Enhancement of Anti-Inflammatory Activity of PEP-1-FK506 Binding Protein by Silk Fibroin Peptide
- Authors
- Kim, Dae Won; Hwang, Hyun Sook; Kim, Duk-Soo; Sheen, Seung Hoon; Heo, Dong Hwa; Hwang, Gyojun; Kang, Suk Hyung; Kweon, HaeYong; Jo, You-Young; Kang, Seok Woo; Lee, Kwang-Gill; Park, Jinseu; Eum, Won Sik; Cho, Yong-Jun; Choi, Soo Young
- Issue Date
- Apr-2012
- Publisher
- 한국미생물·생명공학회
- Keywords
- Inflammation; PEP-1-FK506BP; protein transduction; reactive oxygen species; silk fibroin peptide; TPA
- Citation
- Journal of Microbiology and Biotechnology, v.22, no.4, pp 494 - 500
- Pages
- 7
- Journal Title
- Journal of Microbiology and Biotechnology
- Volume
- 22
- Number
- 4
- Start Page
- 494
- End Page
- 500
- URI
- https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/15297
- DOI
- 10.4014/jmb.1111.11024
- ISSN
- 1017-7825
1738-8872
- Abstract
- Silk fibroin (SF) peptide has been traditionally used as a treatment for flatulence, spasms, and phlegm. In this study, we examined whether SF peptide enhanced the anti-inflammatory effect of PEP-1-FK506 binding protein (PEP-1-FK506BP) through comparing the anti-inflammatory activities of SF peptide and/or PEP-1-FK506BP. In the presence or absence of SF peptide, transduction levels of PEP-1-FK506BP into HaCaT cells and mice skin and anti-inflammatory activities of PEP-1-FK506BP were identified by Western blot and histological analyses. SF peptide alone effectively reduced both mice ear edema and the elevated levels of cyclooxygenase-2, interleukin-6 and -1 beta, and tumor necrosis factor-alpha, showing similar anti-inflammatory effect to that of PEP-1-FK506BP. Furthermore, co-treatment with SF peptide and PEP-1-FK506BP exhibited more enhanced anti-inflammatory effects than the samples treated with SF peptides or PEP-1-FK506BP alone, suggesting the possibility that SF peptide and PEP-1-FK506BP might interact with each other. Moreover, the transduction data demonstrated that SF peptide did not affect the transduction of PEP-1-FK506BP into HaCaT cells and mice skin, indicating that the improvement of anti-inflammatory effect of PEP-1-FK506BP was not caused by enhanced transduction of PEP-1-FK506BP. Thus, these results suggest the possibility that co-treatment with SF peptide and PEP-1-FK506BP may be exploited as a useful therapy for various inflammation-related diseases.
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