curcumin and catechol

curcumin has been researched along with catechol* in 4 studies

Other Studies

4 other study(ies) available for curcumin and catechol

ArticleYear
Quality by Design-Based Crystallization of Curcumin Using Liquid Antisolvent Precipitation: Micromeritic, Biopharmaceutical, and Stability Aspects.
    Assay and drug development technologies, 2020, Volume: 18, Issue:1

    Topics: Biological Availability; Catechols; Crystallization; Curcumin; Particle Size; Polyethylene Glycols; Solubility; Surface Properties; Temperature

2020
Design, synthesis, and evaluation of curcumin derivatives as Nrf2 activators and cytoprotectors against oxidative death.
    European journal of medicinal chemistry, 2017, Jul-07, Volume: 134

    Activation of nuclear factor erythroid-2-related factor 2 (Nrf2) has been proven to be an effective means to prevent the development of cancer, and natural curcumin stands out as a potent Nrf2 activator and cancer chemopreventive agent. In this study, we synthesized a series of curcumin analogs by introducing the geminal dimethyl substituents on the active methylene group to find more potent Nrf2 activators and cytoprotectors against oxidative death. The geminally dimethylated and catechol-type curcumin analog (compound 3) was identified as a promising lead molecule in terms of its increased stability and cytoprotective activity against the tert-butyl hydroperoxide (t-BHP)-induced death of HepG2 cells. Mechanism studies indicate that its cytoprotective effects are mediated by activating the Nrf2 signaling pathway in the Michael acceptor- and catechol-dependent manners. Additionally, we verified by using copper and iron ion chelators that the two metal ion-mediated oxidations of compound 3 to its corresponding electrophilic o-quinone, contribute significantly to its Nrf2-dependent cytoprotection. This work provides an example of successfully designing natural curcumin-directed Nrf2 activators by a stability-increasing and proelectrophilic strategy.

    Topics: Antioxidants; Catechols; Cell Death; Curcumin; Cytoprotection; Hep G2 Cells; Humans; NF-E2-Related Factor 2; Oxidative Stress; Signal Transduction

2017
Selected dietary (poly)phenols inhibit periodontal pathogen growth and biofilm formation.
    Food & function, 2015, Volume: 6, Issue:3

    Periodontitis (PD) is a chronic infectious disease mediated by bacteria in the oral cavity. (Poly)phenols (PPs), ubiquitous in plant foods, possess antimicrobial activities and may be useful in the prevention and management of periodontitis. The objective of this study was to test the antibacterial effects of selected PPs on periodontal pathogens, on both planktonic and biofilm modes of growth. Selected PPs (n = 48) were screened against Streptococcus mitis (S. mitis), Aggregatibacter actinomycetemcomitans (A. actinomycetemcomitans), Fusobacterium nucleatum (F. nucleatum) and Porphyromonas gingivalis (P. gingivalis). The antibacterial potential of each compound was evaluated in terms of planktonic minimum inhibitory concentration (PMIC) and planktonic minimum bactericidal concentration (PMBC) using standardized broth microdilution assays. The most active PPs were further tested for their effect on mono-species and multi-species biofilms using a colorimetric resazurin-based viability assay and scanning electron microscopy. Of the 48 PPs tested, 43 showed effective inhibition of planktonic growth of one or more test strains, of which curcumin was the most potent (PMIC range = 7.8-62.5 μg mL(-1)), followed by pyrogallol (PMIC range = 2.4-2500 μg mL(-1)), pyrocatechol (MIC range = 4.9-312.5 μg mL(-1)) and quercetin (PMIC range = 31.2-500 μg mL(-1)). At this concentration, adhesion of curcumin and quercetin to the substrate also inhibited adhesion of S. mitis, and biofilm formation and maturation. While both curcumin and quercetin were able to alter architecture of mature multi-species biofilms, only curcumin-treated biofilms displayed a significantly reduced metabolic activity. Overall, PPs possess antibacterial activities against periodontopathic bacteria in both planktonic and biofilm modes of growth. Further cellular and in vivo studies are necessary to confirm their beneficial activities and potential use in the prevention and or treatment of periodontal diseases.

    Topics: Adsorption; Aggregatibacter actinomycetemcomitans; Anti-Bacterial Agents; Bacterial Adhesion; Biofilms; Catechols; Curcumin; Durapatite; Fusobacterium nucleatum; Humans; Microbial Sensitivity Tests; Microbial Viability; Mouthwashes; Periodontitis; Polyphenols; Porphyromonas gingivalis; Pyrogallol; Quercetin; Streptococcus mitis; Structure-Activity Relationship

2015
Cytotoxic effects of catechol to neuroblastoma N2a cells.
    General physiology and biophysics, 2008, Volume: 27, Issue:4

    The mechanisms of catechol-induced cytotoxicity were studied in cultures of neuroblastoma N2a cells. The minimal cytotoxic concentration after 72 h was 20 micromol x l(-1). The EC50 after 72 h was 38 micromol x l(-1). There was not a correlation between the cytotoxicity and the formation of quinones in the medium. Catechol-induced cytotoxicity was increased significantly when superoxide dismutase (SOD) was added. The addition of catalase did not protect cells, but this enzyme reverted the deleterious effect of SOD. The experimental studies showed a detrimental effect of deferoxamine on catechol-induced cytotoxicity suggesting that cells need iron to maintain its metabolism. NF-kappaB inhibitors increased the cytotoxicity, suggesting that this factor is also important for cell viability. L-cysteine and N-acetyl-L-cysteine protected cells significantly in a dose-dependent manner. The use of monochlorobimane showed that catechol induced reduced glutathione (GSH) depletion after 24 h, prior to cell death. The mode of cell death was studied by flow cytometry after double staining with annexin V and propidium iodide. Catechol induced apoptosis after 72 h. Furthermore, catechol also induced nuclear fragmentation. These data showed that catechol-induced cytotoxicity to N2a cell was not directly a consequence of reactive oxygen species production. Rather, it was due to GSH depletion followed by the induction of apoptosis.

    Topics: Animals; Antioxidants; Apoptosis; Ascorbic Acid; Catechols; Cell Line, Tumor; Cell Survival; Curcumin; Cysteine; Cytotoxins; Deferoxamine; Glutathione; Mice; Neuroblastoma; NF-kappa B; Reactive Oxygen Species; Sesquiterpenes; Superoxide Dismutase

2008