Journal of oral microbiology · 2026
Dihydromyricetin attenuates biofilm formation and virulence in Streptococcus mutans, the key pathogen underlying dental caries.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
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Liao Yuntong, Li Xinxin, Sethupathy Sivasamy, Zhong Lili, Cheng Xin, Wang Fang, Ding Zhiwen, Hao Chunbo, Ye Lianmeng, Li Yuqing, Dar Owias Iqbal, Wang Min
Аннотация
OBJECTIVE: Streptococcus mutans is a primary pathogen linked to dental caries. This study evaluated the effects of dihydromyricetin (DHM), a flavonoid from Ampelopsis grossedentata, on the biofilm formation and virulence of S. mutans UA159 and explored the underlying mechanisms.
METHODS: Antibacterial activity was determined by minimum inhibitory concentration (MIC) and growth assays. Biofilm formation, metabolic activity and viable counts were assessed using crystal violet staining, MTT and CFU assays. Biofilm architecture was examined by electron and confocal microscopy. Acid production, extracellular polysaccharide (EPS) synthesis, adhesion and aggregation were evaluated. Expression of virulence genes (gtfB, gtfC and spaP) and the quorum sensing gene luxS was analyzed by RT-qPCR.
RESULTS: DHM showed an MIC of 250 μg/mL and significantly inhibited biofilm formation, EPS synthesis, acid production, adhesion and aggregation. Biofilm structure was disrupted and viable cell counts were reduced. DHM markedly downregulated virulence-associated and quorum sensing-related genes.
CONCLUSION: DHM suppresses biofilm formation and cariogenic virulence of S. mutans, partly through the modulation of quorum sensing, indicating its potential as a natural anticariogenic agent.
METHODS: Antibacterial activity was determined by minimum inhibitory concentration (MIC) and growth assays. Biofilm formation, metabolic activity and viable counts were assessed using crystal violet staining, MTT and CFU assays. Biofilm architecture was examined by electron and confocal microscopy. Acid production, extracellular polysaccharide (EPS) synthesis, adhesion and aggregation were evaluated. Expression of virulence genes (gtfB, gtfC and spaP) and the quorum sensing gene luxS was analyzed by RT-qPCR.
RESULTS: DHM showed an MIC of 250 μg/mL and significantly inhibited biofilm formation, EPS synthesis, acid production, adhesion and aggregation. Biofilm structure was disrupted and viable cell counts were reduced. DHM markedly downregulated virulence-associated and quorum sensing-related genes.
CONCLUSION: DHM suppresses biofilm formation and cariogenic virulence of S. mutans, partly through the modulation of quorum sensing, indicating its potential as a natural anticariogenic agent.