ArticleCurrent medical science2024
Kaempferol Improved Rheumatoid Arthritis by Regulating the Immune Imbalance of Treg/Th17.
Article in Current medical science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Kaempferol as a multi-targeted phytotherapeutic for arthritis: systematic review and meta-analysis of preclinical models.Inflammopharmacology · 2025Pooled it
- Physicochemically-guided immunomodulatory biomaterials for regulating immune responses in rheumatoid arthritis.Materials today. Bio · 2026Article
- Kaempferol: advances in biosynthesis, molecular mechanisms, and therapeutic applications.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Tripterygium wilfordii multi-glycoside alleviates ankylosing spondylitis via gut microbiota modulation and metabolite reprogramming.Journal of advanced research · 2026Article
- Mechanism of Qiling Fuzheng Qingjie granules in alleviating doxorubicin-induced T cell immune dysfunction via mitochondrial energy metabolism.Chinese medicine · 2026Article
- OptiSyn: an interpretable, multi-omics-driven graph convolutional network framework for synergy-oriented drug combination design in disease treatment.Chinese medicine · 2026Article
- Dual role of IL-17A in COPD: amplifier of inflammatory cascades and mediator of airway remodeling and alveolar destruction.Frontiers in immunology · 2026Review
- Targeting neuroimmune interactions: the therapeutic potential of kaempferol in immune-related central nervous system disorders.Frontiers in immunology · 2026Review
- Mining personalized core traditional Chinese medicine prescriptions for rheumatoid arthritis and elucidating their mechanisms via frequent closed Itemset compression and multilevel network pharmacology.Frontiers in molecular biosciences · 2026Article
- Promotion of Treg/Th17 balance in MRL/lpr mice by Jianpi-Zishen Formula via modulation of DNMT1-mediated Foxp3 methylation.Frontiers in immunology · 2025Article
- Kaempferol as a multifaceted immunomodulator: implications for inflammation, autoimmunity, and cancer.Frontiers in immunology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThe objective of this study was to explore the therapeutic effects of kaempferol (Kae) on rheumatoid arthritis (RA) and to elucidate the underlying mechanisms.
methodsThe collagen-induced arthritis (CIA) model was established using collagen II to induce RA. Mice were treated with Kae at a dose of 25 or 50 mg/kg/day via gavage. Pathological changes in the ankle joint were analyzed. Enzyme-linked immunosorbent assay (ELISA) was employed to measure the levels of inflammatory factors. Reverse transcription quantitative polymerase chain reaction (RT-qPCR) was used to assess the expression of genes associated with the balance of regulatory T (Treg)/T helper 17 (Th17) cells. Flow cytometry was utilized to determine the Treg/Th17 ratio. Furthermore, these techniques were employed to evaluate the impact of miR-34a and Foxp3 dysregulation on cellular functions in RA under the influence of Kae. Dual luciferase reporter assay was conducted to analyze the binding of miR-34a to Foxp3.
resultsTreatment with Kae led to a downregulation of receptor-related orphan receptor gamma t (RORγt) and IL-17 expression, and an upregulation of Foxp3, IL-10, and TGF-β expression in CIA mice. Kae intervention inhibited the production of proinflammatory cytokines and increased the production of anti-inflammatory cytokines. Furthermore, Kae treatment suppressed the expression of miR-34a, which was identified as a target of miR-34a. Finally, Kae regulated Treg/ Th17 balance-related genes and cellular inflammation through the miR-34a/Foxp3 axis.
conclusionThe study demonstrated that Kae effectively ameliorates CIA in mice by modulating the Treg/Th17 balance and related genes via the miR-34a/Foxp3 axis. These findings suggest that Kae may serve as a promising therapeutic agent for the treatment of RA and for restoring immune homeostasis.
Indexed as
Identifiers
39673582What 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.