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PEP-1-FK506BP inhibits alkali burn-induced corneal inflammation on the rat model of corneal alkali injury

Authors
Kim, Dae WonLee, Sung HoShin, Min JeaKim, KibomKu, Sae KwangYoun, Jong KyuCho, Su BinPark, Jung HwanLee, Chi HernSon, OraSohn, Eun JeongCho, Sung-WooPark, Jong HoonKim, Hyun AhHan, Kyu HyungPark, JinseuEum, Won SikChoi, Soo Young
Issue Date
Nov-2015
Publisher
KOREAN SOCIETY BIOCHEMISTRY & MOLECULAR BIOLOGY
Keywords
Corneal alkali burn injury; Corneal inflammation; Corneal neovascularization; PEP-1-FK506BP; Protein therapy
Citation
BMB REPORTS, v.48, no.11, pp 618 - 623
Pages
6
Journal Title
BMB REPORTS
Volume
48
Number
11
Start Page
618
End Page
623
URI
https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/10193
DOI
10.5483/BMBRep.2015.48.11.041
ISSN
1976-6696
1976-670X
Abstract
FK506 binding protein 12 (FK506BP) is a small peptide with a single FK506BP domain that is involved in suppression of immune response and reactive oxygen species. FK506BP has emerged as a potential drug target for several inflammatory diseases. Here, we examined the protective effects of directly applied cell permeable FK506BP (PEP-1-FK506BP) on corneal alkali burn injury (CAI). In the cornea, there was a significant decrease in the number of cells expressing pro-inflammation, apoptotic, and angiogenic factors such as TNF-alpha, COX-2, and VEGF. Both corneal opacity and corneal neovascularization (CNV) were significantly decreased in the PEP-1-FK506BP treated group. Our results showed that PEP-1-FK506BP can significantly inhibit alkali burn-induced corneal inflammation in rats, possibly by accelerating corneal wound healing and by reducing the production of angiogenic factors and inflammatory cytokines. These results suggest that PEP-1-FK506BP may be a potential therapeutic agent for CAI.
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