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

BMB Rep. 2015 Nov;48(11):618-23. doi: 10.5483/bmbrep.2015.48.11.041.

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-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.

Publication types

  • News
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Burns, Chemical / drug therapy*
  • Burns, Chemical / pathology
  • Cornea / drug effects*
  • Cornea / pathology
  • Corneal Injuries / prevention & control*
  • Corneal Neovascularization / metabolism
  • Disease Models, Animal
  • Eye Burns / drug therapy*
  • Eye Burns / pathology
  • Inflammation / metabolism
  • Male
  • Peptides / metabolism
  • Rats
  • Rats, Sprague-Dawley
  • Tacrolimus Binding Proteins / pharmacology*
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Peptides
  • Tumor Necrosis Factor-alpha
  • Tacrolimus Binding Proteins