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Transduced PEP-1-ribosomal protein S3 (rpS3) ameliorates 12-O-tetradecanoylphorbol-13-acetate-induced inflammation in mice

Authors
Ahn, Eun HeeKim, Dae WonKang, Hye WonShin, Min JaeWon, Moo HoKim, JoonKim, Dong JoonKwon, Oh-ShinKang, Tae-CheonHan, Kyu HyungPark, JinseuEum, Won SikChoi, Soo Young
Issue Date
29-10월-2010
Publisher
ELSEVIER IRELAND LTD
Keywords
Inflammation; MAPK; PEP-1-rpS3; TPA
Citation
TOXICOLOGY, v.276, no.3, pp.192 - 197
Indexed
SCIE
SCOPUS
Journal Title
TOXICOLOGY
Volume
276
Number
3
Start Page
192
End Page
197
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/115489
DOI
10.1016/j.tox.2010.08.004
ISSN
0300-483X
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-kappa B) 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-kappa B and MAPK, prompting the suggestion that PEP-1-rpS3 can be used as a therapeutic agent against skin inflammation. (C) 2010 Elsevier Ireland Ltd. All rights reserved.
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