Melatonin reduces inflammatory injury through inhibiting NF-kappaB activation in rats with colitis

Mediators Inflamm. 2005 Aug 31;2005(4):185-93. doi: 10.1155/MI.2005.185.

Abstract

Proinflammatory mediators are important in the pathogenesis of IBD, which are regulated by activation of NF-kappaB. The aim of this study was to investigate whether melatonin reduces inflammatory injury and inhibits proinflammatory molecule and NF-kappaB in rats with colitis. Rat colitis model was established by TNBS enema. NF-kappaB p65, TNF-alpha, ICAM-1, and IkappaBalpha in colon tissue were examined by immunohistochemistry, EMSA, RT-PCR, and Western blot analysis. Expression of proinflammatory molecule and activation of NF-kappaB were upregulated and IkappaB level decreased in rats with colitis. Melatonin reduces colonic inflammatory injury through downregulating proinflammatory molecule mediated by NF-kappaB inhibition and blockade of IkappaBalpha degradation.

MeSH terms

  • Animals
  • Antioxidants / administration & dosage*
  • Colitis, Ulcerative / chemically induced
  • Colitis, Ulcerative / drug therapy
  • Colitis, Ulcerative / metabolism*
  • Down-Regulation / drug effects*
  • Female
  • I-kappa B Proteins / biosynthesis
  • Inflammation / chemically induced
  • Inflammation / drug therapy
  • Inflammation / metabolism
  • Intercellular Adhesion Molecule-1 / biosynthesis
  • Male
  • Melatonin / administration & dosage*
  • NF-KappaB Inhibitor alpha
  • Rats
  • Rats, Sprague-Dawley
  • Transcription Factor RelA / antagonists & inhibitors
  • Transcription Factor RelA / metabolism*
  • Tumor Necrosis Factor-alpha / biosynthesis
  • Up-Regulation / drug effects

Substances

  • Antioxidants
  • I-kappa B Proteins
  • Nfkbia protein, rat
  • Transcription Factor RelA
  • Tumor Necrosis Factor-alpha
  • Intercellular Adhesion Molecule-1
  • NF-KappaB Inhibitor alpha
  • Melatonin