ArticleACS omega2025
Baitong Decoction Ameliorates DSS-Induced Colitis via Modulation of STING and JAK/STAT Pathways.
Article in ACS omega, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- The bidirectional immunoregulatory effects of Traditional Chinese Medicine on the cGAS-STING signaling pathway and their translational prospects.Chinese medicine · 2026Review
- A systems pharmacology-basedFrontiers in veterinary science · 2026Article
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Baitong decoction (BTD), a classical traditional Chinese medicine formulation, is widely recognized for its pharmacological potential in treating digestive diseases, yet its mechanisms of action in ulcerative colitis (UC) remain unclear. This study investigated the therapeutic effects of BTD in a dextran sodium sulfate (DSS)-induced murine model of UC, using six mice per group. The chemical profile of BTD was standardized via HPLC. Treatment with BTD significantly ameliorated UC symptoms, including weight loss, disease activity index (DAI) scores, colon shortening, and histopathological damage. AB-PAS staining indicated that BTD restored goblet cell numbers and mucus secretion. Additionally, BTD reduced levels of proinflammatory cytokines (TNF-α, IL-1β, IL-6, IL-18) and myeloperoxidase (MPO) activity. Immunohistochemical (IHC) analysis further revealed suppressed expression of NF-κB p65 and IL-6 in colon tissues. Network pharmacology suggested the involvement of TNF, JAK/STAT, and STING pathways, targeting molecules such as IL-6, TNF-α, STAT3, and STAT6. Molecular docking demonstrated strong binding between BTD's active compounds and these targets. Results from Western blotting, enzyme-linked immunosorbent assay and IHC collectively indicated that BTD could inhibit the expression of proteins related to the JAK/STAT and STING signaling pathways in vivo. BTD exerts significant therapeutic effects in DSS-induced UC model mice by suppressing inflammatory responses and modulating the JAK/STAT and STING signaling pathways, providing a solid theoretical foundation for its clinical translation and mechanistic exploration.
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Registered trials
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