4.4 Article

Efficacy of β-caryophyllene for periodontal disease related factors

期刊

ARCHIVES OF ORAL BIOLOGY
卷 100, 期 -, 页码 113-118

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PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.archoralbio.2019.02.015

关键词

beta-Caryophyllene; Periodontal disease; Antimicrobial activity; Anti-inflammation; Prevention of halitosis

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Objective: This study aimed to investigate the antimicrobial activity of beta-caryophyllene against periodontopathogens as well as its inhibitory effects on the expression of inflammatory cytokines and production of volatile sulfur compounds by lipopolysaccharide and periodontopathogenic enzymes, respectively. Design: The antimicrobial activity of beta-caryophyllene againstPorphyromonas gingivalis, Tannerella forsythia, and Treponema denticola was investigated via a susceptibility assay using a microplate reader. THP-1 cells were treated with lipopolysaccharide in the presence or the absence of beta-caryophyllene, and the expression and production of inflammatory cytokines were then analyzed by a real-time reverse transcription polymerase chain reaction and enzyme-linked immunosorbent assay. After fluorescence-labelling lipopolysaccharide, the effect of beta-caryophyllene on the binding of lipopolysaccharide to the cell wall was investigated via flow cytometry. The spent culture media of P. gingivalis was shaken with or without beta-caryophyllene and gaseous volatile sulfur compounds (VSCs) were measured by a gas chromatograph. Results: beta-caryophyllene showed strong the antimicrobial activity against periodontopathogens. It also reduced lipopolysaccharide-induced expression and production of cytokines, thereby inhibiting the binding of lipopolysaccharide-binding to toll-like receptors by interfering with the complex of lipopolysaccharide and CD14 or lipopolysaccharide-binding protein. beta-caryophyllene also inhibited the emission of gaseous VSCs produced byP. gingivalis. Conclusions: beta-caryophyllene may improve periodontal health via antimicrobial activity against periodontopathogens, reducing inflammation caused by lipopolysaccharide, and by neutralizing VSCs.

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