Cardamonin inhibits the expression of inflammatory mediators in TNF-α-stimulated human periodontal ligament cells

Abstract

Objective

Periodontis is a chronic inflammatory disease induced by periodontopathogenic bacteria. The excessive immune response caused by persistent bacterial infection leads to alveolar bone resorption and ultimately tooth loss. Cardamonin is a biologically active substance that is found in the Zingiberaceae family, such as Alpinia zerumbet, and is classified as a natural chalcone. There have been no attempts to use cardamonin for the treatment of periodontitis, and no reports have examined the effects of cardamonin on periodontal tissue component cells. The aim of this study was to analyze effects of cardamonin on expression of inflammation mediators produced by TNFα-stimulated human periodontal ligament cells (HPDLCs), including its effects on signal transduction molecules.

Methods

Cytokine and chemokine levels were measured by ELISA. Protein expression in HPDLCs and activations of signal transduction pathway were determined by Western blotting.

Results

Our results indicate that cardamonin suppresses C-C motif chemokine ligand (CCL)2, CCL20, C-X-C motif chemokine ligand (CXCL)10, and interleukin (IL)-6 production and intercellular adhesion molecule (ICAM)-1 and cyclooxygenase (COX)-2 expression in TNF-α-stimulated HPDLCs. In addition, cardamonin induced the expression of the antioxidant enzyme, Heme Oxygenase (HO)-1, in HPDLCs. Furthermore, cardamonin suppressed TNF-α-stimulated c-Jun N-terminal kinase (JNK), nuclear factor (NF)-κB, and signal transducer and activator of transcription (STAT)3 signaling pathways in HPDLCs.

Conclusion

We show that cardamonin reduces inflammatory mediator production by inhibiting the activation of several signaling pathways in this manuscript.

Keywords:

• Cardamonin
• anti-inflammatory effect
• antioxidant enzyme
• signal transduction
• periodontal ligament cells

Author contributions

Conceptualization, Y.H.; investigation, R.O., Y.H., I.H.; methodology, R.O., Y.H., I.H., and K.O.; writing—original draft, R,O., Y.H.; writing—review and editing, K.O. and K.H. All authors have read and agreed to the published version of the manuscript.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Data availability statement

The data in this manuscript are available from the corresponding author on reasonable request.

Additional information

Funding

This work was supported by JSPS KAKENHI [Grant Numbers: 22K09966 and 22K09984] and Research Cluster program of Tokushima University [Grant Number: 2202006].