MODULATION OF TNBS-INDUCED COLITIS BY ELECTOPORATION-MEDIATED KALLISTATIN GENE THERAPY

摘要

Recent studies have demonstrated kallistatin to be a potent anti-inflammatory agent The aim of this article was to evaluate the prophylactic effect of electroporation-mediated kallistatin gene delivery for experimental colitis in mice. Mice received recombinant plasmid containing kallistatin gene by electroporation prior to the induction of colitis with 2-4-6-trinitrobenzene sulphonic acid(TNBS). All the animals were assessed systemically and histologically. Kallistatin expression and inflammatory cytokine levels in the serum were measured by ELISA. In the TNBS model, kallistatin expression significantly reduced the macroscopic and microscopic damages, attenuated weight loss, and suppressed the levels of both serum tumor necrosis factor-a(TNF-α) and serum amyloid A. Gene therapy strategy using nonviral vectors encoding kallistatin may provide a beneficial approach to chronic inflammatory conditions.