ArticleFrontiers in pharmacology2026
Qitu qushi formula ameliorates diabetic kidney disease potentially through gut microbiota-derived indole-3-propionic Acid-Mediated regulation of the Sirt1/FoxO1 pathway.
Article in Frontiers in pharmacology, 2026. 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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11 authors.
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Abstract
Background: Diabetic kidney disease (DKD) is a leading cause of end-stage renal disease, and current pharmacotherapies provide limited renal protection. Qitu Qushi Formula (QTQSF), a traditional Chinese medicine prescription, has shown therapeutic potential in DKD, but its underlying mechanisms remain unclear. This study aimed to elucidate whether QTQSF alleviates DKD Methods: Clinical, animal, and cellular studies were integrated to investigate the therapeutic effects of QTQSF. Clinical samples from 30 patients with type 2 DKD received QTQSF treatment for 6 months was used to assess renal function and gut microbiota. To explore microbiota-mediated mechanisms, db/db mice, pseudo-germ-free models, and fecal microbiota transplantation (FMT) were utilized. Multi-omics analyses, including 16S rRNA sequencing, untargeted and targeted metabolomics, and transcriptomics, were conducted to uncover key pathways underlying QTQSF's efficacy. Results: QTQSF significantly improved renal function and remodeled gut microbial composition in DKD patients. In db/db mice, QTQSF reduced albuminuria, fibrosis, and apoptosis, whereas these protective effects were attenuated after gut microbiota depletion. FMT supported that gut microbiota mediated the renoprotective effects of QTQSF. Integrated multi-omics analyses revealed that QTQSF enhanced microbial tryptophan metabolism and increased the gut microbiota-derived metabolite indole-3-propionic acid (IPA). Elevated IPA levels were associated with regulation of the renal Sirt1/FoxO1 pathway, which was further validated in podocytes as a key mechanism underlying the anti-apoptotic effects. Conclusion: QTQSF may ameliorate DKD by enhancing gut microbiota-derived IPA production and regulating the Sirt1/FoxO1 signaling pathway, thereby attenuating renal injury. These findings provide mechanistic insight into the renoprotective effects of QTQSF and highlight a gut microbiota-metabolite-host signaling axis in DKD.
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