保坂啓一先生らの論文「Sudachitin reduces inflammatory mediator expression in toll-like receptor 2 ligand-stimulated human dental pulp cells」が掲載されました。

 

掲載誌等：Cell Biochemistry and Biophysics, 83, 2, 2431-2439, 2025.
DOI：10.1007/s12013-024-01652-8
著者：Katsuhiro Mieda, Tadashi Nakanishi, Hitomi Kuramoto, Yoshitaka Hosokawa, Ikuko Hosokawa, Daisuke Takegawa and Keiichi Hosaka

 

要約：Sudachitin, which is a polymethoxy flavonoid derived from the peer of Citrus sudachi, has several biological properties. However, the effect of sudachitin on human dental pulp cells (HDPCs) remains unclear. The aim of this study was to investigate whether sudachitin could decrease the expression of inflammatory mediators such as cytokines and prostaglandin in HDPCs stimulated with Pam3CSK4, a ligand for toll-like receptor (TLR) 2. HDPCs were pre-incubated with different concentrations of sudachitin (6.25, 12.5, 25, or 50 μM) and stimulated with Pam3CSK4 (100 ng/mL). The quantification of inflammatory cytokines (interleukin (IL)-6, IL-8, and C-X-C motif chemokine ligand (CXCL) 10) and prostaglandin E (PGE) were performed by enzyme-linked immunosorbent assay (ELISA). The expression of cyclooxygenase (COX)-2, a key enzyme for PGE formation, was analyzed by western blot. Moreover, the activations of cell signal pathways were examined by western blot analysis. Sudachitin suppressed IL-6, IL-8, CXCL10, and PGE production and COX-2 protein expression in Pam3CSK4-stimulated HDPCs. In addition, we revealed that nuclear factor-kappa B (NF-κB) and protein kinase B (Akt) pathways in the Pam3CSK4-stimulated HDPCs were inhibited by sudachitin treatment. These findings suggest that sudachitin can reduce inflammatory mediator production in HDPCs stimulated with TLR2 ligand by inhibiting NF-κB and Akt activations.

 

キーワード：Dental pulp cells / 歯髄炎 (pulpitis) / Sudachitin / Anti-inflammatory / サイトカイン (cytokine) / Prostaglandin E2