ArticleFrontiers in microbiology2026
Qijiao Shengbai capsule ameliorates ulcerative colitis in mice by modulating gut microbiota and protecting the intestinal barrier, associated with suppression of the TLR4/MyD88/NF-κB pathway.
Article in Frontiers in microbiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Qijiao Shengbai capsule (QJSB) is a classic traditional Chinese compound formulation composed of seven herbal ingredients, primarily used clinically to treat leukopenia. Individual herbs and their active components within QJSB demonstrate favorable efficacy against ulcerative colitis (UC). Nevertheless, no evidence exists of QJSB being a full-form prescription for treating UC. Methods: This study identified the chemical composition of QJSB using UHPLC-ESI-Q-Exactive Plus Orbitrap-MS. At the same time, a mouse model of ulcerative colitis (UC) was established using DSS to examine the effects of QJSB on disease symptoms, inflammatory factors, intestinal barrier function, and colonic histopathological changes. Furthermore, metabolomics, 16S rRNA sequencing, and network pharmacology were combined to analyze the potential mechanisms underlying the effects of QJSB intervention in UC-affected mice, and key pathways predicted by network pharmacology were validated using Western blot analysis. Results: The results showed that QJSB treatment significantly alleviated DSS-induced colitis symptoms in UC mice, as evidenced by weight recovery, a decrease in the disease activity index (DAI), improvement in colonic shortening, and reduced tissue damage. Gut microbiota analysis indicated that QJSB modulates the composition of the gut microbiota by upregulating the abundance of Conclusion: The present findings suggest that QJSB may exert therapeutic effects against UC, potentially through mechanisms involving the inhibition of inflammatory responses, protection of intestinal barrier function, regulation of metabolic homeostasis, and restoration of gut microbial ecology. These results imply that QJSB could serve as a potential therapeutic candidate for UC and provide a new basis for its clinical application.
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