Phytomedicine : international journal of phytotherapy and phytopharmacology · 2025
Kaji-ichigoside F1 alleviates the effect of ulcerative colitis: An integrated strategy of gut microbiota, metabolomics, and transcriptomics.
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Liu Jinlong, Wu Hao, Wu Jinying, Jiang Xiaoyuan, Fan Yuzhu, Liu Yue, Wang Lina, Sun Xin
Аннотация
BACKGROUND: Kaji-ichigoside F1 (KF1) is widely recognized for its antibacterial and anti-inflammatory properties. However, its specific effects on ulcerative colitis (UC) and the associated mechanisms remain unclear.
PURPOSE: We investigated the effect of KF1 in alleviating UC and elucidated its potential pharmacological mechanisms.
METHODS: We established a UC mouse model by inducing UC with sodium dextran sulfate (DSS) and then treating or not treating it with KF1. 16S rRNA gene sequencing, metabolomics, and transcriptomics techniques were used to explore the alleviative effect of KF1 on UC. Finally, we elucidated the important roles of key functional bacteria and metabolism regulated by KF1 in UC.
RESULTS: The KF1 intervention ameliorated UC and altered the composition of the gut microbiota, increasing the abundance of the beneficial bacterium Bacteroides vulgatus. Furthermore, KF1 increased the levels of the beneficial metabolic pathway. Notably, KF1 significantly suppressed inflammatory factors and improved DSS-induced UC. Transcriptomic analysis revealed that KF1 inhibited the PI3K/AKT signaling pathway.
CONCLUSION: KF1 ameliorates UC by modulating the gut microbiota and metabolism to create a more favorable state while inhibiting pro-inflammatory pathways.
PURPOSE: We investigated the effect of KF1 in alleviating UC and elucidated its potential pharmacological mechanisms.
METHODS: We established a UC mouse model by inducing UC with sodium dextran sulfate (DSS) and then treating or not treating it with KF1. 16S rRNA gene sequencing, metabolomics, and transcriptomics techniques were used to explore the alleviative effect of KF1 on UC. Finally, we elucidated the important roles of key functional bacteria and metabolism regulated by KF1 in UC.
RESULTS: The KF1 intervention ameliorated UC and altered the composition of the gut microbiota, increasing the abundance of the beneficial bacterium Bacteroides vulgatus. Furthermore, KF1 increased the levels of the beneficial metabolic pathway. Notably, KF1 significantly suppressed inflammatory factors and improved DSS-induced UC. Transcriptomic analysis revealed that KF1 inhibited the PI3K/AKT signaling pathway.
CONCLUSION: KF1 ameliorates UC by modulating the gut microbiota and metabolism to create a more favorable state while inhibiting pro-inflammatory pathways.