curcumin and hydroquinone

Topics: Binding Sites; Carotenoids; Curcumin; Enzyme Inhibitors; Enzymes, Immobilized; Humans; Hydroquinones; Kinetics; Molecular Docking Simulation; Monophenol Monooxygenase; Protein Binding; Protein Interaction Domains and Motifs; Protein Structure, Secondary; Pyrogallol; Recombinant Proteins; Surface Plasmon Resonance; Tannins

NF-E2-related factor2 (Nrf2)-antioxidant response element (ARE) signaling pathway is the major defensive mechanism against oxidative stress and is up regulated by specific antioxidants and oxidants to comprise the chemoptotective response. Detection of ARE-activating compounds helps to develop new drugs and identify/quantify the tension range of the oxidants. Important reasons promoting this work are high throughput, rapid and inexpensive experiments relative to the in vitro studies for ARE-Nrf2 pathway monitoring of chemicals and environmental samples.. In this study hepatoma Huh7 reporter cell line was generated which contains a luciferase gene under the control of an ARE. This is the first example of ARE construct containing one copy of extended consensus response element. The cells were treated with hydroquinone (HQ) and p-benzoquinone (BQ) (oxidative stress inducers) and the antioxidant, curcumin.. The luciferase activity was induced in a concentration-dependent manner in a concentration range of 1-2 μM for BQ and HQ. Curcumin was also validated as an ARE inducer in concentration above 10 μM. In addition, this reporter cell line provides a rapid detection as early as 4 h to respond to the ARE inducers.. It is a powerful tool for the sensitive and selective screening of chemicals, drugs and environmental samples for their antioxidant and oxidant activities.

Topics: Antioxidant Response Elements; Antioxidants; Benzoquinones; Cell Line, Tumor; Curcumin; Genes, Reporter; Humans; Hydroquinones; Luciferases, Firefly; NF-E2-Related Factor 2; Oxidants; Oxidative Stress

Catharanthus roseus cell suspension cultures converted exogenously supplied curcumin to a series of glucosides, none of which has been found in nature so far. The efficiency of glucosylation was dependent on culture stage of the cells and medium sucrose concentration. Methyl jasmonate and salicylic acid enhanced the glucoside formation only when they were added to the cultures prior to the addition of curcumin. The glucoside yield was 2.5 micromol/g fresh weight of the cells at an optimal culture condition. The water solubility of curcumin-4',4"-O-beta-D-digentiobioside was 0.65 mmol/ml, which was 20 million-fold higher than that of curcumin.

Topics: Acetates; Catharanthus; Cells, Cultured; Culture Media, Conditioned; Curcumin; Cyclopentanes; Flavonoids; Glucosides; Glycosylation; Hydroquinones; Luteolin; Magnetic Resonance Spectroscopy; Molecular Structure; Oxylipins; Salicylic Acid; Solubility; Sucrose; Suspensions; Water

The APP gene promoter has multiple regulatory sequences, some of which may contribute to the neuropathology of Alzheimer's disease (AD). In this study, we investigated the effects of phorbol ester (PMA), IL-1, retinoic acid and reactive oxygen species on APP promoter activity in primary hippocampal neurons. We transfected neurons with either of two APP promoter constructs, a -2.8 kb and a shorter -488 bp upstream fragment fused to the chloramphenicol transferase (CAT) reporter gene. We demonstrated that phorbol 12-myristate-13 acetate (PMA), retinoic acid and IL-1 all stimulated both APP promoter constructs in hippocampal neurons after 24 h treatment. PMA and IL-1 treatments led to 2-fold increases of APP promoter activity. Retinoic acid induced a 3-fold increase. In addition, the magnitude of APP promoter responses to PMA and IL-1 treatment was similar between APP -2.8 kb and -488 bp plasmid transfected neurons. This suggests that the AP-1 sequence at -350 to -344 in the APP promoter may mediate the stimulatory effects of PMA and IL-1, as previously observed in endothelial and HeLa cells. In contrast, hydrogen peroxide, which was shown to activate NF-kappaB in primary neurons, failed to stimulate APP promoter activity, suggesting that the regulatory elements in the APP promoter may not respond to reactive oxygen species. Overall, these data indicate that APP expression in primary neurons can be modulated by PMA, IL-1 and retinoic acid. However, the contribution of reactive oxygen to Alzheimer's disease may not be directly related to the activation of the APP gene promoter but instead to neuronal damage associated with oxidative stress. Since elevated levels of IL-1 have been observed in AD brain, IL-1 could contribute to development of Alzheimer's disease by stimulating APP synthesis in primary neurons.

Topics: Amyloid beta-Protein Precursor; Animals; Antineoplastic Agents; Benzoflavones; Carcinogens; Cation Exchange Resins; Cell Survival; Cells, Cultured; Curcumin; DNA; Gene Expression Regulation; Hippocampus; Hydrogen Peroxide; Hydroquinones; Indicators and Reagents; Interleukin-1; Lipids; Mutagens; Neurons; NF-kappa B; Phorbol Esters; Promoter Regions, Genetic; Rats; Reactive Oxygen Species; Transfection; Tretinoin; Tumor Necrosis Factor-alpha