ベイトウウェンタンはデキストラン硫酸ナトリウム誘発性潰瘍性大腸炎マウスの症状を緩和する：ネットワーク薬理学と実験的研究の組み合わせ

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.

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.

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.

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.