The Quasipaa spinosa skin peptide GFGFGGF prevents dextran sodium sulfate‐induced colitis by improving the intestinal barrier and gut microbiota
- 19 July 2025
- journal article
- Published by Wiley in Journal of the Science of Food and Agriculture
- Vol. 105 (14) , 7743-7757
Abstract
Background: Ulcerative colitis is a chronic inflammatory disease affecting the colon and is supposed to be related to intestinal barrier dysfunction and gut microbiota disorders. Previous study identified the potential antioxidant effects of the peptide GFGFGGF derived from Quasipaa spinosa skin (QSP), but its other bioactive functions require further research. The aim of this study was to assess the function of QSP in a mouse model of colitis induced by dextran sodium sulfate (DSS). Results: The results showed that QSP ameliorated the symptoms of DSS‐induced colitis in mice, such as weight loss, colon shortening, splenomegaly and histopathological changes. Further investigations revealed that QSP treatment suppressed the production of pro‐inflammatory cytokines (IL‐1 β , IL‐6 and TNF‐ α ). Results from RT‐qPCR and Western blot analyses demonstrated that QSP inhibited the activation of the NF‐ κ B signaling pathway and reduced the mRNA levels of its downstream inflammation‐related genes (IL‐1 β , IL‐6 and TNF‐ α ). Meanwhile, QSP increased the mRNA level of tight junction proteins (ZO‐1, Occludin) and adherens junction proteins (E‐cadherin) to maintain the integrity of the colonic barrier thus improving intestinal health. Meanwhile, QSP treatment modulated the composition of the intestinal microbiota, reversing the relative abundance of harmful and beneficial bacteria, and increased the levels of short‐chain fatty acids. Conclusion: Our results indicated that peptide GFGFGGF had a notable function in preventing colitis induced by DSS. The restoration of the gut barrier and the regulation of gut microbiota were achieved by it, and it may be a promising prebiotic for the treatment of colitis. © 2025 Society of Chemical Industry.Keywords
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