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Alkannin inhibits CCL3 and CCL5 production in human periodontal ligament cells
Author(s) -
Hosokawa Yoshitaka,
Hosokawa Ikuko,
Shindo Satoru,
Ohta Yoshihiro,
Ozaki Kazumi,
Matsuo Takashi
Publication year - 2016
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1002/cbin.10692
Subject(s) - ccl5 , ccl3 , periodontal fiber , business , production (economics) , chemokine , chemistry , ccl2 , biology , medicine , immunology , dentistry , economics , inflammation , biochemistry , in vitro , cytotoxic t cell , il 2 receptor , macroeconomics
Alkannin, which is found in Alkanna tinctoria , a member of the borage family, is used as a food coloring. Alkannin has recently been reported to have certain biological functions, such as anti‐microbial and anti‐oxidant effects. It is known that CC chemokine receptor (CCR) 5‐positive leukocytes contribute to alveolar bone resorption in periodontal lesions. The aim of this study was to examine whether alkannin inhibits the production of CC chemokine ligand (CCL) 3 and CCL5, which are CCR5 ligands, in human periodontal ligament cells (HPDLC). Interleukin (IL)‐1β induced CCL3 and CCL5 production in HPDLC. Alkannin inhibited IL‐1β‐mediated CCL3 and CCL5 production in HPDLC in a dose‐dependent manner. Moreover, we revealed that alkannin suppressed inhibitor of kappa B‐α degradation in IL‐1β‐stimulated HPDLC. In addition, a nuclear factor (NF)‐κB inhibitor significantly inhibited CCL3 and CCL5 production in IL‐1β‐stimulated HPDLC. These results demonstrate that alkannin inhibits CCR5 ligand production in IL‐1β‐stimulated HPDLC by attenuating the NF‐κB signaling pathway.