ArticleBMC complementary medicine and therapies2025
QuYuShengXin formula reshapes bile-acid-mediated macrophage polarization in the treatment of ulcerative colitis.
Article in BMC complementary medicine and therapies, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Senkyunolide I Inhibits mtDNA-cGAS-STING Signaling in Macrophages via Targeting VDAC1 Oligomerization to Attenuate Ulcerative Colitis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
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10 authors.
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Abstract
backgroundQuYuShengXin Formula (QYSX), a multi-herbal preparation, has previously demonstrated robust clinical efficacy against ulcerative colitis (UC), with preliminary evidence suggesting that QYSX could reconfigure the fecal bile acid BA landscape and restore the M2/M1 macrophage balance, but their interaction remains unknown. We therefore dissected the therapeutic footprint of QYSX in a dextran sulfate sodium (DSS)-induced mice model of UC, focusing on its specific mechanism of regulating BA metabolism and macrophage polarization.
methodsDSS-induced mice received QYSX or mesalazine for comparative efficacy. Disease activity index (DAI), body-weight trajectory and stool consistency were monitored daily. Colonic histopathology was graded after H&E staining. Liquid chromatography-mass spectrometry, enzyme-linked immunosorbent assay, flow cytometry, western blot and real-time quantitative PCR were conducted to evaluate the possible mechanism of QYSX.
resultsQYSX markedly attenuated he symptoms and colonic pathology of UC. It simultaneously downregulated IL-1β, IL-6, TNF-α, LPS and NF-κB p65, while elevating TGR5 expression. DSS-elicited disruption of the fecal BAs structure and concentration were largely reversed by QYSX. Flow-cytometric profiling revealed a decreased expression of M1 macrophages without alteration of M2 macrophages, yielding a rise in the M2/M1 ratio.
conclusionBy re-instating the physiologic fecal BA landscape, QYSX engages TGR5 to inhibit NF-κB signaling, thereby suppressing LPS- and TNF-α-driven M1 hyper-activation. This restoration of M2/M1 homeostasis curbs mucosal inflammation and maintains intestinal immune equilibrium, providing a mechanistic rationale for the clinical efficacy of QYSX in UC.
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