Related Experiment Video
Updated: Jul 4, 2025

Induction of Periodontitis via a Combination of Ligature and Lipopolysaccharide Injection in a Rat Model
Published on: February 17, 2023
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.
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.
Background:
Cardamonin is classified as a natural chalcone, and has been reported to possess various bioactive effects. However, there have been limited attempts to utilize cardamonin in the treatment of periodontitis. This study aimed to investigate whether cardamonin has anti-inflammatory effects on human periodontal ligament cells (HPDLCs), which are a component cell of periodontal tissue. Specifically, the study seeks to determine whether cardamonin affects the expression of inflammatory mediators, such as cytokines and adhesion molecules, induced by interleukin-1β (IL-1β) in HPDLCs, as well as the signaling pathways activated by IL-1β.
Methods:
Cytokine and chemokine levels in supernatants of HPDLCs were measured by ELISA. Western blot analysis was used to measure protein expression and signal transduction pathway activation in HPDLCs.
Results:
We found that IL-1β-induced CC chemokine ligand (CCL)2, CCL5, CCL20, CXC-chemokine ligand (CXCL)10, and interleukin (IL)-6 production and intercellular adhesion molecule (ICAM)-1 and cyclooxygenase (COX)-2 expression in HPDLCs were suppressed by cardamonin treatment. We also found that cardamonin suppressed IL-1β-activated nuclear factor (NF)-κB pathway, and the phosphorylation of signal transducer and activator of transcription (STAT)3. Furthermore, cardamonin treatment enhanced the expression of the antioxidant enzymes, heme oxygenase (HO)-1 and NAD(P)H dehydrogenase [quinone] 1 (NQO1), in HPDLCs.
Conclusion:
In this study, we found that cardamonin could suppress the production of inflammatory mediators in HPDLCs as well as the activation of several signaling pathways induced by IL-1β treatment.

