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DOI 10.1159/000356675

Медицинская библиотека · Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2014

Genipin inhibits IL-1β-induced CCL20 and IL-6 production from human periodontal ligament cells.

Shindo Satoru, Hosokawa Yoshitaka, Hosokawa Ikuko, Ozaki Kazumi, Matsuo Takashi

СтатьяПоддержка исследования: вне правительства СШАПеревод в очереди

Аннотация

BACKGROUND/AIMS: Genipin, the aglycon of geniposide found in gardenia fruit has long been considered for treatment of various diseases in traditional oriental medicine. Genipin has been used as a blue colorant in food industry. Genipin has recently been reported to have some pharmacological functions, such as antimicrobial, antitumor, and anti-inflammatory effects. The aim of this study was to examine whether genipin could modify CCL20 and IL-6, which are related to bone resorption in periodontal disease, expression in human periodontal ligament cells (HPDLCs).

METHODS

CCL20 and IL-6 productions from HPDLCs were determined by ELISA. Western blot analysis was used for the detection of signal transduction molecules expressions in HPDLCs.

RESULTS

Genipin prevented IL-1β-mediated CCL20 and IL-6 production in HPDLCs. Moreover, genipin could suppress nuclear factor kappa B (NF-κB) p65, extracellular signalregulated kinase (ERK) and MAPK/ERK kinase (MEK) phosphorylations in IL-1β-stimulated HPDLCs. NF-κB inhibitor and ERK inhibitor significantly inhibited IL-6 and CCL20 productions from IL-1β-stimulated HPDLCs.

CONCLUSIONS

These data provide a novel mechanism through which genipin could be used to provide direct benefits in periodontal disease to inhibit IL-6 and CCL20 productions in periodontal lesions.

Для цитирования: Shindo Satoru, Hosokawa Yoshitaka, Hosokawa Ikuko, Ozaki Kazumi, Matsuo Takashi. Genipin inhibits IL-1β-induced CCL20 and IL-6 production from human periodontal ligament cells.. Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology. 2014. DOI: 10.1159/000356675.

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