Kaempferol Improved Rheumatoid Arthritis by Regulating the Immune Imbalance of Treg/Th17

Curr Med Sci. 2024 Dec;44(6):1259-1269. doi: 10.1007/s11596-024-2925-8. Epub 2024 Dec 14.

Abstract

Objective: The objective of this study was to explore the therapeutic effects of kaempferol (Kae) on rheumatoid arthritis (RA) and to elucidate the underlying mechanisms.

Methods: The 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.

Results: Treatment 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.

Conclusion: The 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.

Keywords: Foxp3; Treg/Th17; kaempferol; miR-34a; rheumatoid arthritis.

MeSH terms

  • Animals
  • Arthritis, Experimental* / drug therapy
  • Arthritis, Experimental* / immunology
  • Arthritis, Rheumatoid* / drug therapy
  • Arthritis, Rheumatoid* / genetics
  • Arthritis, Rheumatoid* / immunology
  • Cytokines / genetics
  • Cytokines / metabolism
  • Disease Models, Animal
  • Forkhead Transcription Factors* / genetics
  • Forkhead Transcription Factors* / metabolism
  • Interleukin-10 / genetics
  • Interleukin-10 / metabolism
  • Interleukin-17 / genetics
  • Interleukin-17 / metabolism
  • Kaempferols* / administration & dosage
  • Kaempferols* / pharmacology
  • Male
  • Mice
  • Mice, Inbred DBA
  • MicroRNAs* / genetics
  • Nuclear Receptor Subfamily 1, Group F, Member 3 / genetics
  • Nuclear Receptor Subfamily 1, Group F, Member 3 / metabolism
  • T-Lymphocytes, Regulatory* / drug effects
  • T-Lymphocytes, Regulatory* / immunology
  • Th17 Cells* / drug effects
  • Th17 Cells* / immunology

Substances

  • Kaempferols
  • kaempferol
  • MicroRNAs
  • Forkhead Transcription Factors
  • Foxp3 protein, mouse
  • Nuclear Receptor Subfamily 1, Group F, Member 3
  • Interleukin-17
  • Rorc protein, mouse
  • Cytokines
  • Interleukin-10