rutin and taxifolin

rutin has been researched along with taxifolin* in 3 studies

Other Studies

3 other study(ies) available for rutin and taxifolin

ArticleYear
Adenosine/guanosine preferring nucleoside ribohydrolase is a distinct, druggable antitrichomonal target.
    Bioorganic & medicinal chemistry letters, 2015, Nov-15, Volume: 25, Issue:22

    Nucleoside salvage pathway enzymes used by Trichomonas vaginalis are distinct from the pathway involved in activation of existing 5-nitroimidazole drugs. They thus represent excellent targets for developing novel, mechanism-based antitrichomonal agents. The purine-specific adenosine/guanosine preferring ribohydrolase (AGNH) was screened against the NIH Clinical Collection to assess its druggability. Eight compounds, including five flavonoids, were identified with IC50 values ⩽10 μM and confirmed in counter screens run in the presence of detergent. The inhibitors are structurally distinct from inhibitors of the pyrimidine-specific uridine ribohydrolase (UNH) thus indicating that AGNH is a distinct, druggable target from UNH.

    Topics: Adenosine; Antitrichomonal Agents; Flavonoids; High-Throughput Screening Assays; N-Glycosyl Hydrolases; Quercetin; Small Molecule Libraries; Stereoisomerism; Trichomonas vaginalis

2015
Quercetin, quercetin glycosides and taxifolin differ in their ability to induce AhR activation and CYP1A1 expression in HepG2 cells.
    Phytotherapy research : PTR, 2012, Volume: 26, Issue:11

    The natural flavonoid quercetin is a low affinity ligand of the aryl hydrocarbon receptor (AhR), a transcription factor regulating the expression of cytochrome P450 (CYP) 1A enzymes. This study examined the ability of quercetin, isoquercitrin (quercetin-3-O-glucoside), rutin (quercetin-3-O-rutinoside) and taxifolin (dihydroquercetin) to activate AhR and to induce CYP1A1 expression in human hepatoma HepG2 cells. Gene reporter assays showed that quercetin significantly activated AhR and triggered CYP1A1 transcription after 24 h exposure. These effects were, however, much lower than those of 2,3,7,8-tetrachlorodibenzo-p-dioxin, a prototypical AhR ligand. Quercetin also induced a significant increase in CYP1A1 mRNA levels together with a moderate increase in the level of CYP1A1 activity. In contrast, isoquercitrin and rutin had negligible effects on AhR activity and CYP1A1 expression. Taxifolin at the highest concentration tested (50 µm) produced a mild non-significant increase in AhR activity and CYP1A1 transcription. Taxifolin also significantly increased CYP1A1 mRNA expression, but this effect was approximately 15 times weaker than that of quercetin and was not accompanied by induction of CYP1A1 activity. It is concluded that quercetin, but not its 3-O-glycosides isoquercitrin and rutin, induces AhR activation and CYP1A1 expression in HepG2 cells and that the CYP1A1-inducing activity of taxifolin has a low toxicological potential.

    Topics: Cytochrome P-450 CYP1A1; Glucosides; Hep G2 Cells; Humans; Quercetin; Receptors, Aryl Hydrocarbon; Rutin

2012
Monohydroxyethylrutoside, a dose-dependent cardioprotective agent, does not affect the antitumor activity of doxorubicin.
    Clinical cancer research : an official journal of the American Association for Cancer Research, 1997, Volume: 3, Issue:10

    The cumulative dose-related cardiotoxicity of doxorubicin is believed to be caused by the production of oxygen- free radicals. 7-Monohydroxyethylrutoside (monoHER), a semisynthetic flavonoid and powerful antioxidant, was investigated with respect to the prevention of doxorubicin-induced cardiotoxicity in mice and to its influence on the antitumor activity of doxorubicin in vitro and in vivo. Non-tumor-bearing mice were equipped with a telemeter in the peritoneal cavity. They were given six weekly doses of 4 mg/kg doxorubicin i.v., alone or in combination with either 100 or 250 mg/kg monoHER i.p., 1 h prior to doxorubicin administration and for the following 4 days. Cardiotoxic effects were measured from electrocardiogram changes up to 2 weeks after treatment. Protection against cardiotoxicity was found to be dose dependent, with 53 and 75% protection, respectively, as calculated from the reduction in the increase in the ST interval. MonoHER and several other flavonoids with good antioxidant properties were tested for their antiproliferative effects in the absence or the presence of doxorubicin in A2780 and OVCAR-3 human ovarian cancer cells and MCF-7 human breast cancer cells in vitro. Some flavonoids were directly toxic at 50 and 100 microM, whereas others, including monoHER, did not influence the antiproliferative effects of doxorubicin at these concentrations. The influence of monoHER was further tested on the growth-inhibitory effect of 8 mg/kg doxorubicin i.v., given twice with an interval of 1 week in A2780 and OVCAR-3 cells that were grown as s.c. xenografts in nude mice. MonoHER, administered 1 h before doxorubicin in a dose schedule of 500 mg/kg i.p. 2 or 5 days per week, was not toxic and did not decrease the antitumor activity of doxorubicin. It can be concluded that monoHER showed a dose-dependent protection against chronic cardiotoxicity and did not influence the antitumor activity of doxorubicin in vitro or in vivo.

    Topics: Animals; Antibiotics, Antineoplastic; Antioxidants; Breast Neoplasms; Cardiomyopathies; Catechin; Chelation Therapy; Cystadenocarcinoma, Serous; Dose-Response Relationship, Drug; Doxorubicin; Drug Interactions; Electrocardiography; Female; Flavonoids; Flavonols; Free Radical Scavengers; Free Radicals; Humans; Hydroxyethylrutoside; Iron; Iron Chelating Agents; Kaempferols; Mice; Mice, Nude; Molecular Structure; Neoplasm Transplantation; Ovarian Neoplasms; Quercetin; Razoxane; Rutin; Telemetry; Tumor Cells, Cultured; Weight Loss

1997