Cardamonin decreases inflammatory mediator expression in IL-1β-stimulated human periodontal ligament cells

Risa Okamoto1, Yoshitaka Hosokawa2, Ikuko Hosokawa1

  • 1Department of Regenerative Dental Medicine, Tokushima University Graduate School of Biomedical Sciences, 3-18-15 Kuramoto-cho, Tokushima, Tokushima, 770-8504, Japan.

Molecular Biology Reports
|January 28, 2024
PubMed

Insights

Cardamonin, a natural chalcone, reduces inflammation in human periodontal ligament cells by inhibiting key inflammatory mediators and pathways. This suggests potential therapeutic applications for periodontitis treatment.

Area of Science:

  • Natural Product Chemistry
  • Cell Biology
  • Immunology

Background:

  • Cardamonin is a chalcone with reported bioactivity.
  • Periodontitis involves inflammation of periodontal tissues.
  • Limited research exists on cardamonin for periodontitis treatment.

Purpose of the Study:

  • Investigate cardamonin's anti-inflammatory effects on human periodontal ligament cells (HPDLCs).
  • Determine cardamonin's impact on interleukin-1β (IL-1β)-induced inflammatory mediators.
  • Analyze cardamonin's influence on IL-1β-activated signaling pathways.

Main Methods:

  • Enzyme-linked immunosorbent assay (ELISA) for cytokine and chemokine quantification.
  • Western blot analysis for protein expression and signal transduction pathway assessment.
  • Utilized HPDLCs stimulated with IL-1β.

Main Results:

  • Cardamonin suppressed IL-1β-induced production of CCL2, CCL5, CCL20, CXCL10, and IL-6.
  • Cardamonin reduced intercellular adhesion molecule (ICAM)-1 and cyclooxygenase (COX)-2 expression.
  • Cardamonin inhibited IL-1β-activated nuclear factor (NF)-κB and signal transducer and activator of transcription (STAT)3 phosphorylation.
  • Cardamonin enhanced antioxidant enzyme expression (HO-1, NQO1).

Conclusions:

  • Cardamonin exhibits anti-inflammatory properties in HPDLCs.
  • Cardamonin effectively suppresses inflammatory mediator production induced by IL-1β.
  • Cardamonin modulates key inflammatory signaling pathways, including NF-κB and STAT3.
Abstract