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

• Published in: BMB reports Vol. 48; no. 11; pp. 618 - 623
• Main Authors: Kim, Dae Won, Lee, Sung Ho, Shin, Min Jea, Kim, Kibom, Ku, Sae Kwang, Youn, Jong Kyu, Cho, Su Bin, Park, Jung Hwan, Lee, Chi Hern, Son, Ora, Sohn, Eun Jeong, Cho, Sung-Woo, Park, Jong Hoon, Kim, Hyun Ah, Han, Kyu Hyung, Park, Jinseu, Eum, Won Sik, Choi, Soo Young
• Format: Journal Article
• Language: Korean
• Published: 생화학분자생물학회 30.11.2015
• Subjects: Corneal alkali burn injury; Corneal inflammation; Corneal neovascularization; PEP-1-FK506BP; Protein therapy; Corneal inflammation; PEP-1-FK506BP; Corneal neovascularization; Corneal alkali burn injury; Protein therapy
• ISSN: 1976-6696; 1976-670X

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-, 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. [BMB Reports 2015; 48(11): 618-623]