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Background <p>QuYuShengXin 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.</p> Methods <p>DSS-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&amp;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.</p> Results <p>QYSX 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.</p> Conclusion <p>By 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.</p>

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QuYuShengXin formula reshapes bile-acid-mediated macrophage polarization in the treatment of ulcerative colitis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月22日

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  • Jiachun Ni,
  • Yuchang Lu,
  • Jiaying Tan,
  • Jiaqi Jiang,
  • Yunyun Wang,
  • Dan Gan,
  • Can Cui,
  • Jiong Wu,
  • Haojie Yang,
  • Zhenyi Wang

摘要

Background

QuYuShengXin 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.

Methods

DSS-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.

Results

QYSX 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.

Conclusion

By 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.