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<p>Sanren Decoction (SRD), a traditional Chinese medicine formula historically used to relieve damp-heat and gastrointestinal disorders, demonstrates targeted efficacy in ulcerative colitis (UC)—a disease marked by chronic inflammation and mucosal damage—by acting on multiple pathological pathways. This study employed an integrative methodology comprising network pharmacology, molecular docking, and in vivo experimentation to elucidate the underlying pharmacological mechanisms of SRD in the management of UC. The findings identified 87 genes targeted by SRD that are associated with UC, highlighting PTGS2 (Prostaglandin-Endoperoxide Synthase 2) as a crucial target involved in inflammatory processes. Molecular docking analysis confirmed significant interactions between the active compounds of SRD and PTGS2, suggesting a potential anti-inflammatory pathway. In vivo experiments utilizing a DSS-induced colitis mouse model demonstrated that SRD effectively ameliorates clinical symptoms and histopathological damage, enhances intestinal barrier integrity, and modulates macrophage polarization from a pro-inflammatory M1 state to an anti-inflammatory M2 phenotype. Furthermore, SRD was found to alter gut microbiota composition by increasing the abundance of beneficial bacteria and influencing metabolic pathways. These findings establish a strong scientific foundation for the potential of SRD as a comprehensive therapeutic approach for UC, offering promising prospects for its integration into clinical practice.</p>

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Sanren decoction ameliorates ulcerative colitis by modulating gut microbiota and macrophage polarization to enhance intestinal barrier function

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年8月20日

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  • Shujuan Zhang,
  • BangHua Li,
  • Xiaoqun Han,
  • LinLin Ruan,
  • Xingxing Fu,
  • Yanglin Chen,
  • Hongtao Wan,
  • Xiaojian Zhu,
  • Dan Liu,
  • Bo Yi

摘要

Sanren Decoction (SRD), a traditional Chinese medicine formula historically used to relieve damp-heat and gastrointestinal disorders, demonstrates targeted efficacy in ulcerative colitis (UC)—a disease marked by chronic inflammation and mucosal damage—by acting on multiple pathological pathways. This study employed an integrative methodology comprising network pharmacology, molecular docking, and in vivo experimentation to elucidate the underlying pharmacological mechanisms of SRD in the management of UC. The findings identified 87 genes targeted by SRD that are associated with UC, highlighting PTGS2 (Prostaglandin-Endoperoxide Synthase 2) as a crucial target involved in inflammatory processes. Molecular docking analysis confirmed significant interactions between the active compounds of SRD and PTGS2, suggesting a potential anti-inflammatory pathway. In vivo experiments utilizing a DSS-induced colitis mouse model demonstrated that SRD effectively ameliorates clinical symptoms and histopathological damage, enhances intestinal barrier integrity, and modulates macrophage polarization from a pro-inflammatory M1 state to an anti-inflammatory M2 phenotype. Furthermore, SRD was found to alter gut microbiota composition by increasing the abundance of beneficial bacteria and influencing metabolic pathways. These findings establish a strong scientific foundation for the potential of SRD as a comprehensive therapeutic approach for UC, offering promising prospects for its integration into clinical practice.