{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,19]],"date-time":"2026-01-19T14:30:25Z","timestamp":1768833025200,"version":"3.49.0"},"reference-count":44,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2024,8,22]],"date-time":"2024-08-22T00:00:00Z","timestamp":1724284800000},"content-version":"vor","delay-in-days":21,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Immunity Inflam &amp;amp; Disease"],"published-print":{"date-parts":[[2024,8]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Purpose<\/jats:title><jats:p>The aim of this study was to explore whether MAF bZIP transcription factor B (MAFB) might alleviate ulcerative colitis (UC) in dextran sulfate sodium (DSS)\u2010induced mice and LPS\u2010induced IEC\u20106 cells.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>UC in vivo and in vitro model was established by using DSS and LPS, respectively. The mice body weight and disease activity index (DAI) score were recorded daily, and colon length was measured. Moreover, the permeability was evaluated utilizing a fluorescein isothiocyanate dextran (FITC\u2010Dextran) probe. Histopathological changes of DSS\u2010induced colitis mice was assessed utilizing H&amp;E staining. Next, qRT\u2010PCR was performed to detect IL\u20101\u03b2, IL\u20106, TNF\u2010\u03b1, and IL\u201010 level in in vivo and in vitro. Furthermore, the level of MDA, SOD, CAT, and GSH were evaluated in colon tissues. Besides, the expressions of tight junction proteins and NF\u2010\u03baB pathway relative proteins were examined in colitis mice and IEC\u20106 cells using western blot, immunohistochemistry and immunofluorescence.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>MAFB level was downregulated in DSS\u2010induced colitis mice. Moreover, the upregulation of MAFB protected mice from DSS\u2010induced colitis by suppressing DSS\u2010induced inflammation, oxidative stress, and intestinal barrier impairment. We also demonstrated that the upregulation of MAFB inactivated NF\u2010\u03baB pathway in DSS\u2010caused colitis mice. Subsequently, we observed that MAFB upregulation could inhibit LPS\u2010caused epithelial barrier impairment and inflammation in IEC\u20106 cells. Additionally, MAFB overexpression could suppress the activation of NF\u2010\u03baB pathway in IEC\u20106 cells.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>The upregulation of MAFB could protect against UC via the suppression of inflammation and the intestinal barrier impairment through inhibiting the NF\u2010\u03baB pathway.<\/jats:p><\/jats:sec>","DOI":"10.1002\/iid3.1372","type":"journal-article","created":{"date-parts":[[2024,8,22]],"date-time":"2024-08-22T21:25:11Z","timestamp":1724361911000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Expression of MAF bZIP transcription factor B protects against ulcerative colitis through the inhibition of the NF\u2010\u03baB pathway"],"prefix":"10.1002","volume":"12","author":[{"ORCID":"https:\/\/orcid.org\/0009-0001-7496-027X","authenticated-orcid":false,"given":"Jingwen","family":"Li","sequence":"first","affiliation":[{"name":"Department 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