ArticleScientific reports2025
Butin regulates the NLRP3/CASP-1/GSDMD pyroptosis axis to inhibit proliferation and pyroptosis in human fibroblast-like synoviocytes of rheumatoid arthritis.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Global research trends in programmed cell death in rheumatoid arthritis from 2001 to 2025: a bibliometric analysis.Frontiers in immunology · 2026Pooled it
- Beyond the Prevention of Anti-drug Antibody Formation with Uricase Therapy: Mechanistic Roles of DMARDs in Modifying Gout Flare Risk.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
To investigate the mechanism by which Butin inhibits proliferation and pyroptosis in human fibroblast-like synoviocytes of rheumatoid arthritis (HFLS-RA) via the NLRP3/Caspase-1/ GSDMD pyroptosis axis. Flavonoid compounds were extracted from Hei Gu Teng, and Butin was analyzed for its interaction with RA target proteins and signaling pathways using network pharmacology. An in vitro HFLS-RA model was established, and cells were induced with IL-1β. Groups included control, IL-1β-stimulated, IL-1β + Leflunomide, and IL-1β + Butin at low, medium, and high concentrations. Cell inhibition rates were measured using the MTT assay to determine the optimal Butin concentration, while scratch and Transwell assays assessed cell proliferation, migration, and invasion. LDH assays measured cell membrane damage; ELISA, RT-qPCR, and Western blot analyzed the expression of inflammation-related proteins NLRP3, GSDMD, CASP1, CASP3, IL1β, and IL18; Hoechst33342/PI staining and flow cytometry examined the cell cycle and pyroptosis. Hei Gu Teng yielded Butin (> 96% purity). Network pharmacology identified 48 target genes, predominantly involved in pathways like IL-1 signaling, HIF-1 signaling, sphingolipid signaling, and osteoclast differentiation. Cell assays demonstrated significantly reduced proliferation in Butin-treated groups compared to control (P < 0.05). Compared to the IL-1β + Leflunomide group, the Butin group showed decreased LDH release and lower levels of NLRP3, GSDMD, IL-1β, IL-18, CASP1, and CASP3 proteins and mRNAs (P < 0.05). Cell cycle analysis indicated increased DNA content in G0/G1 phases and decreased in G2/S phases for medium and high Butin concentrations (P < 0.05). Butin suppresses the expression of multiple inflammatory factors induced by IL-1β within the NLRP3/CASP-1/GSDMD pyroptosis axis, reducing proliferation and pyroptosis of HFLS-RA, thus alleviating synovial inflammation and representing a potential mechanism for RA treatment.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.