Journal of ethnopharmacology · 2026
Tong-Xie-Yao-Fang ameliorates IBS-D: Potential role of Alistipes finegoldii-associated gut tryptophan indole metabolism.
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Ying YiTian, Zheng XiangHou, Yang Jing, Ye Huiwen, Dong Zhenhao, Ji Youqi, Li Shengyu, Tan Xun, Zhang Wei
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: Irritable bowel syndrome with diarrhea (IBS-D) is a prevalent chronic gastrointestinal condition characterized by visceral hypersensitivity, low-grade mucosal inflammation, and impaired epithelial barrier integrity. Current therapies remain limited, highlighting the need for more alternative strategies. Tong-Xie-Yao-Fang (TXYF), a classical Chinese herbal formula, has shown clinical efficacy in IBS-D, however, the mechanisms underlying its therapeutic effects remain unclear.
AIM OF THE STUDY: This study aimed to investigate whether and how TXYF exerts therapeutic effects by modulating colonic tryptophan metabolism, with a particular focus on the gut microbiota.
MATERIALS AND METHODS: IBS-D model was induced by combining chemical irritation and wrap restraint stress in C57BL/6J mice, and multi-omics approaches were employed to identify specific microbiota and metabolites modulated by TXYF. The multi-omics findings were further verified in vivo and in vitro.
RESULTS: TXYF treatment significantly alleviated IBS-D symptoms in our model. Non-targeted metabolomics identified the tryptophan-indole pathway as a key axis modulated by TXYF, with indole-3-acetic acid (IAA) emerging as a prominent differential metabolite in colonic tissue. Western blot analysis showed that TXYF activated the aryl hydrocarbon receptor (AhR) in the colon. Integrative metagenomic and metabolomic analyses revealed a strong association between Alistipes finegoldii and colonic indole and IAA levels. Consistent with these findings, transplantation of A. finegoldii combined with tryptophan supplementation, or administration of IAA alone, recapitulated the therapeutic effects of TXYF against IBS-D. In vitro, both IAA and faecal supernatant from TXYF-treated mice protected against tumour necrosis factor-induced epithelial barrier disruption in an AhR-dependent manner.
CONCLUSION: Collectively, the present study suggests that the therapeutic efficiency of TXYF against IBS-D is closely associated with its ability to modify microbiota-derived colonic IAA production, with gut microbiota member Alistipes finegoldii playing a key role in this effect.
AIM OF THE STUDY: This study aimed to investigate whether and how TXYF exerts therapeutic effects by modulating colonic tryptophan metabolism, with a particular focus on the gut microbiota.
MATERIALS AND METHODS: IBS-D model was induced by combining chemical irritation and wrap restraint stress in C57BL/6J mice, and multi-omics approaches were employed to identify specific microbiota and metabolites modulated by TXYF. The multi-omics findings were further verified in vivo and in vitro.
RESULTS: TXYF treatment significantly alleviated IBS-D symptoms in our model. Non-targeted metabolomics identified the tryptophan-indole pathway as a key axis modulated by TXYF, with indole-3-acetic acid (IAA) emerging as a prominent differential metabolite in colonic tissue. Western blot analysis showed that TXYF activated the aryl hydrocarbon receptor (AhR) in the colon. Integrative metagenomic and metabolomic analyses revealed a strong association between Alistipes finegoldii and colonic indole and IAA levels. Consistent with these findings, transplantation of A. finegoldii combined with tryptophan supplementation, or administration of IAA alone, recapitulated the therapeutic effects of TXYF against IBS-D. In vitro, both IAA and faecal supernatant from TXYF-treated mice protected against tumour necrosis factor-induced epithelial barrier disruption in an AhR-dependent manner.
CONCLUSION: Collectively, the present study suggests that the therapeutic efficiency of TXYF against IBS-D is closely associated with its ability to modify microbiota-derived colonic IAA production, with gut microbiota member Alistipes finegoldii playing a key role in this effect.