Exploring the mechanism of action of Qufengzhitong pills in treating rheumatoid arthritis via the PI3K/AKT, NF-κB, and MAPK pathways.

Authors

Jie Li, Rongxue Li, Yule Wang, Marwan M A Rashed, Dejun Qi, Yuanjie He, Chenghui He, Yanxu Chang, Sihui Nian, Hong Duan, Henggui Hu, Kefeng Zhai

Published in

The Journal of pharmacy and pharmacology. Volume 78. Issue 6. Jun 02, 2026.

Abstract

To elucidate the therapeutic mechanism of Qufengzhitong Pills (QFZTP) in the treatment of rheumatoid arthritis (RA).
Blood-absorbed active components of QFZTP and its potential therapeutic targets for RA were screened via liquid chromatography-tandem mass spectrometry (LC-MS/MS) and network pharmacology. Core targets were analyzed using protein-protein interaction networks, with key pathways identified via Gene Ontology/Kyoto Encyclopedia of Genes and Genomes enrichment. Molecular docking was performed for major components and core targets. An IL-1β-induced MH7A cell-based RA model was established; CCK-8, ELISA (IL-6/TNF-α), wound-healing/Transwell, flow cytometry, EdU, and western blot (PI3K/AKT/NF-κB/MAPK pathways) were used to assess cell viability, cytokines, migration, apoptosis, proliferation, and protein expression.
LC-MS/MS identified 92 active components in rat serum, and network pharmacology identified 369 potential QFZTP targets for RA, enriched mainly in TNF signaling, PI3K/AKT, MAPK, and apoptosis pathways. Core components (crocetin, epigallocatechin, bergapten) showed stable binding (<-5.0 kcal/mol) to AKT1, EGFR, and PI3K, occupying similar active pockets as native inhibitors. In vitro, QFZTP-containing serum significantly reduced IL-1β-induced MH7A cell viability; inhibited IL-6/TNF-α secretion (comparable to native QFZTP solution); attenuated migration/proliferation; induced apoptosis; downregulated EGFR, p-PI3K, p-AKT, p-p38, p-NF-κB, and Bcl-2; and up-regulated Bax.
QFZTP synergistically regulates the PI3K/AKT, NF-κB, and MAPK pathways to inhibit synovial cell proliferation and migration, induce apoptosis, and attenuate inflammation. This study provides a robust theoretical and experimental basis for its clinical application in RA.

PMID:
42335406
Bibliographic data and abstract were imported from PubMed on 24 Jun 2026.

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