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KMID : 0624620150480110618
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BMB Reports
2015 Volume.48 No. 11 p.618 ~ p.623
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PEP-1-FK506BP inhibits alkali burn-induced corneal inflammation on the rat model of corneal alkali injury
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Kim Dae-Won
Lee Sung-Ho
Shin Min-Jea
Kim Ki-Bom
Ku Sae-Kwang
Youn Jong-Kyu
Cho Su-Bin
Park Jung-Hwan
Lee Chi-Hern
Son O-Ra
Sohn Eun-Jeong
Cho Sung-Woo
Park Jong-Hoon
Kim Hyun-Ah
Han Kyu-Hyung
Park Jin-Seu
Eum Won-Sik
Choi Soo-Young
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Abstract
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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-α, 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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KEYWORD
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Corneal alkali burn injury, Corneal inflammation, Corneal neovascularization, PEP-1-FK506BP, Protein therapy
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