Toxicological Research

Korean Society of Toxicology & Korea Environmental Mutagen Society (한국독성학회)
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Gliotoxin Protects Trinitrobenzene Sulfonic Acid-Induced Colonic Damage through Induction of Heme Oxygenase-1

  • Oh, Jaemin (Wonkwang University School of Medicine and Institute of Medical Science) ;
  • Hur, Jungmu (Wonkwang University School of Medicine and Institute of Medical Science) ;
  • Kim, Yourim (Wonkwang University School of Medicine and Institute of Medical Science) ;
  • Kwon, Young-Mi (School of Oriental Medicine, Wonkwang University) ;
  • Kim, Kyungsuk (Wonkwang University School of Medicine and Institute of Medical Science) ;
  • Chung, Yeuntai (Wonkwang University School of Medicine and Institute of Medical Science) ;
  • Choi, Minkyu (Wonkwang University School of Medicine and Institute of Medical Science)
  • Published : 2004.09.01
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Abstract

Background: Crohn's disease is characterized by a chronic relapsing inflammation of the bowel. Gliotoxin has been known to play strong immunosuppressive properties, while mechanisms for its anti-inflammatory actions are not completely understood. Here, we investigated the effects of gliotoxin in trinitrobenzene sulfonic acid (TNBS) induced mouse colitis, an animal model of Crohn's disease. Results: Gliotoxin dramatically improved clinical and histopathological symptoms in accompanied with reduced expression of TNF-$\alpha$, IL-1$\beta$, and ICAM-1 protein levels in TNBS induced colitis. Interestingly Gliotoxin induced Heme oxygenase-1 (HO-1) and the HO-1 inducer cobalt protoporphyrin IX (CoPPIX) completely mimicked the protective effects of gliotoxin in TNBS induced colitis mice. In contrast, the HO-1 inhibitor zinc protoporphyrin IX (ZnPPIX) could reverse the anti-inflammatory effects of gliotoxin and CoPPIX. Conclusions: Gliotoxin is a potential therapeutic agent targeting for the treatment of Crohn's disease by inducing HO-1.

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References

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