curcumin and kaempferol

curcumin has been researched along with kaempferol* in 5 studies

Other Studies

5 other study(ies) available for curcumin and kaempferol

ArticleYear
Antidiabetic potential of polyherbal formulation DB14201: Preclinical development, safety and efficacy studies.
    Journal of ethnopharmacology, 2017, Feb-02, Volume: 197

    The poly-herbal formulation DB14201 is a new combination of ayurvedic ingredients for treatment of diabetes. The aim of present study was to investigate safety and in vivo efficacy of DB14201 extract. Further this work was aimed to develop, characterize and standardize DB14201 extract and develop it as a botanical drug.. The polyherbal extract was standardized using four chemical markers. The LC-MS/MS method was developed for identification and quantification of mangiferin, berberine, kaempferol and curcumin. The extract was standardized for heavy metal content, aflotoxins, and microbial tests. The mechanism of action of DB14201 extract was explored through glucose uptake by adipocytes, TNF-α production and free fatty acid release, in vitro, was studied using murine adipocytes (3T3-L1). The effect of extract on insulin release was evaluated using murine pancreatic beta cell (β TC-6). The safety and in vivo efficacy of extract was studied using suitable animal model. Hematology and blood biochemistry parameters were also assessed.. In vitro studies of DB14201 in murine adipocytes and murine pancreatic beta cells demonstrated the plausible mechanism of action of DB14201 could be through increase in glucose uptake and by stimulation of insulin release by RIN-5f cells. The microbial load, heavy metals were found to be within the AYUSH permissible limits and aflotoxins were absent. Preclinical efficacy studies in animal models proved the anti-diabetic potential of the extract. The preclinical acute dose toxicity study and 90-days repeated dose toxicity study of DB14201 extract in wistar rats by oral route indicated that the extract is safe up to 1000mg/kg dose. Hematology and blood biochemistry parameters were within the normal range.. The data presented herein demonstrated anti-diabetic potential of developed DB14201 extract and this study will serve as the benchmark for the further research on this polyherbal formulation.

    Topics: 3T3-L1 Cells; Adipocytes; Animals; Berberine; Blood Glucose; Chromatography, Liquid; Curcumin; Diabetes Mellitus, Experimental; Glucose; Hypoglycemic Agents; Insulin; Insulin-Secreting Cells; Kaempferols; Male; Metals, Heavy; Mice; Mice, Inbred C57BL; Plant Extracts; Rats; Rats, Wistar; Tandem Mass Spectrometry; Tumor Necrosis Factor-alpha; Xanthones

2017
Curcumin and kaempferol prevent lysozyme fibril formation by modulating aggregation kinetic parameters.
    Biochimica et biophysica acta, 2014, Volume: 1844, Issue:3

    Interaction of small molecule inhibitors with protein aggregates has been studied extensively, but how these inhibitors modulate aggregation kinetic parameters is little understood. In this work, we investigated the ability of two potential aggregation inhibiting drugs, curcumin and kaempferol, to control the kinetic parameters of aggregation reaction. Using thioflavin T fluorescence and static light scattering, the kinetic parameters such as amplitude, elongation rate constant and lag time of guanidine hydrochloride-induced aggregation reactions of hen egg white lysozyme were studied. We observed a contrasting effect of inhibitors on the kinetic parameters when aggregation reactions were measured by these two probes. The interactions of these inhibitors with hen egg white lysozyme were investigated using fluorescence quench titration method and molecular dynamics simulations coupled with binding free energy calculations. We conclude that both the inhibitors prolong nucleation of amyloid aggregation through binding to region of the protein which is known to form the core of the protein fibril, but once the nucleus is formed the rate of elongation is not affected by the inhibitors. This work would provide insight into the mechanism of aggregation inhibition by these potential drug molecules.

    Topics: Circular Dichroism; Curcumin; Fluorescence; Guanidine; Kaempferols; Kinetics; Microscopy, Electron, Scanning; Molecular Dynamics Simulation; Muramidase; Spectrophotometry, Ultraviolet

2014
The inhibition of human glutathione S-transferases activity by plant polyphenolic compounds ellagic acid and curcumin.
    Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association, 2007, Volume: 45, Issue:2

    Glutathione S-transferases (GSTs) are multifunctional detoxification proteins that protect the cell from electrophilic compounds. Overexpression of GSTs in cancer results in resistance to chemotherapeutic agents and inhibition of the over expressed GST has been suggested as an approach to combat GST-induced resistance. The inhibition of human recombinant GSTs by natural plant products was investigated in this study. Using 1-chloro-2,4 dinitrobenzene (CDNB) as a substrate, ellagic acid and curcumin were shown to inhibit GSTs A1-1, A2-2, M1-1, M2-2 and P1-1 with IC(50) values ranging from 0.04 to 5 microM whilst genistein, kaempferol and quercetin inhibited GSTs M1-1 and M2-2 only. The predominant mode of inhibition with respect to the G and H-sites were mixed inhibition and uncompetitive to a lesser extent. The K(i) (K(i)(')) values for ellagic acid and curcumin with respect to GSH and CDNB were in the range 0.04-6 microM showing the inhibitory potency of these polyphenolic compounds. Ellagic acid and curcumin also showed time- and concentration-dependent inactivation of GSTs M1-1, M2-2 and P1-1 with curcumin being a more potent inactivator than ellagic acid. These results facilitate the understanding of the interaction of human GSTs with plant polyphenolic compounds with regards to their role as chemomodulators in cases of GST-overexpression in malignancies.

    Topics: Curcumin; Dinitrochlorobenzene; Dose-Response Relationship, Drug; Drug Resistance, Multiple; Ellagic Acid; Enzyme Inhibitors; Flavonoids; Genistein; Glutathione Transferase; Humans; Inhibitory Concentration 50; Kaempferols; Kinetics; Phenols; Phytotherapy; Polyphenols; Quercetin; Substrate Specificity

2007
Dietary compounds inhibit proliferation and contraction of keloid and hypertrophic scar-derived fibroblasts in vitro: therapeutic implication for excessive scarring.
    The Journal of trauma, 2003, Volume: 54, Issue:6

    Keloid and hypertrophic scars commonly occur after injuries. Overproliferation of fibroblasts, overproduction of collagen, and contraction characterize these pathologic scars. Current treatment of excessive scars with intralesional corticosteroid injections used individually or in combination with other methods often have unsatisfactory outcome, frustrating both the patient and the clinician. The phytochemical compounds are well known as potential anticancer agents. We have investigated the inhibitory effects of compounds on keloid fibroblasts (KF) and hypertrophic scar-derived fibroblasts (HSF).. Fibroblasts were cultured from nontreated earlobe keloids and burn hypertrophic scars. Ten compounds (three hydroxybenzoic and four hydroxycinnamic acid derivatives, two flavonols [quercetin and kaempferol], and turmeric curcumin) were tested with fibroblasts. The inhibitory effects of compounds on fibroblasts was assessed by proliferation assays, fibroblast-populated collagen lattice (FPCL) contraction, and electron microscopy.. The phytochemicals significantly inhibited KF and HSF proliferation in a dose- and time-dependent manner. In the hydroxybenzoic and flavonol groups, increasing inhibitory effects seemed to depend on increasing numbers of hydroxyl groups in their chemical structures. This phenomenon was not observed in the hydroxycinnamic acid group. The phytochemicals inhibited fibroblast proliferation by inducing cell growth arrest but not apoptosis. The reversibility of growth inhibition occurred when the compounds were removed from the culture and fresh media was replaced. Slower reversibility of growth inhibition was observed in the groups treated with quercetin, chlorogenic acid, or curcumin. The compounds quercetin, gallic acid, protocatechuic acid, and chlorogenic acid were the strongest inhibitors of FPLC contraction by HTFs. When the compounds were washed out of the lattices and replaced by fresh medium, the FPCL contraction was resumed. The resumption of FPCL contraction was slowest in the quercetin-treated group, indicating again the strong inhibitory effect of quercetin.. From this in vitro study, quercetin seemed to have good potent effects to inhibit proliferation and contraction of excessive scar-derived fibroblasts.

    Topics: Adolescent; Biological Assay; Burns; Cell Division; Cells, Cultured; Cicatrix, Hypertrophic; Collagen; Coumaric Acids; Curcumin; Ear; Enzyme Inhibitors; Female; Fibroblasts; Flavonoids; Flavonols; Humans; Hydroxybenzoates; Kaempferols; Keloid; Quercetin

2003
Modulation of aflatoxin B1 activated protein kinase C by phenolic compounds.
    Cancer letters, 1997, Dec-16, Volume: 121, Issue:1

    Several natural phenolic compounds were tested in vitro for their effect on the activity of protein kinase C isolated from liver cytosol, particulate and nuclear fractions of normal and aflatoxin B1 treated rats. Quercetin and kaempferol inhibited the enzyme activity of all these fractions at very low dose levels. These phenolics were particularly effective in inhibiting the elevated enzyme activity following aflatoxin B1 administration. Ellagic acid and curcumin were found to be inhibitory only towards particulate enzymes obtained after carcinogen treatment, while curcumin and rutin were moderately active against nuclear enzymes. Constitutive activation of protein kinase C can drive the cell to a proliferative state, thereby initiating the process of carcinogenesis, however, suppression of this activation by phenolic compounds may be an effective way to control carcinogenesis.

    Topics: Aflatoxin B1; Animals; Cell Nucleus; Curcumin; Cytosol; Dose-Response Relationship, Drug; Ellagic Acid; Enzyme Activation; Flavonoids; Kaempferols; Male; Phenols; Protein Kinase C; Quercetin; Rats; Rats, Wistar

1997