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Journal of ethnopharmacology · 2026

Exploring the mechanism of Bazheng San on rats with Interstitial Cystitis/Bladder Pain Syndrome (IC/BPS) based on TLR4/NF-κB/NLRP3 signaling pathway.

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Wenjie Yang, Xin Jiang, Yang Li, Chenxi Li, Xiaoxue Gao

Аннотация

ETHNOPHARMACOLOGICAL RELEVANCE: Bazheng San (BZS) is a traditional Chinese herbal formula commonly used to treat urinary disorders described as "Lin syndrome" in traditional Chinese medicine. Interstitial cystitis/bladder pain syndrome (IC/BPS) presents similar clinical manifestations, including urinary frequency, urgency, and pelvic pain. However, the pharmacological mechanisms underlying the therapeutic effects of BZS on IC/BPS remain unclear.

AIM OF THE STUDY: This study aimed to evaluate the therapeutic effects of Bazheng San on IC/BPS and to explore whether its anti-inflammatory activity involves regulation of the TLR4/NF-κB/NLRP3 signaling pathway.

MATERIALS AND METHODS: An IC/BPS rat model was established to assess urinary function, bladder histopathology, mast cell activation, and inflammatory responses. Histological staining, ELISA, qPCR, Western blot, and immunohistochemistry were used to evaluate inflammatory mediators and pathway-related molecules. An in vitro inflammatory model was induced in human bladder epithelial cells (5637) using lipopolysaccharide (LPS). BZS-containing serum and the TLR4 inhibitor Tak-242 were used to explore pathway regulation.

RESULTS: BZS reduced urinary frequency and urinary histamine levels and alleviated bladder pathological injury and mast cell infiltration in IC/BPS rats. Serum inflammatory cytokines (TNF-α, IL-6, and IL-1β) were also significantly decreased. BZS downregulated the expression of TLR4, MyD88, NF-κB p65, and NLRP3 and inhibited p65 nuclear translocation. In LPS-stimulated 5637 cells, BZS-containing serum suppressed inflammatory cytokine production and pathway activation and showed a synergistic effect with Tak-242.

CONCLUSION: Bazheng San alleviates IC/BPS-related inflammation and bladder injury, possibly through inhibition of the TLR4/NF-κB/NLRP3 signaling pathway.

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