ArticleJournal of traditional Chinese medicine = Chung i tsa chih ying wen pan2026
Baitouweng Tang alleviates dextran sulfate sodium-induced ulcerative colitis in mice: a network pharmacology combined with experimental study.
Article in Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
objectiveTo explore the mechanism of Baitouweng Tang (, Pulsatilla decoction, PD) alleviates dextran sulfate sodium (DSS)-induced ulcerative colitis (UC) in mice by integrating network pharmacology prediction with experimental validation, focusing on the modulation of inflammatory signaling.
methodsA chronic UC model was induced in C57BL/6 mice by cyclical administration of DSS. Mice were treated with either a low (15 mL/kg) or high (30 mL/kg) dose of PD. Disease severity was assessed clinically and via histopathology. Serum levels of inflammatory cytokines were quantified. A network pharmacology approach was employed to predict the core targets and pathways of PD against UC. Key predictions concerning the toll-like receptor 4/nuclear factor-kappa B (TLR4/NF-κB) pathway were subsequently verified in colonic tissue using quantitative polymerase chain reaction and Western blotting.
resultsPD treatment significantly ameliorated DSS-induced UC symptoms, including reducing disease activity, preventing colon shortening, and improving histological architecture. PD effectively rebalanced the systemic inflammatory milieu by decreasing pro-inflammatory cytokines interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) and elevating anti-inflammatory cytokines interleukin-10 (IL-10). Network pharmacology analysis identified the TLR4/NF-κB signaling pathway as a central target. Experimental validation confirmed that PD markedly suppressed the upregulation of both TLR4 and NF-κB at the transcriptional and protein levels in the inflamed colon.
conclusionPD demonstrates protective effects against experimental UC. Its mechanism is associated with the inhibition of the TLR4/NF-κB signaling pathway and the subsequent attenuation of inflammatory responses. This study provides a modern pharmacological basis for the classical application of PD in treating heat-toxin related intestinal disorders, bridging traditional use and mechanistic understanding.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.