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Nrf2-deficient mice have an increased susceptibility to dextran sulfate sodium-induced colitis.

Nrf2-deficient mice have an increased susceptibility to dextran sulfate sodium-induced colitis. Research Abstract Details 

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  • Nrf2-deficient mice have an increased susceptibility to dextran sulfate sodium-induced colitis. Abstract Text:

    tin oo khorTin Oo Khor,mou-tuan huangMou-Tuan Huang,ki han kwonKi Han Kwon,jefferson y chanJefferson Y Chan,bandaru s reddyBandaru S Reddy,ah-ng kongAh-Ng Kong,

    Inflammatory bowel diseases, chronic inflammatory disorders, have been strongly linked with an increased risk of the development of colorectal cancer. Understanding the etiology of these diseases is pivotal for the improvement of currently available strategies to fight against inflammatory bowel disease, and more importantly, to prevent colorectal cancer. Nuclear factor-erythroid 2-related factor 2 (Nrf2) has been known to be a transcriptional factor which plays a crucial role in cytoprotection against inflammation, as well as oxidative and electrophilic stresses. The aim of this study is to investigate the role of Nrf2 in the regulation of dextran sulfate sodium (DSS)-induced experimental colitis in mice. Nrf2-deficient mice were found to be more susceptible to DSS-induced colitis as shown by the increased severity of colitis following 1 week of oral administration of 1% DSS. The increased severity of colitis in Nrf2(-/-) mice was found to be associated with decreased expression of antioxidant/phase II detoxifying enzymes including heme-oxygenase-1, NAD(P)H-quinone reductase-1, UDP-glucurosyltransferase 1A1, and glutathione S-transferase Mu-1. In addition, proinflammatory mediators/cytokines such as COX-2, inducible nitric oxide, interleukin 1beta, interleukin 6, and tumor necrosis factor alpha were significantly increased in the colonic tissues of Nrf2(-/-) mice compared with their wild-type (Nrf2+/+) counterparts. In summary, we show for the first time that mice lacking Nrf2 are more susceptible to DSS-induced colitis. Our data suggests that Nrf2 could play an important role in protecting intestinal integrity, through regulation of proinflammatory cytokines and induction of phase II detoxifying enzymes.

    Nrf2-deficient mice have an increased susceptibility to dextran sulfate sodium-induced colitis. Publishing Authors By Initials

    to khorTO Khor,mt huangMT Huang,kh kwonKH Kwon,jy chanJY Chan,bs reddyBS Reddy,an kongAN Kong,

    For similar investigative techniques: genetic techniques: nucleic acid amplification techniques: polymerase chain reaction research abstracts see: investigative techniques: genetic techniques: nucleic acid amplification techniques: polymerase chain reaction research

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    Nrf2-deficient mice have an increased susceptibility to dextran sulfate sodium-induced colitis. Journal Published:

    PUBLICATION TYPE: Research Support, N.I.H., Extr

    Journal: Cancer research

    VOLUME: 66

    Page Numbers: 11580-4

    Journal Abbreviation: Cancer Res.

    ISSN: 0008-5472

    DAY: 15

    MONTH: Dec

    YEAR: 2006

    Nrf2-deficient mice have an increased susceptibility to dextran sulfate sodium-induced colitis. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 2984705

    Nrf2-deficient mice have an increased susceptibility to dextran sulfate sodium-induced colitis. Keywords Mesh Terms:

    KEYWORDS: Polymerase Chain Reaction

    MESH TERMS: genetics

    Chemical & Substance for Abstract: Nrf2-deficient mice have an increased susceptibility to dextran sulfate sodium-induced colitis. Information

    Substance Name: Dextran Sulfate

    Registry Number: 9042-14-2

    Grant and Affiliation Information for Nrf2-deficient mice have an increased susceptibility to dextran sulfate sodium-induced colitis.

    AFFILIATION: Department of Pharmaceutics, Ernest Mario School of Pharmacy, Rutgers, The State University of New Jersey, Piscataway, New Jersey 08854, USA.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NCI

    GRANT: R01 CA094828

    ACRONYM: CA

    MEDLINETA: Cancer Res

    REFSOURCE:

    DATABASENAME:

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