This study was designed to investigate the tumor-inhibitory effects of quercetin (Que) and its water-soluble metabolites, quercetin-3'-sulfate (Q3'S) and quercetin-3-glucuronide (Q3G), as well as to make the molecular mechanism and structure-antitumor relationship clear. It was found that Que, Q3'S, and Q3G could inhibit the growth of human breast cancer MCF-7 cells in a dose-dependent manner, with the IC values of 23.1, 27.6, and 73.2 μM, respectively, and their anticancer effect was ranked as Que > Q3'S > Q3G. Furthermore, flow cytometric assay revealed that Que, Q3'S, and Q3G mediated the cell-cycle arrest principally at the S phase and decreased the number of G0/G1 and G2/M after a 48 h treatment with human breast MCF-7 cells. Moreover, it was found that 70.8%, 58.2%, and 48.0% of MCF-7 cancer cells entered the early phase of apoptosis when treated with 100 μM Que, Q3'S, and Q3G for 48 h, respectively. In addition, induction of apoptosis by Que, Q3'S, and Q3G was accompanied by marginal generation of intracellular reactive oxygen species (ROS) in the MCF-7 cancer cells. Overall, these results demonstrate that Que, Q3'S, and Q3G possess strong antitumor effects through induction of an ROS-dependent apoptosis pathway in MCF-7 cells.

Differential effects of quercetin and its two derivatives (isorhamnetin and isorhamnetin-3-glucuronide) in inhibiting proliferation of human breast cancer MCF-7 cells

Fuzhuan brick tea can improve non-alcoholic fatty liver disease (NAFLD) and intestinal microbiota imbalance induced by a high fructose diet (HFD) intake in mice.

No abstract

This article studied the effects of high L-carnitine consumption on intestinal microbiota, liver function, and metabolite distribution in mice. 16S rRNA results showed that high L-carnitine supplementation could induce the accumulation of Anaerobiospirillum, Coriobacteriaceae, Akkermansia_muciniphila, and Helicobacter. High intake of L-carnitine also induced liver injury, which was proved by the increases in the serum AST and ALT activities, production of inflammatory liver cytokines (IL-1, IL-6, TNF-α, and TNF-β), lipid metabolism (TC, TG, HDL, and LDL) disorder, and decline in antioxidant ability (SOD, GSH-Px, MDA, and RAHFR). The correlation analysis results showed that Anaerobiospirillum, Akkermansia_muciniphila, and Helicobacter were strongly positively correlated with AST, IL-1, TNF-α, TNF-β, and MDA levels (r > 0.5, p < 0.01 or p < 0.05). All in all, high Lcarnitine ingestion could induce a decline in the liver function by disorder in the gut bacteria composition, resulting in an increase in TMAO metabolism.

Gut microbiota-dependent metabolites trimethylamine N-oxide (TMAO), trimethylamine (TMA) and dimethylamine (DMA) from dietary methylamines have recently gained much attention due to their high association with chronic kidney disease risk.

L-carnitine could be metabolized to trimethylamine (TMA) by gut microbiota and further converted into trimethylamine N-oxide (TMAO) in the liver, leading to liver damage. This study aimed to investigate the...

(2018) Stachyose combined with tea polyphenols mitigated metabolic disorders in high fructose diet-fed mice as studied by GC-MS metabolomics approach, CyTA -Journal of Food, 16:1,[516][517][518][519][520][521][522][523][524] To link to this article: https://doi.org/10. 1080/19476337.2017 High fructose (HF) ingestion is a common risk factor for the development of nonalcoholic fatty liver disease (NAFLD), which has become a serious health problem. The underlying mechanism of HFinduced NAFLD needs to be further understood and an effective prevention needs to be established urgently. Gas chromatography-mass spectrometer-based metabonomic method was employed to characterize the serum metabolic profile of HF-induced NAFLD in mice. β-Hydroxybutyric acid, elaidic acid and oleic acid that contributed to energy and lipid metabolism were confirmed as potential biomarkers for HF-induced NAFLD. With these changed metabolic pathways as possible drug targets, different administrations revealed that co-administration of stachyose and tea polyphenols was a more effective method than treatment of stachyose or tea polyphenols alone for preventing HF-induced negative changes of metabolic pathways in mice. These findings suggest that β-hydroxybutyric acid, elaidic acid and oleic acid are potential biomarkers in HF-induced NAFLD, and co-administration is a novel preventive strategy.Estaquiosa combinada con polifenoles de té para mitigar los trastornos metabólicos en ratones alimentados con una dieta alta en fructosa, estudio realizado mediante un enfoque metabolómico GC-MS RESUMEN La ingesta elevada de fructosa (HF) constituye un factor de riesgo común en el desarrollo de esteatohepatitis no alcohólica (NAFLD), padecimiento que se ha convertido en un problema de salud serio. El mecanismo subyacente de la NAFLD inducida por HF debe ser mejor comprendido, al tiempo que urge establecer mecanismos de prevención que resulten efectivos. En este sentido, para caracterizar el perfil metabólico del suero de ratones con NAFLD inducida por HF se utilizó el método metabolómico basado en GC-MS. Ello permitió constatar que los ácidos betahidroxibutírico, elaídico y oleico, que contribuyen al metabolismo energético y lipídico, son biomarcadores potenciales para la NAFLD inducida por el HF. A partir de la identificación de estas vías metabólicas alteradas como posibles dianas de los medicamentos, la administración diferenciada de sustancias (combinadas o por separado) reveló que, para prevenir los cambios negativos inducidos por la HF en las vías metabólicas de ratones, la coadministración de estaquiosa y polifenoles de té resultó ser un método más efectivo que el tratamiento con estaquiosa o con polifenoles de té por separado. Estos hallazgos sugieren que los ácidos betahidroxibutírico, elaídico y oleico son biomarcadores potenciales para la NAFLD inducida por HF y que la coadministración constituye una estrategia preventiva innovadora. ARTICLE HISTORY