阿魏酸通过抑制自诱导剂-2的产生和受体活性来抑制牙龈卟啉单胞菌生物膜的形成。

IF 2.1
Archives of oral biology Pub Date : 2025-10-01 Epub Date: 2025-07-26 DOI:10.1016/j.archoralbio.2025.106365
Daiki Ando, Hnin Yu Lwin, Yukari Aoki-Nonaka, Aoi Matsugishi-Nasu, Yukako Minato, Yuko Warita, Naoki Takahashi, Koichi Tabeta
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引用次数: 0

摘要

目的:研究阿魏酸对牙周致病菌的抗菌及抗生物膜作用。设计:采用MTT法检测阿魏酸对人口腔上皮细胞系Ca9-22的细胞毒性。采用阿魏酸处理牙龈卟啉单胞菌ATCC 33277、核梭菌ATCC 25586、中间普雷伏菌ATCC 25611、放线菌comitans聚集菌JP2和mittis链球菌ATCC 903,测定最小抑菌浓度和最小杀菌浓度。结晶紫染色评价其对生物膜形成的抑制作用。利用感应菌株哈维弧菌(Vibrio harveyi) BB170对牙龈卟啉卟啉(P. gingivalis)自诱导物-2 (AI-2)的产生和受体活性进行了发光测定。结果:阿魏酸对人口腔上皮细胞无细胞毒性。阿魏酸对牙龈假单胞菌和放线菌的mic分别为1000和500 µg/mL。结果表明,阿魏酸对具核假单胞菌、中间假单胞菌和密氏链球菌的抑菌活性较弱。然而,阿魏酸在1/8 MIC以下的低浓度下显著抑制牙龈假单胞菌生物膜的形成。特异性抑制1/8 MIC以下牙龈假单胞菌产生AI-2,抑制AI-2受体活性。结论:阿魏酸对牙周病细菌的抑菌活性较弱,但具有较低的细胞毒性,可抑制牙龈假单胞菌生物膜的形成。阿魏酸抑制AI-2的产生和受体活性,提示阿魏酸是有效的群体感应抑制剂,可控制牙龈假单胞菌生物膜的形成。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Ferulic acid suppresses Porphyromonas gingivalis biofilm formation via the inhibition of autoinducer-2 production and receptor activity.

Objective: This study aimed to clarify the antibacterial and antibiofilm effects of ferulic acid against periodontal pathogenic bacteria.

Design: The cytotoxicity of ferulic acid was examined using the MTT assay on the human oral epithelial cell line Ca9-22. To determine the minimum inhibitory concentration (MIC) and minimum bactericidal concentration, Porphyromonas gingivalis ATCC 33277, Fusobacterium nucleatum ATCC 25586, Prevotella intermedia ATCC 25611, Aggregatibacter actinomycetemcomitans JP2, and Streptococcus mitis ATCC 903 were treated with ferulic acid. The inhibition of biofilm formation was evaluated by crystal violet staining. The inhibition of P. gingivalis autoinducer-2 (AI-2) production and receptor activity was evaluated by luminescence measurements using the sensor strain Vibrio harveyi BB170.

Results: Ferulic acid did not exhibit any cytotoxicity on human oral epithelial cells. The MICs of ferulic acid against P. gingivalis and A. actinomycetemcomitans were 1000 and 500 µg/mL, respectively. It did not show antibacterial activity against F. nucleatum, P. intermedia, and S. mitis, indicating the weak antibacterial activity of ferulic acid. However, ferulic acid significantly inhibited P. gingivalis biofilm formation at low concentrations below 1/8 MIC. It specifically inhibited AI-2 production from P. gingivalis below 1/8 MIC and suppressed the receptor activity of AI-2.

Conclusions: Although ferulic acid showed weak antibacterial activity against periodontopathogenic bacteria, it had low cytotoxicity and inhibited P. gingivalis biofilm formation. Ferulic acid inhibited AI-2 production and receptor activity, suggesting that ferulic acid is an efficient quorum-sensing inhibitor for controlling P. gingivalis biofilm formation.

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