Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 10 de 10
Filter
Add more filters










Publication year range
1.
Nat Prod Res ; 26(3): 203-8, 2012.
Article in English | MEDLINE | ID: mdl-21815723

ABSTRACT

A new flavone glucoside, apigenin 4'-(6″-methylglucuronide) (1), together with six known compounds, cirsilineol, jaceosidin, melitensin, apigenin, apigenin 7-(6″-methylglucuronide) and prunasin, were isolated from the ethanolic extract of the aerial parts of Centaurea nicaeensis All. var. walliana M. (Asteraceae) collected from Souk-Ahras, eastern Algeria. The structures were established by spectral analysis, mainly HRESI-MS, UV and 2D-NMR experiments (COSY, HSQC and HMBC).


Subject(s)
Centaurea/chemistry , Flavonoids/isolation & purification , Flavonoids/chemistry , Magnetic Resonance Spectroscopy , Spectrometry, Mass, Electrospray Ionization , Spectrophotometry, Ultraviolet
2.
Mol Nutr Food Res ; 54 Suppl 2: S171-83, 2010 Jul.
Article in English | MEDLINE | ID: mdl-20440695

ABSTRACT

Phenolic extracts from red wine (RWPs) have been shown to induce nitric oxide (NO)-mediated vasoprotective effects, mainly by causing the PI3-kinase/Akt-dependent activation of endothelial NO synthase (eNOS). RWPs contain several hundreds of phenolic compounds. The aim of the present study was to identify red wine phenolic compounds capable of activating eNOS in endothelial cells using multi-step fractionation. The red wine phenolic extract was fractionated using Sephadex LH-20 and preparative RP-HPLC approaches. The ability of a fraction to activate eNOS was assessed by determining the phosphorylation level of Akt and eNOS by Western blot analysis, and NO formation by electron spin resonance spectroscopy. Tentative identification of phenolic compounds in fractions was performed by MALDI-TOF and HPLC-MS techniques. Separation of RWPs by Sephadex LH-20 generated nine fractions (fractions A to I), of which fractions F, G, H and I caused significant eNOS activation. Fraction F was then subjected to semi-preparative RP-HPLC to generate ten subfractions (subfraction SF1 to SF10), all of which caused eNOS activation. The active fractions and subfractions contained mainly procyanidins and anthocyanins. Isolation of phenolic compounds from SF9 by semi-preparative RP-HLPC lead to the identification of petunidin-O-coumaroyl-glucoside as a potent activator of eNOS.


Subject(s)
Endothelium, Vascular/drug effects , Flavonoids/pharmacology , Nitric Oxide Synthase Type III/metabolism , Phenols/pharmacology , Wine/analysis , Animals , Anthocyanins/chemistry , Anthocyanins/isolation & purification , Anthocyanins/pharmacology , Cells, Cultured , Chemical Fractionation , Chromatography, High Pressure Liquid , Coronary Vessels/cytology , Coronary Vessels/drug effects , Coronary Vessels/metabolism , Electron Spin Resonance Spectroscopy , Endothelium, Vascular/metabolism , Enzyme Activation/drug effects , Flavonoids/chemistry , Flavonoids/isolation & purification , Glucosides/chemistry , Glucosides/isolation & purification , Glucosides/pharmacology , Molecular Structure , Nitric Oxide/analysis , Phenols/chemistry , Phenols/isolation & purification , Phosphorylation/drug effects , Polyphenols , Proanthocyanidins/chemistry , Proanthocyanidins/isolation & purification , Proanthocyanidins/pharmacology , Proto-Oncogene Proteins c-akt/metabolism , Spectrometry, Mass, Electrospray Ionization , Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization , Sus scrofa
3.
Biochem Biophys Res Commun ; 393(1): 162-7, 2010 Feb 26.
Article in English | MEDLINE | ID: mdl-20117080

ABSTRACT

Several rich sources of polyphenols stimulate the endothelial formation of nitric oxide (NO), a potent vasoprotecting factor, via the redox-sensitive activation of the PI3-kinase/Akt pathway leading to the phosphorylation of endothelial NO synthase (eNOS). The present study examined the molecular mechanism underlying the stimulatory effect of epicatechins on eNOS. NO-mediated relaxation was assessed using porcine coronary artery rings in the presence of indomethacin, and charybdotoxin plus apamin, inhibitors of cyclooxygenases and EDHF-mediated responses, respectively. The phosphorylation level of Akt and eNOS was assessed in cultured coronary artery endothelial cells by Western blot, and ROS formation using dihydroethidine. (-)-Epigallocatechin-3-O-gallate (EGCg) caused endothelium-dependent relaxations in coronary artery rings and the phosphorylation of Akt and eNOS in endothelial cells. These responses were inhibited by membrane-permeant analogues of superoxide dismutase and catalase, whereas native superoxide dismutase, catalase and inhibitors of major enzymatic sources of reactive oxygen species including NADPH oxidase, xanthine oxidase, cytochrome P450 and the mitochondrial respiration chain were without effect. The EGCg derivative with all hydroxyl functions methylated induced neither relaxations nor the intracellular formation of ROS, whereas both responses were observed when the hydroxyl functions on the gallate moiety were present. In conclusion, EGCg causes endothelium-dependent NO-mediated relaxations of coronary artery rings through the Akt-dependent activation of eNOS in endothelial cells. This response is initiated by the intracellular formation of superoxide anions and hydrogen peroxide, and is critically dependent on the gallate moiety and on the presence of hydroxyl functions possibly through intracellular auto-oxidation.


Subject(s)
Catechin/analogs & derivatives , Coronary Vessels/drug effects , Endothelium, Vascular/drug effects , Nitric Oxide Synthase Type III/biosynthesis , Vasodilation , Animals , Catechin/chemistry , Catechin/pharmacology , Coronary Vessels/enzymology , Coronary Vessels/physiology , Endothelium, Vascular/enzymology , Endothelium, Vascular/physiology , Enzyme Activation , Hydrogen Peroxide/metabolism , Oxidation-Reduction , Reactive Oxygen Species/metabolism , Superoxides/metabolism , Swine
4.
Z Naturforsch C J Biosci ; 64(3-4): 210-4, 2009.
Article in English | MEDLINE | ID: mdl-19526714

ABSTRACT

A phytochemical study of the stem bark of Vismia laurentii resulted in the isolation of a tetracyclic triterpene, tirucalla-7,24-dien-3-one (1), and seven other known compounds: 3-geranyloxyemodin (2), vismiaquinone A (3), vismiaquinone B (4), bivismiaquinone (5), epifriedelinol (6), betulinic acid (7) and stigmasta-7,22-dien-3-ol (8). The structure of all these compounds was elucidated by spectroscopic means. The stem bark extract and compounds 1 and 3 showed good antimalarial activity against the W2 strain of Plasmodium falciparum.


Subject(s)
Antimalarials/isolation & purification , Clusiaceae/chemistry , Plant Stems/chemistry , Anthracenes/chemistry , Anthracenes/isolation & purification , Anthracenes/toxicity , Antimalarials/chemistry , Antimalarials/toxicity , Cameroon , Erythrocytes/drug effects , Erythrocytes/physiology , Humans
5.
Apoptosis ; 13(10): 1232-42, 2008 Oct.
Article in English | MEDLINE | ID: mdl-18726190

ABSTRACT

Our study aimed to compare death signalling pathways triggered by lupulone in TRAIL-sensitive human colon cancer cells (SW480) and in their derived TRAIL-resistant metastatic cells (SW620). Lupulone (40 microg/ml) up-regulated expression of TRAIL DR4/DR5 death receptors at the cell surface of both cell lines, even in the absence of exogenous TRAIL ligand. Cell death induced by lupulone was inhibited in SW480 and SW620 cells exposed to blocking anti-DR4/DR5 antibodies. In SW480 cells, lupulone triggered cell death through a cross-talk between TRAIL-DR4/DR5 and the mitochondrial (intrinsic) pathways involving caspase-8 activation and Bid protein cleavage. As a consequence mitochondrial cytochrome c was released into the cytosol and activation of caspases-9 and -3 was observed. In the metastatic SW620 cells, lupulone restored the sensibility of these cells to TRAIL ligand and activated the extrinsic apoptotic pathway via DR4/DR5 death receptors and the involvement of the caspase-8/caspase-3 cascade. The demonstration that lupulone is able to activate TRAIL-death signalling pathways even in TRAIL resistant cancer cells highlights the potential of this natural compound for cancer prevention and therapy.


Subject(s)
Apoptosis/drug effects , Colonic Neoplasms/pathology , Receptors, TNF-Related Apoptosis-Inducing Ligand/metabolism , Terpenes/pharmacology , Antibodies, Blocking/pharmacology , BH3 Interacting Domain Death Agonist Protein/metabolism , Caspase Inhibitors , Caspases/metabolism , Cell Line, Tumor , Colonic Neoplasms/enzymology , Cytochromes c/metabolism , Drug Screening Assays, Antitumor , Drug Synergism , Enzyme Inhibitors/pharmacology , Humans , Mitochondrial Membranes/drug effects , Mitochondrial Membranes/metabolism , Models, Biological , Neoplasm Metastasis , Oxidative Stress/drug effects , Permeability/drug effects , Reactive Oxygen Species/metabolism , TNF-Related Apoptosis-Inducing Ligand/pharmacology
6.
Phytochemistry ; 69(4): 1024-8, 2008 Feb.
Article in English | MEDLINE | ID: mdl-18067931

ABSTRACT

Phytochemical study of the fruits of Vismia laurentii resulted in the isolation of five structurally related compounds. Three of them are constituents, namely, laurentiquinone A (1) (methyl 1,6,8-trihydroxy-3-methyl-7-(3-methylbut-2-enyl)-9,10-dioxo-9,10-dihydroanthracene-2-carboxylate), laurentiquinone B (2) (methyl 5,7-dihydroxy-2,2,9-trimethyl-6,11-dioxo-6,11-dihydro-2H-anthra[2,3-b]pyran-8-carboxylate) and laurentiquinone C (3) (methyl 9-(ethanoyloxymethyl)-5,7-dihydroxy-2,2-dimethyl-6,11-dioxo-6,11-dihydro-2H-anthra[2,3-b]pyran-8-carboxylate) and two are known compounds, emodin (4) and isoxanthorin (5). Their structures were elucidated by spectroscopic means. Crude extracts of hexane and EtOAc showed anti-plasmodial activity against the W2 strain of Plasmodium falciparum.


Subject(s)
Anthraquinones/chemistry , Clusiaceae/chemistry , Fruit/chemistry , Anthraquinones/isolation & purification , Magnetic Resonance Spectroscopy , Molecular Structure
7.
Z Naturforsch C J Biosci ; 63(11-12): 801-7, 2008.
Article in English | MEDLINE | ID: mdl-19227826

ABSTRACT

Bioguided fractionation of a leaves extract from Limoniastrum feei (Girard) Batt. (Plumbaginaceae) led to the isolation of seven polyphenolic constituents: gallic acid (1), myrciaphenone A (2), myricetin-3-O-beta-galactopyranoside (3-1), epigallocatechin gallate (3-2), myricetin 3-O-alpha-rhamnopyranoside (4), quercetin (5) and myricetin (6). Gallic acid was the most antioxidant compound in DPPH [(0.94 +/- 0.68) microg/mL] and FRAP [(0.83 +/- 0.15) microM Fe2+/mL] tests, whereas myricetin was a more specific superoxide radical scavenger since it was the most active product in the superoxide nitroblue tetrazolium hypoxanthine/xanthine oxidase test [(1.86 +/- 0.12) microg/mL].


Subject(s)
Antioxidants/isolation & purification , Flavonoids/isolation & purification , Phenols/isolation & purification , Plant Leaves/chemistry , Plumbaginaceae/chemistry , Algeria , Antioxidants/pharmacology , Catechin/analogs & derivatives , Catechin/isolation & purification , Catechin/pharmacology , Flavonoids/pharmacology , Free Radical Scavengers/isolation & purification , Free Radical Scavengers/pharmacology , Gallic Acid/isolation & purification , Gallic Acid/pharmacology , Magnetic Resonance Spectroscopy , Mass Spectrometry , Phenols/pharmacology , Polyphenols
8.
Planta Med ; 73(12): 1284-6, 2007 Oct.
Article in English | MEDLINE | ID: mdl-17893835

ABSTRACT

A phytochemical study of an ethyl acetate extract of Decussocarpus rospigliosii leaves led to the isolation of six 3'-8''-biapigenin derivatives identified as amentoflavone (1), podocarpusflavone A (2), sequoiaflavone (3), podocarpusflavone B (4), 7,7''-di-O-methylamentoflavone (5) and heveaflavone (6). Biflavones 1-4 showed strong inhibitory activity on several PDE isoforms. Biflavone (5) showed selective and potent inhibition of the PDE4 isoform (IC50=1.48+/-0.21 microM) and was almost as active as the reference drug Rolipram (IC50=1.1+/-0.2 microM).


Subject(s)
Biflavonoids/pharmacology , Phosphodiesterase Inhibitors/pharmacology , Tracheophyta/chemistry , Animals , Biflavonoids/isolation & purification , Cattle , Humans , Phosphodiesterase Inhibitors/isolation & purification , Plant Leaves/chemistry , Substrate Specificity
9.
Carcinogenesis ; 28(7): 1575-81, 2007 Jul.
Article in English | MEDLINE | ID: mdl-17434926

ABSTRACT

The bitter acids of hops (Humulus lupulus L.) mainly consist of humulones or alpha-acids and lupulones or beta-acids. We aimed to evaluate the antiproliferative mechanisms of lupulones on a human metastatic colon carcinoma-derived cell line (SW620 cells) and to assess their chemopreventive effects in a model of colon carcinogenesis. SW620 cell growth was inhibited by 70% after a 48 h exposure to lupulones (40 microg/ml). Lupulones up-regulated the expression of Fas receptor (Fas) and Fas ligand (FasL) as well as TNF-related apoptosis inducing ligand (TRAIL)-R1 (DR4) and -R2 (DR5) receptor proteins, suggesting the involvement of Fas and TRAIL receptors-mediated pathways in lupulone-induced apoptosis. Lupulones also increased the mitochondrial membrane permeability. Colon carcinogenesis was initiated in Wistar rats by intra-peritoneal injections of azoxymethane (AOM), once a week for 2 weeks. One week after the last injection, rats received lupulones (0.001 or 0.005%) in drinking water, and AOM-control rats received the excipient. After 7 months of treatment, the colon of rats receiving 0.001 and 0.005% lupulones showed, respectively, a 30 and a 50% reduction (P < 0.05) of the number of preneoplastic lesions (aberrant crypt foci). In addition, we observed a drastic reduction (70-80%) of the total number of tumors in the colon of rats treated with lupulones when compared with the AOM control group. Lupulones induced apoptosis in SW620 colon-derived metastatic cells by activating both Fas and TRAIL death receptor signaling pathways, and antagonize at a low dose (4 mg/kg/day) colon cancer development. These observations suggest the use of lupulones for colon cancer chemoprevention trials.


Subject(s)
Anticarcinogenic Agents/pharmacology , Apoptosis/drug effects , Colonic Neoplasms/prevention & control , Terpenes/pharmacology , Animals , Anticarcinogenic Agents/therapeutic use , Azoxymethane , Cell Line, Tumor , Cell Proliferation/drug effects , Colonic Neoplasms/chemically induced , Colonic Neoplasms/pathology , Disease Models, Animal , Fas Ligand Protein/metabolism , Humans , Intestinal Mucosa/metabolism , Intestinal Mucosa/pathology , Male , Mitochondrial Membranes/drug effects , Mitochondrial Membranes/physiology , Neoplasm Metastasis , Permeability , Plant Preparations/chemistry , Rats , Rats, Wistar , Receptors, TNF-Related Apoptosis-Inducing Ligand/metabolism , Terpenes/therapeutic use , fas Receptor/metabolism
10.
Anticancer Res ; 26(5A): 3381-5, 2006.
Article in English | MEDLINE | ID: mdl-17094456

ABSTRACT

BACKGROUND: Procyanidins are apple constituents with potential in colon cancer chemoprevention. MATERIALS AND METHODS: Human colon cancer derived metastatic cells (SW620), growing under standardized conditions, were exposed to procyanidins and lysosomotropic compounds. Growth, apoptosis and lysosomal integrity was determined using published methods. RESULTS: Lysosomotropic drugs (MDL 72527, phenylalanine methylester and chloroquine) amplified procyanidin-induced growth inhibition and apoptosis in SW620 cells at non-cytotoxic concentrations. The improved toxicity of the drug combinations relies primarily on the enhancement of lysosomal membrane permeability. CONCLUSION: Combinations with non-toxic concentrations of lysosomotropic compounds improve the anti-carcinogenic properties of apple procyanidins.


Subject(s)
Antioxidants/pharmacology , Apoptosis/drug effects , Biflavonoids/pharmacology , Catechin/pharmacology , Chemoprevention , Colonic Neoplasms/prevention & control , Malus/chemistry , Proanthocyanidins/pharmacology , Antimalarials/pharmacology , Cell Proliferation/drug effects , Chloroquine/pharmacology , Colonic Neoplasms/pathology , Drug Synergism , Humans , Lysosomes/metabolism , Oxidoreductases Acting on CH-NH Group Donors/antagonists & inhibitors , Phenylalanine/analogs & derivatives , Phenylalanine/pharmacology , Putrescine/analogs & derivatives , Putrescine/pharmacology , Tumor Cells, Cultured
SELECTION OF CITATIONS
SEARCH DETAIL
...