In order to investigate the antibacterial mechanism of tea polyphenols and theaflavins against oral cariogenic bacteria, the pH value of the culture medium, the number of bacteria adhering to the smooth glass tube wall, and the electrical conductivity value within 10 h were measured, respectively. The effects of four concentrations of tea polyphenols and theaflavins below the MIC value were studied on acid production, adhesion, and electrical conductivity of oral cariogenic bacteria. The live/dead staining method was used to observe the effects of four concentrations of tea polyphenols and theaflavins below the MIC value on the biofilm formation of oral cariogenic bacteria under a laser scanning confocal microscope. With the increase in concentrations of tea polyphenols and theaflavins, the acid production and adhesion of the cariogenic bacteria gradually decreased, and the conductivity gradually increased. However, the conductivity increase was not significant (p < 0.05). Compared with the control group, the 1/2MIC and 1/4MIC tea polyphenols and theaflavins treatments significantly reduced the biomass of the cariogenic biofilm (p < 0.05). The confocal laser scanning microscope showed that the integrated optical density of green fluorescence of the cariogenic biofilm gradually decreased with the increase in agent concentration after the action of tea polyphenols and theaflavins.

Scutellarein (SCU) is an herbal flavonoid, showing hepatoprotective potentials. The study was aimed to investigate whether the hepatoprotective effect of SCU is dependent on the integrity of gut microbiota. Mice received repeated intraperitoneal injections of CCl₄, followed with or without SCU treatment (15, 30, and 60 mg/kg). Gut microbial community of mice was disrupted by administrating a cocktail of antibiotics (ampicillin, neomycin sulfate, metronidazole, and vancomycin) in drinking water. The results showed SCU plus antibiotics aggravated CCl₄‐induced chronic liver injury, as demonstrated by liver function analysis, histological analysis, and TUNEL assay. SCU activated CYP2E1 expression and worsened CYP2E1‐mediated lipid peroxidation and oxidative stress as coadministered with antibiotics. Moreover, when gut microbiota was disrupted by antibiotics, SCU activated IκBα/NF‐κB pathway and promoted the release of subsequent proinflammatory cytokines including interleukin‐6 (IL‐6), interleukin‐1β (IL‐1β), and tumor necrosis factor‐α (TNF‐α). Remarkably, the 16 S rRNA sequencing demonstrated that SCU greatly decreased the relative abundance of Bifidobacterium and Lactobacillus and increased the relative abundance of Enterococcus in gut microbiota‐dysbiosis mice. Spearman correlation analysis showed that Lactobacillus was positively correlated with SOD and negatively correlated with AST. Collectively, the hepatoprotective effect of SCU is reversed under antibiotics intervention, which may partly involve the activation of CYP2E1 and IκBα/NF‐κB pathway and diminishment of Lactobacillus.