artepillin-c and Colonic-Neoplasms

artepillin-c has been researched along with Colonic-Neoplasms* in 2 studies

Other Studies

2 other study(ies) available for artepillin-c and Colonic-Neoplasms

ArticleYear
Dietary artepillin C suppresses the formation of aberrant crypt foci induced by azoxymethane in mouse colon.
    Cancer letters, 2006, Aug-18, Volume: 240, Issue:1

    Artepillin C, a prenylated phenylpropanoid found specifically in Brazilian propolis, has been shown to be a bioavailable antioxidant. In this study, artepillin C was tested for colon cancer-preventing activity using azoxymethane-challenged ddY mice. Oral doses of 80 and 160 mg/kg body weight of propolis or 10mg/kg of artepillin C (equi-amounts to 160 mg propolis) reduced significantly the frequency of colonic aberrant crypt foci (ACF) by 39.2, 43.7 and 43.4%, respectively. In liver of the mice, glutathione S-transferase and NADPH:quinone reductase activity increased with the doses of propolis or artepillin C, and an antioxidant-responsive element (ARE) was found to be activated for binding DNA. Artepillin C is considered to suppress the formation of colonic ACF through the activation of ARE and induction of phase II enzymes in liver.

    Topics: Animals; Antineoplastic Agents; Antioxidants; Azoxymethane; Carcinogens; Colonic Neoplasms; Diet; Dose-Response Relationship, Drug; Glutathione Transferase; Intestinal Mucosa; Liver; Male; Mice; NAD(P)H Dehydrogenase (Quinone); Phenylpropionates; Precancerous Conditions; Propolis; Response Elements; Up-Regulation

2006
Artepillin C in Brazilian propolis induces G(0)/G(1) arrest via stimulation of Cip1/p21 expression in human colon cancer cells.
    Molecular carcinogenesis, 2005, Volume: 44, Issue:4

    Potential chemopreventive agents exist in foods. Artepillin C in Brazilian propolis was investigated for its effects on colon carcinogenesis. We had found that artepillin C was a bioavailable antioxidant, which could be incorporated into intestinal Caco-2 and hepatic HepG2 cells without any conjugation and inhibited the oxidation of intracellular DNA. Artepillin C was then added to human colon cancer WiDr cells. It dose-dependently inhibited cell growth, inducing G(0)/G(1) arrest. The events involved a decrease in the kinase activity of a complex of cyclin D/cyclin-dependent kinase 4 and in the levels of retinoblastoma protein phosphorylated at Ser 780 and 807/811. The inhibitors of the complex, Cip1/p21 and Kip1/p27, increased at the protein level. On the other hand, Northern blotting showed that artepillin C did not affect the expression of Kip1/p27 mRNA. According to the experiments using isogenic human colorectal carcinoma cell lines, artepillin C failed to induce G(0)/G(1) arrest in the Cip1/p21-deleted HCT116 cells, but not in the wild-type HCT116 cells. Artepillin C appears to prevent colon cancer through the induction of cell-cycle arrest by stimulating the expression of Cip1/p21 and to be a useful chemopreventing factor in colon carcinogenesis.

    Topics: Blotting, Northern; Cell Proliferation; Colonic Neoplasms; Cyclin D; Cyclin-Dependent Kinase 4; Cyclin-Dependent Kinase Inhibitor p21; Cyclin-Dependent Kinase Inhibitor p27; Cyclins; Flow Cytometry; G1 Phase; HCT116 Cells; Humans; Immunoprecipitation; Nucleic Acid Synthesis Inhibitors; Phenylpropionates; Phosphorylation; Propolis; Resting Phase, Cell Cycle; Retinoblastoma Protein; RNA, Messenger

2005