3-4-di-o-caffeoylquinic-acid and Colonic-Neoplasms

3-4-di-o-caffeoylquinic-acid has been researched along with Colonic-Neoplasms* in 2 studies

Other Studies

2 other study(ies) available for 3-4-di-o-caffeoylquinic-acid and Colonic-Neoplasms

ArticleYear
Dicaffeoylquinic acids in Yerba mate (Ilex paraguariensis St. Hilaire) inhibit NF-κB nucleus translocation in macrophages and induce apoptosis by activating caspases-8 and -3 in human colon cancer cells.
    Molecular nutrition & food research, 2011, Volume: 55, Issue:10

    The biological functions of caffeoylquinic acid (CQA) derivatives from various plant sources have been partially elucidated. The objectives were to isolate and purify diCQAs from Yerba mate tea leaves and assess their anti-inflammatory and anti-cancer capabilities in vitro and explore their mechanism of action.. Methanol extracts of dried mate leaves were resolved by flash chromatography and further purified resulting in two fractions one containing 3,4- and 3,5-diCQAs and the other 4,5-diCQA with NMR-confirmed structures. Both fractions inhibited LPS-induced RAW 264.7 macrophage inflammation by suppressing nitric oxide/inducible nitric oxide and prostaglandin E(2) /cyclooxygenase-2 pathways through inhibiting nucleus translocation of Nuclear factor κB subunits, p50 and p65. The diCQA fractions inhibited Human colon cancer cells CRL-2577 (RKO) and HT-29 cell proliferation by inducing apoptosis in a time- and concentration-dependent manner, but did not affect the protein levels of p21, p27, p53, and Bax:Bcl-2 ratio in RKO cells. In HT-29 cells, however, the diCQA fractions increased Bax:Bcl-2 ratio. The diCQA fractions increased the activation of caspase-8 leading to cleavage of caspase-3 in both RKO and HT-29 colon cancer cells.. The results suggest that diCQAs in Yerba mate could be potential anti-cancer agents and could mitigate other diseases also associated with inflammation.

    Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Antineoplastic Agents, Phytogenic; Apoptosis; bcl-2-Associated X Protein; Caspase 3; Caspase 8; Cell Nucleus; Cell Proliferation; Chlorogenic Acid; Colonic Neoplasms; Cyclooxygenase 2; Dinoprostone; Drug Evaluation, Preclinical; Enzyme Activation; HT29 Cells; Humans; Ilex paraguariensis; Lipopolysaccharides; Macrophages; Magnetic Resonance Spectroscopy; Mice; NF-kappa B; Nitric Oxide; Nitric Oxide Synthase Type II; Plant Extracts; Plant Leaves; Protein Transport; Proto-Oncogene Proteins c-bcl-2

2011
Cell cycle arrest and apoptosis induced by methyl 3,5-dicaffeoyl quinate in human colon cancer cells: Involvement of the PI3K/Akt and MAP kinase pathways.
    Chemico-biological interactions, 2011, Oct-15, Volume: 194, Issue:1

    Methyl 3,5-dicaffeoyl quinate (MDQ) is a flavonoid glucoside found in several plants that scavenges 1,1-diphenyl-2-picrylhydrazyl (DPPH) free radicals and peroxynitrite, and inhibits the formation of cholesteryl ester hydroperoxide during the copper ion-induced oxidation of blood plasma in rats. In this study, MDQ inhibited proliferation and induced apoptosis in HT-29 cells in a dose-dependent manner as detected by 1-(4,5-dimethylthiazol-2-yl)-3,5-diphenylformazan (MTT), trypan blue exclusion, and flow cytometric assays. Western blot analysis showed that apoptosis was dependent on caspase-3 activity. PARP cleavage and the cytosolic release of cytochrome c from mitochondria increased significantly. In addition, these events were accompanied by a collapse in the mitochondrial membrane potential and a decreased Bcl-2/Bax ratio. Furthermore, the MDQ-induced G(0)/G(1) arrest was correlated with an increase in p27 and a decrease in cyclin D1 and p53. MDQ also inhibited the phosphorylation of PI3K/Akt and ERK; significantly reduced NF-κB; and in general displayed a significant anti-proliferative effect via a cell cycle arrest and apoptotic induction in HT-29 cells. These results suggest that MDQ has therapeutic potential against human colon carcinoma.

    Topics: Antineoplastic Agents, Phytogenic; Apoptosis; Caspase 3; Cell Cycle; Chlorogenic Acid; Colonic Neoplasms; Cyclooxygenase 2; Cytochromes c; Dose-Response Relationship, Drug; HT29 Cells; Humans; Membrane Potential, Mitochondrial; Mitochondria; Mitogen-Activated Protein Kinases; NF-kappa B; Phosphatidylinositol 3-Kinases; Phosphorylation; Proto-Oncogene Proteins c-akt; Tumor Cells, Cultured

2011