Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2026
Baitouweng Tang alleviates dextran sulfate sodium-induced ulcerative colitis in mice: a network pharmacology combined with experimental study.
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Yan Sun, Haozheng Zhou, Jianhui Feng, Zikai Lin, Jie H E, Zhenhua Wang, Yuting Guo, Shaohong Wen, Gang L I
Аннотация
OBJECTIVE: To 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.
METHODS: A 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.
RESULTS: PD 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.
CONCLUSION: PD 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.
METHODS: A 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.
RESULTS: PD 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.
CONCLUSION: PD 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.