4.7 Article

Protective Effect of Cicer arietinum L. (Chickpea) Ethanol Extract in the Dextran Sulfate Sodium-Induced Mouse Model of Ulcerative Colitis

Journal

NUTRIENTS
Volume 12, Issue 2, Pages -

Publisher

MDPI
DOI: 10.3390/nu12020456

Keywords

Cicer arietinum; colitis; dextran sodium sulfate; NF-kappa B; STAT3

Funding

  1. Medical Research Program through the National Research Foundation of Korea (NRF) - Ministry of Science and ICT [NRF-2017R1A5A2014768]
  2. National Research Foundation of Korea (NRF) - Korea government (MSIT) [2019R1F1A1058332]
  3. National Research Foundation of Korea [2019R1F1A1058332] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)

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Inflammatory bowel disease (IBD) is a major risk factor of colorectal cancer. Drugs currently used for IBD exhibit adverse effects including vomiting, nausea, and diarrhea. Naturally derived novel alternative therapies are required to overcome these limitations. In this study, we investigated the protective effects of ethanol extract of Cicer arietinum (CEE) in a dextran sodium sulfate (DSS)-induced mouse model of colitis. CEE markedly improved DSS-induced clinical symptoms and histological status, such as the disease activity index, spleen weight, and colon length. Moreover, CEE-treated mice showed significant recovery of DSS-induced crypt damage and cell death. CEE suppressed myeloperoxidase (MPO) activity and macrophage marker F4/80 mRNA expression in colonic tissue of mice with DSS-induced colitis, indicating neutrophil infiltration and macrophage accumulation, respectively. Although DSS upregulated pro-inflammatory mediators and activated transcription factors, CEE downregulated the mRNA expression of cytokines including interleukin-6, interleukin-1 beta, and tumor necrosis factor-alpha, protein expression of cyclooxygenase-2 and inducible nitric oxide synthase, as well as activation of nuclear factor-kappa B (NF-kappa B) and signal transducer and activator of transcription 3 (STAT3). Hence, our findings reveal that the anti-inflammatory properties of CEE, involving the downregulation of the expression of pro-inflammatory mediators by inactivating NF-kappa B and STAT3 in DSS-induced colitis mice.

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