Phytomedicine : international journal of phytotherapy and phytopharmacology · 2025
Jiangu formula modulates the gut microbiota structure and the NF-κB/NLRP3 signaling pathway to alleviate synovitis.
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Li Shuying, Zhang Aoyu, Qiao Jie, Yang Jingjing, Chen Haozhu, Shang Shiyan, Fu Tingshuai, Zhang Beier, Xu Kemin, Yang Gongxu, Zhang Qing
Аннотация
BACKGROUND: Synovitis is a pivotal pathological hallmark of arthritis, and timely intervention is essential for mitigating joint degeneration. Jiangu formula (JGF) can reduce inflammation in joint synovial fluid. However, its mechanism in treating synovial inflammation remains unclear.
METHOD: Chemical characterization of JGF's principal constituents was achieved through liquid chromatography-tandem mass spectrometry analysis. This study established a CFA -induced adjuvant arthritis model and investigated both the joint synovium and gut ecology. Through methodologies including 16S rRNA gene sequencing, it elucidated the mechanism by which JGF influences joint inflammation by modulating the NF-κB/NLRP3 signaling pathway and regulating gut microbiota structure.
RESULTS: JGF significantly improved behavioral and histopathological alterations in the CFA-induced mouse, enhanced locomotor function, reduced serum inflammatory factor levels, downregulated NF-κB/NLRP3 pathway in joint and gut tissues, and modulated the structure of gut microbiota. It may reduce inflammation by promoting arginine and proline metabolism, inhibiting amino sugar and nucleotide sugar metabolism, aiding in the repair of the intestinal mucosa.
CONCLUSION: JGF ameliorates synovial inflammatory response in mice model through modulation of gut microbiota structure and intervention in the NF-κB/NLRP3 signaling pathway, with the beneficial effects demonstrating gut microbiota dependency.
METHOD: Chemical characterization of JGF's principal constituents was achieved through liquid chromatography-tandem mass spectrometry analysis. This study established a CFA -induced adjuvant arthritis model and investigated both the joint synovium and gut ecology. Through methodologies including 16S rRNA gene sequencing, it elucidated the mechanism by which JGF influences joint inflammation by modulating the NF-κB/NLRP3 signaling pathway and regulating gut microbiota structure.
RESULTS: JGF significantly improved behavioral and histopathological alterations in the CFA-induced mouse, enhanced locomotor function, reduced serum inflammatory factor levels, downregulated NF-κB/NLRP3 pathway in joint and gut tissues, and modulated the structure of gut microbiota. It may reduce inflammation by promoting arginine and proline metabolism, inhibiting amino sugar and nucleotide sugar metabolism, aiding in the repair of the intestinal mucosa.
CONCLUSION: JGF ameliorates synovial inflammatory response in mice model through modulation of gut microbiota structure and intervention in the NF-κB/NLRP3 signaling pathway, with the beneficial effects demonstrating gut microbiota dependency.