British journal of pharmacology · 2025
FGF1ΔHBS ameliorates DSS-induced ulcerative colitis by reducing neutrophil recruitment through the MAPK pathway.
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Feng Shuang, Jin Yanyan, Ni Xinrui, Zheng Haoxin, Wu Linling, Xia Ying, Zhou Changzhi, Liang Tong, Zhu Yunfei, Xu Juyi, Wu Qijin, Yang Yong, Zhao Longwei, Zhuang Shentian, Li Xianjing
Аннотация
BACKGROUND AND PURPOSE: Inflammatory bowel diseases (IBDs) constitute chronic inflammatory disease of the gastrointestinal tract, with escalating global prevalence. There is a pressing demand for safe and effective treatments for IBDs. Fibroblast growth factor 1 (FGF1) variant FGF1ΔHBS, 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 FGF1ΔHBS on colitis is warranted.
EXPERIMENTAL APPROACH: The protective role of FGF1ΔHBS was evaluated using a dextran sulphate sodium (DSS)-induced colitis model in mice. RNA-seq analysis was performed on colonic tissues. Inflammatory factor expression was examined by quantitative real-time polymerase chain reaction (PCR) and enzyme-linked immunosorbent assay. Flow cytometry and immunofluorescence staining were employed to confirm the inhibitory effect of FGF1ΔHBS on neutrophil recruitment. Western blotting was performed to explore the mitogen-activated protein kinase (MAPK) signalling pathway.
KEY RESULTS: FGF1ΔHBS significantly alleviated DSS-induced colitis, as indicated by reduced Disease Activity Index scores and less histological injury to the colon. Additionally, FGF1ΔHBS decreased the expression of pro-inflammatory factors. Mechanistically, FGF1ΔHBS inhibited neutrophil-associated chemokine expression in intestinal epithelial cells by suppressing the MAPK signalling pathway, thereby reducing neutrophil recruitment and attenuating neutrophil-mediated intestinal inflammation.
CONCLUSION AND IMPLICATIONS: FGF1ΔHBS protects against DSS-induced colitis in mice by inhibiting neutrophil recruitment through MAPK activity suppression, suggesting a potential therapeutic strategy for preventing IBDs.
LINKED ARTICLES: 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 http://onlinelibrary.wiley.com/doi/10.1111/bph.v182.20/issuetoc.
EXPERIMENTAL APPROACH: The protective role of FGF1ΔHBS was evaluated using a dextran sulphate sodium (DSS)-induced colitis model in mice. RNA-seq analysis was performed on colonic tissues. Inflammatory factor expression was examined by quantitative real-time polymerase chain reaction (PCR) and enzyme-linked immunosorbent assay. Flow cytometry and immunofluorescence staining were employed to confirm the inhibitory effect of FGF1ΔHBS on neutrophil recruitment. Western blotting was performed to explore the mitogen-activated protein kinase (MAPK) signalling pathway.
KEY RESULTS: FGF1ΔHBS significantly alleviated DSS-induced colitis, as indicated by reduced Disease Activity Index scores and less histological injury to the colon. Additionally, FGF1ΔHBS decreased the expression of pro-inflammatory factors. Mechanistically, FGF1ΔHBS inhibited neutrophil-associated chemokine expression in intestinal epithelial cells by suppressing the MAPK signalling pathway, thereby reducing neutrophil recruitment and attenuating neutrophil-mediated intestinal inflammation.
CONCLUSION AND IMPLICATIONS: FGF1ΔHBS protects against DSS-induced colitis in mice by inhibiting neutrophil recruitment through MAPK activity suppression, suggesting a potential therapeutic strategy for preventing IBDs.
LINKED ARTICLES: 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 http://onlinelibrary.wiley.com/doi/10.1111/bph.v182.20/issuetoc.