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