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Cited by 48Inflammatory Bowel DiseaseInflammatory mediators and NSAID effectsOcular Diseases and Behçet’s Syndrome

Oral nitrite ameliorates dextran sulfate sodium-induced acute experimental colitis in mice

Ohtake, Kazuo, Koga, Midori, Uchida, Hiroyuki, Sonoda, Kunihiro, Ito, Junta, Uchida, Masaki, Natsume, Hideshi, Kobayashi, Jun·2010·Nitric Oxide
DOI 10.1016/j.niox.2010.04.004
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Abstract

Inflammatory bowel diseases (IBDs) such as Crohn's disease and ulcerative colitis are chronic inflammatory disorders of the intestinal tract with excessive production of cytokines, adhesion molecules, and reactive oxygen species. Although nitric oxide (NO) is reported to be involved in the onset and progression of IBDs, it remains controversial as to whether NO is toxic or protective in experimental colitis. We investigated the effects of oral nitrite as a NO donor on dextran sulfate sodium (DSS)-induced acute colitis in mice. Mice were fed DSS in their drinking water with or without nitrite for up to 7days. The severity of colitis was assessed by disease activity index (DAI) observed over the experimental period, as well as by the other parameters, including colon lengths, hematocrit levels, and histological scores at day 7. DSS treatment induced severe colitis by day 7 with exacerbation in DAI and histological scores. We first observed a significant decrease in colonic nitrite levels and increase in colonic TNF-alpha expression at day 3 after DSS treatment, followed by increased colonic myeloperoxidase (MPO) activity and increased colonic expressions of both inducible NO synthase (iNOS) and heme oxygenase-1 (HO-1) at day 7. Oral nitrite supplementation to colitis mice reversed colonic nitrite levels and TNF-alpha expression to that of normal control mice at day 3, resulting in the reduction of MPO activity as well as iNOS and HO-1 expressions in colonic tissues with clinical and histological improvements at day 7. These results suggest that oral nitrite inhibits inflammatory process of DSS-induced experimental colitis by supplying nitrite-derived NO instead of impaired colonic NOS activity.

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  • Nitrite normalizes inflammation in a mouse model of inflammatory bowel disease.

    “normalizes inflammation in a mouse model of inflammatory bowel disease (139)”

    From Inorganic nitrite supplementation for healthy arterial aging (2014) · cites this paper as [139]

  • During the development of colitis, tissue levels of nitrite drop quickly along with a concomitant increase in colonic TNF-α expression by day three followed by increased myeloperoxidase activity, and iNOS and HO-1 expression at day 7.

    “It was reported that during the development of colitis, tissue levels of nitrite dropped quickly along with a concomitant increase in colonic TNF-α expression by day three followed by increased myeloperoxidase activity, and iNOS and HO-1 expression at day 7.”

    From Inorganic nitrite therapy: historical perspective and future directions (2011) · cites this paper as [233]

  • Therapeutic intervention with a high dose (25 mM ≈ 1.73 g/L) of oral nitrite confers significant protection against tissue histopathology in DSS-induced colitis in mice.

    “They found that therapeutic intervention with a high dose (25 mM ≈ 1.73 g/L) of oral nitrite conferred significant protection against tissue histopathology.”

    From Inorganic nitrite therapy: historical perspective and future directions (2011) · cites this paper as [233]

  • Oral nitrite therapy reverses the loss of colonic nitrite levels and decreases TNF-α expression, which is associated with clinical and histological improvements.

    “Oral nitrite therapy reversed the loss of colonic nitrite levels and decreased TNF-α expression, which was associated with clinical and histological improvements.”

    From Inorganic nitrite therapy: historical perspective and future directions (2011) · cites this paper as [233]

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Authors
Ohtake, K., Koga, M., Uchida, H., Sonoda, K., Ito, J., Uchida, M., Natsume, H., & Kobayashi, J.
Affiliations
  • Josai University (JP)
  • Kinjo Gakuin University (JP)
Corresponding author
Kobayashi, Jun
ORCID
Venue
Nitric Oxide
Publisher
Elsevier BV
Published
2010-08
Volume
23
Issue
1
Pages
65-73
ISSN
1089-8603 (ISSN-L)
DOI
10.1016/j.niox.2010.04.004
OpenAlex
W2001328285
Cited by
48
References
49
Citations by year
2026: 3 · 2025: 2 · 2024: 2 · 2023: 2 · 2022: 2 · 2020: 2 · 2019: 1 · 2018: 2 · 2017: 3 · 2016: 4 · 2015: 4 · 2014: 8 · 2013: 2 · 2012: 8
FWCI
2.34
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Nitric Oxide (publishedVersion)
  • PubMed (publishedVersion)
  • Josai University Repository of Academia (Josai University) (submittedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Inflammatory Bowel Disease
  • Health Sciences › Medicine › Pharmacology › Inflammatory mediators and NSAID effects
  • Health Sciences › Medicine › Ophthalmology › Ocular Diseases and Behçet’s Syndrome
Keywords
DSS-induced colitis, experimental colitis, inflammatory bowel disease, ulcerative colitis, Crohn's disease, TNF-α, inducible nitric oxide synthase, heme oxygenase-1, myeloperoxidase, nitrite supplementation, colonic inflammation
MeSH terms
Analysis of Variance, Animals, Blood Pressure, Colitis, Ulcerative, Colon, Disease Models, Animal, Heart Rate, Hematocrit, Histocytochemistry, Male, Methemoglobin, Mice, Inbred ICR, Peroxidase, Nitrates, Nitrites, Sodium Nitrite, Specific Pathogen-Free Organisms, Tumor Necrosis Factor-alpha, Dextran Sulfate, Mice, Heme Oxygenase-1, Nitric Oxide Synthase Type II

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