The Polymethoxy Flavonoid Sudachitin Inhibits Interleukin-1β-Induced Inflammatory Mediator Production in Human Periodontal Ligament Cells
Author(s) -
Yoshitaka Hosokawa,
Ikuko Hosokawa,
Kazumi Ozaki,
Takashi Matsuo
Publication year - 2021
Publication title -
biomed research international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.772
H-Index - 126
eISSN - 2314-6141
pISSN - 2314-6133
DOI - 10.1155/2021/8826586
Subject(s) - chemokine , matrix metalloproteinase , chemistry , mediator , protein kinase b , microbiology and biotechnology , proinflammatory cytokine , periodontal fiber , interleukin , cancer research , inflammation , cxcl14 , interleukin 8 , cytokine , signal transduction , cxc chemokine receptors , chemokine receptor , pharmacology , receptor , immunology , biology , medicine , biochemistry , dentistry
Sudachitin, which is a polymethoxylated flavonoid found in the peel of Citrus sudachi, has some biological activities. However, the effect of sudachitin on periodontal resident cells is still uncertain. The aim of this study was to examine if sudachitin could decrease the expression of inflammatory mediators such as cytokines, chemokines, or matrix metalloproteinase (MMP) in interleukin- (IL-) 1 β -stimulated human periodontal ligament cells (HPDLC). Sudachitin inhibited IL-1 β -induced IL-6, IL-8, CXC chemokine ligand (CXCL)10, CC chemokine ligand (CCL)2, MMP-1, and MMP-3 production in HPDLC. On the other hand, tissue inhibitor of metalloproteinase- (TIMP-) 1 expression was increased by sudachitin treatment. Moreover, we found that the nuclear factor- (NF-) κ B and protein kinase B (Akt) pathways in the IL-1 β -stimulated HPDLC were inhibited by sudachitin treatment. These findings indicate that sudachitin is able to reduce inflammatory mediator production in IL-1 β -stimulated HPDLC by inhibiting NF- κ B and Akt pathways.
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