ArticleMediators of inflammation2026
Hydroxysafflor Yellow A Induces Apoptosis and Inhibits Inflammatory Cytokine Expression in Rheumatoid Arthritis Synovial Fibroblasts Through the MEK-ERK Pathway.
Article in Mediators of inflammation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
objectiveThe objective of this study was to investigate whether hydroxysafflor yellow A (HSYA) affects the proliferation and apoptosis of fibroblast-like synoviocytes (FLSs) in rheumatoid arthritis (RA). Synovial fibroblast hyperplasia is a key pathological feature of RA, and its inhibition may slow disease progression. Although HSYA has attracted significant interest, its effects on RA are not yet fully understood. Thus, we performed a series of experiments to examine the impact of HSYA on FLSs.
methodsTo investigate the effects of HSYA on FLSs, we exposed FLSs to Interleukin-1 beta (IL-1β) and assessed their proliferation via CCK8, scratch, transwell, TUNEL, and flow cytometry assays. Inflammatory cytokine levels were determined by ELISA. The involvement of the MEK-ERK signaling pathway was validated via RT-qPCR and immunofluorescence analyses.
resultsTreatment with HSYA significantly inhibited FLSs proliferation, while promoting their apoptosis. Moreover, HSYA altered the expression of the inflammatory cytokines IL-6, IL-10, and TNF-α in FLSs. The anti-inflammatory and anti-proliferative effects of HSYA on FLSs were mediated, at least in part, through the inhibition of the ERK signaling pathway.
conclusionOur findings demonstrate that HSYA induces apoptosis, inhibits proliferation, and suppresses the production of inflammatory cytokines in FLSs via the ERK/MEK signaling pathway. These findings suggest that HSYA has potential therapeutic value in the treatment of RA and warrants further investigation.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.