BackgroundSome differences have been reported in the biotransformation of ginsenosides, probably due to the types of materials used such as ginseng, enzymes, and microorganisms. Moreover, most microorganisms used for transforming ginsenosides do not meet food-grade standards. We investigated the statistical conversion rate of major ginsenosides in ginsenosides model culture during fermentation by lactic acid bacteria (LAB) to estimate possible pathways.MethodsGinsenosides standard mix was used as a model culture to facilitate clear identification of the metabolic changes. Changes in eight ginsenosides (Rb1, Rb2, Rc, Rd, Re, Rf, Rg1, and Rg2) during fermentation with six strains of LAB were investigated.ResultsIn most cases, the residual ginsenoside level decreased by 5.9–36.8% compared with the initial ginsenoside level. Ginsenosides Rb1, Rb2, Rc, and Re continuously decreased during fermentation. By contrast, Rd was maintained or slightly increased after 1 d of fermentation. Rg1 and Rg2 reached their lowest values after 1–2 d of fermentation, and then began to increase gradually. The conversion of Rd, Rg1, and Rg2 into smaller deglycosylated forms was more rapid than that of Rd from Rb1, Rb2, and Rc, as well as that of Rg1 and Rg2 from Re during the first 2 d of fermentation with LAB.ConclusionGinsenosides Rb1, Rb2, Rc, and Re continuously decreased, whereas ginsenosides Rd, Rg1, and Rg2 increased after 1–2 d of fermentation. This study may provide new insights into the metabolism of ginsenosides and can clarify the metabolic changes in ginsenosides biotransformed by LAB.

Obesity can be caused by microbes producing metabolites; it is thus important to determine the correlation between gut microbes and metabolites. This study aimed to identify gut microbiota-metabolomic signatures that change with a high-fat diet and understand the underlying mechanisms. To investigate the profiles of the gut microbiota and metabolites that changed after a 60% fat diet for 8 weeks, 16S rRNA gene amplicon sequencing and gas chromatography-mass spectrometry (GC-MS)-based metabolomic analyses were performed. Mice belonging to the HFD group showed a significant decrease in the relative abundance of Bacteroidetes but an increase in the relative abundance of Firmicutes compared to the control group. The relative abundance of Firmicutes, such as Lactococcus, Blautia, Lachnoclostridium, Oscillibacter, Ruminiclostridium, Harryflintia, Lactobacillus, Oscillospira, and Erysipelatoclostridium, was significantly higher in the HFD group than in the control group. The increased relative abundance of Firmicutes in the HFD group was positively correlated with fecal ribose, hypoxanthine, fructose, glycolic acid, ornithine, serum inositol, tyrosine, and glycine. Metabolic pathways affected by a high fat diet on serum were involved in aminoacyl-tRNA biosynthesis, glycine, serine and threonine metabolism, cysteine and methionine metabolism, glyoxylate and dicarboxylate metabolism, and phenylalanine, tyrosine, and trypto-phan biosynthesis. This study provides insight into the dysbiosis of gut microbiota and metabolites altered by HFD and may help to understand the mechanisms underlying obesity mediated by gut microbiota.

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Silicon dioxide (SiO 2 ) nanoparticles (NPs) have been widely used in the biomedical field, such as in drug delivery and gene therapy. However, little is known about the biological effects and potential hazards of SiO 2 . Herein, the colloidal SiO 2 NPs with two different sizes (20 nm and 100 nm) and different charges (L-arginine modified: SiO 2 EN20[R] , SiO 2 EN100[R] ; and negative: SiO 2 EN20[−] , SiO 2 EN100[−] were orally administered (750 mg/kg/day) in female C57BL/6 mice for 14 days. Assessments of immunotoxicity include hematology profiling, reactive oxygen species generation and their antioxidant effect, stimulation assays for B- and T-lymphocytes, the activity of natural killer (NK) cells, and cytokine profiling. In vitro toxicity was also investigated in the RAW 264.7 cell line. When the cellularity of mouse spleen was evaluated, there was an overall decrease in the proliferation of B- and T-cells for all the groups fed with SiO 2 NPs. Specifically, the SiO 2 EN20(−) NPs showed the most pronounced reduction. In addition, the nitric oxide production and NK cell activity in SiO 2 NP-fed mice were significantly suppressed. Moreover, there was a decrease in the serum concentration of inflammatory cytokines such as interleukin (IL)-1β, IL-12 (p70), IL-6, tumor necrosis factor-α, and interferon-γ. To elucidate the cytotoxicity mechanism of SiO 2 in vivo, an in vitro study using the RAW 264.7 cell line was performed. Both the size and charge of SiO 2 using murine macrophage RAW 264.7 cells decreased cell viability dose-dependently. Collectively, our data indicate that different sized and charged SiO 2 NPs would cause differential immunotoxicity. Interestingly, the small-sized and negatively charged SiO 2 NPs showed the most potent in vivo immunotoxicity by way of suppressing the proliferation of lymphocytes, depressing the killing activity of NK cells, and decreasing proinflammatory cytokine production, thus leading to immunosuppression.

Polymer–nonleaded metal (tungsten, Sendust) composites were prepared to study the effects of multilayer structure on X-ray shielding ability. Though the metals were nonleaded, the metal contents were low, and the composite films were thin, the composite films showed favorable X-ray shielding ability due to the uniform dispersion of metal particles in the polymer matrix and the flake alignment (Sendust). This means that multi- layered particles can effectively absorb the penetrating photons and they fill the pin holes in the composite. More uniformly aligned Sendust shows better shielding effect than randomly oriented Sendust. The lamination order of tungsten film and Sendust composite film affects the final performance of the laminated composites. This work demonstrates that nonleaded metal–polymer composite can be applied for X-ray shielding as a reliable substitute material for lead.