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There is a pressing demand for safe and effective treatments for IBDs. Fibroblast growth factor 1 (FGF1) variant FGF1<jats:sup>\u0394HBS<\/jats:sup>, characterised by reduced mitogenic capacity, has shown promising therapeutic potential in various inflammatory conditions, including obesity and diabetic nephropathy. Hence, exploring the therapeutic impact of FGF1<jats:sup>\u0394HBS<\/jats:sup> on colitis is warranted.<\/jats:p><\/jats:sec><jats:sec><jats:title>Experimental Approach<\/jats:title><jats:p>The protective role of FGF1<jats:sup>\u0394HBS<\/jats:sup> was evaluated using a dextran sulphate sodium (DSS)\u2010induced colitis model in mice. RNA\u2010seq analysis was performed on colonic tissues. Inflammatory factor expression was examined by quantitative real\u2010time polymerase chain reaction (PCR) and enzyme\u2010linked immunosorbent assay. Flow cytometry and immunofluorescence staining were employed to confirm the inhibitory effect of FGF1<jats:sup>\u0394HBS<\/jats:sup> on neutrophil recruitment. Western blotting was performed to explore the mitogen\u2010activated protein kinase (MAPK) signalling pathway.<\/jats:p><\/jats:sec><jats:sec><jats:title>Key Results<\/jats:title><jats:p>FGF1<jats:sup>\u0394HBS<\/jats:sup> significantly alleviated DSS\u2010induced colitis, as indicated by reduced Disease Activity Index scores and less histological injury to the colon. Additionally, FGF1<jats:sup>\u0394HBS<\/jats:sup> decreased the expression of pro\u2010inflammatory factors. Mechanistically, FGF1<jats:sup>\u0394HBS<\/jats:sup> inhibited neutrophil\u2010associated chemokine expression in intestinal epithelial cells by suppressing the MAPK signalling pathway, thereby reducing neutrophil recruitment and attenuating neutrophil\u2010mediated intestinal inflammation.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion and Implications<\/jats:title><jats:p>FGF1<jats:sup>\u0394HBS<\/jats:sup> protects against DSS\u2010induced colitis in mice by inhibiting neutrophil recruitment through MAPK activity suppression, suggesting a potential therapeutic strategy for preventing IBDs.<\/jats:p><\/jats:sec><jats:sec><jats:title>LINKED ARTICLES<\/jats:title><jats:p>This article is part of a themed issue Drugs and Drug Targets in Metabolic and Chronic Inflammatory Diseases. To view the other articles in this section visit <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"http:\/\/onlinelibrary.wiley.com\/doi\/10.1111\/bph.v182.20\/issuetoc\">http:\/\/onlinelibrary.wiley.com\/doi\/10.1111\/bph.v182.20\/issuetoc<\/jats:ext-link><\/jats:p><\/jats:sec>","DOI":"10.1111\/bph.70049","type":"journal-article","created":{"date-parts":[[2025,4,21]],"date-time":"2025-04-21T19:05:06Z","timestamp":1745262306000},"page":"5057-5070","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":8,"title":["FGF1<sup>\u0394HBS<\/sup> ameliorates DSS\u2010induced ulcerative colitis by reducing neutrophil recruitment through the MAPK pathway"],"prefix":"10.1111","volume":"182","author":[{"given":"Shuang","family":"Feng","sequence":"first","affiliation":[{"name":"Institute of Translational Medicine China Pharmaceutical University  Nanjing China"},{"name":"School of Basic Medicine and Clinical Pharmacy 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