorbol Acetate