Vitamin A deficiency exacerbates inflammation in a rat model of colitis through activation of nuclear factor-κB and collagen formation

R. Reifen*, T. Nur, K. Ghebermeskel, G. Zaiger, R. Urizky, M. Pines

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

73 Scopus citations

Abstract

Inflammatory bowel disease is characterized by oxidative stress, inflammation and tissue damage. Vitamin A is an antioxidant, a regulator of epithelial proliferation and differentiation and vital for optimal immune function. To investigate the effect of vitamin A on the course of colitis, it was induced by administration of trinitrobenzene sulfonic acid (TNBS) into the colons of rats fed for 7 wk vitamin A-deficient (VAD), sufficient (VAS) or supplemented (VASUP) diet, or VAS pair-fed (PF) to the VAD rats. Inflammation and fibrosis were examined by hematoxin and eosin, and Sirius red staining. Activation of nuclear factor-κB (NF-κB) and oxidative stress were determined by electrophoretic mobility shift and plasma malondialdehyde (MDA) and RBC Cu/Zn-superoxide dismutase activity, respectively. Vitamin A deficiency in the noncolitic rats impaired food consumption and weight gain (P < 0.05) and increased plasma MDA, (P = 0.01) activity of NF-κB (P < 0.05) and deposition of collagen in the colon. Our data suggest that vitamin A deficiency induces colonic inflammation. Colitis is amplified by deficiency and ameliorated by supplementation of the vitamin. These findings have implications for the management of inflammatory bowel disease.

Original languageAmerican English
Pages (from-to)2743-2747
Number of pages5
JournalJournal of Nutrition
Volume132
Issue number9
DOIs
StatePublished - Sep 2002

Keywords

  • Colitis
  • Fibrosis
  • Nuclear factor-κB
  • Oxidative stress
  • Vitamin A

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