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At least 1,117 records · Page 62Linked to original sources
PubMed1997

(-)-Epigallocatechin-3-gallate blocks the induction of nitric oxide synthase by down-regulating lipopolysaccharide-induced activity of transcription factor nuclear factor-kappaB.

Nitric oxide (NO) plays an important role in inflammation and multiple stages of carcinogenesis. We investigated the effect of various tea polyphenols and caffeine on the induction of NO synthase (NOS) in thioglycollate-elicited and lipopolysaccharide (LPS)-activated peritoneal macrophages. Gallic acid (GA), (-)-epigallocatechin (EGC), and (-)-epigallocatechin-3-gallate (EGCG), the major tea catechin, were found to inhibit inducible NOS (iNOS) protein in activated macrophages. EGCG, a potent antitumor agent with anti-inflammatory and antioxidant properties, inhibited NO generation, as measured by the amount of nitrite released into the culture medium. Inhibition of NO production was observed when cells were cotreated with EGCG and LPS. iNOS activity in soluble extracts of lipopolysaccharide-activated macrophages treated with EGCG (5 and 10 microM) for 6-24 hr was significantly lower than that in macrophages without EGCG treatment. Western blot, reverse transcription-polymerase chain reaction, and Northern blot analyses demonstrated that significantly reduced 130-kDa protein and 4.5-kb mRNA levels of iNOS were expressed in lipopolysaccharide-activated macrophages with EGCG compared with those without EGCG. Electrophoretic mobility shift assay indicated that EGCG blocked the activation of nuclear factor-kappaB, a transcription factor necessary for iNOS induction. EGCG also blocked disappearance of inhibitor kappaB from cytosolic fraction. These results suggest that EGCG decreases the activity and protein levels of iNOS by reducing the expression of iNOS mRNA and the reduction could occur through prevention of the binding of nuclear factor-kappaB to the iNOS promoter, thereby inhibiting the induction of iNOS transcription.

Animals↗
PubMedDate not supplied

Inhibition of ultraviolet-B radiation induced ornithine decarboxylase activity and edema formation by hydrolyzable and condensed tannins in mouse skin in vivo.

Naturally occurring hydrolyzable (HT) and condensed (CT) tannins and their monomeric units were tested for their ability to inhibit the induction of epidermal ODC activity and the formation of skin edema by UVB, two responses that are linked to the hyperplastic and inflammatory components of skin tumor promotion by this agent. Hairless mice were irradiated with either single (200 mJ/cm2/sec) or multiple (150 mJ/cm2/sec) doses of UVB and epidermal ODC activity was assayed at different times following irradiation. The peak of ODC induction which is observed 30-40 hours after a single UVB irradiation increases by 2.5 fold and shifts to a much earlier time of 5 hours after two UVB treatments repeated at 24-hour intervals. Topical applications of the various plant tannins, before or after irradiation, were found to inhibit, in a dose-dependent manner, epidermal ODC activity induced by single and multiple UVB treatments. Furthermore, the various HT and CT samples resulted in significant protection against UVB radiation-caused cutaneous edema. In general, the polymeric tannins inhibited ODC induction and edema to a greater degree than equal doses of their monomeric units, gallic acid and catechin. These results, in conjunction with our prior publications, suggest that various HTs and CTs may be useful against the hyperplastic and inflammatory responses associated with the exposure of skin to the tumor-promoting effects of both physical and chemical environmental carcinogens.

Animals↗
PubMed1998

Calcium/calmodulin-dependent signaling for appressorium formation in the plant pathogenic fungus Magnaporthe grisea.

Magnaporthe grisea, the causal agent of rice blast, forms a dome-shaped melanized infection structure, an appressorium, to infect its host. Environmental cues that induce appressorium formation by this fungus include hydrophobicity and hardness of contact surface, and chemicals from the host. To determine if the calcium/calmodulin-dependent signaling systems are involved in appressorium formation in M. grisea, we tested the effects of the calcium chelator, calcium ionophore, diverse intracellular calcium modulators, and calmodulin antagonists on appressorium formation. Several calcium modulators and calmodulin antagonists inhibited appressorium formation at the microM level, while conidia germination remained unaffected. There was an inhibition of appressorium formation by EGTA, a calcium chelator, which was restored by the addition of exogenous CaCl2. Neomycin, a phospholipase C inhibitor, specifically inhibited appressorium formation at concentrations from 10 microM to 100 mM. These data suggest that a calcium/calmodulin-dependent signaling system is involved in the appressorium formation of M. grisea.

Adrenergic alpha-Antagonists↗
PubMed2000

Contribution of proanthocyanidins to the peroxy radical scavenging capacity of some Italian red wines.

Highly reactive radicals, ROO(*), were generated from 2, 2'-azobis[2-(2-imidazolin-2-yl)propane] and linoleic acid. The ROO(*) scavenging capacity of some Italian red wines was evaluated following the changes in oxygen consumption. Under the experimental conditions the time course of oxygen consumption shows two typical behaviors: trolox-like (class I) and gallic acid-like (class II). Usually the time course of wine was similar to that of gallic acid. The rate of oxygen consumption was found to decrease exponentially with the amount of wine or gallic acid added to the test solution. On this basis the capacity of red wines to scavenge peroxy radicals was expressed as content of gallic acid (S(GA)). The S(GA) values were found to be correlated to the amount of total proanthocyanidins and total polyphenols of some Italian red wines (p < 0.01). The proanthocyanidins extracted from seeds were shown to make a major contribution to the peroxy radical scavenging capacity of red wines, whereas, interestingly, the chemical class of the low molecular weight tannins reactive to vanillin did not correlate with the S(GA) values.

Anthocyanins↗
PubMed1991

Actions of gallic esters on the arachidonic acid metabolism of human polymorphonuclear leukocytes.

Gallic esters with a varying chain length of its alcohol moiety produced strong inhibition of the conversion of [1-14C]-arachidonic acid to 5S-hydroxy-6E,8Z,11Z,14Z-eicosatetraenoic acid (5-HETE) by isolated human polymorphonuclear leukocytes. Octyl gallate and decyl gallate were the most powerful inhibitors with a concentration of half-inhibition of about 1 mumol . 1-1. Additionally these compounds caused however at 10 mumol . 1-1 a complete inhibition of the incorporation of arachidonic acid in triacylglycerols and phospholipids which is assumed to be a consequence of the damage to the energy metabolism of the cells. In contrast, the other gallic esters enhance the incorporation of arachidonic acid in the ester lipids in addition to moderate inhibition of the 5-lipoxygenase pathway.

Arachidonic Acid↗
PubMed2006

In vitro study of AMP-deaminase from fish (Cyprinus carpio) treated with hydrolyzable tannins.

AMP-deaminase (EC 3.5.4.6) is an enzyme responsible for stabilising adenylate energy changes. The properties of this enzyme are controlled by various ligands of hydrophobic nature. An investigation of enzyme activity alterations under the influence of natural phenolic acids (tannic, ellagic and gallic) which are soluble in water, could evidence the biological toxicity of these compounds. In our study purified AMP-deaminase isolated from white muscle of Cyprinus carpio was exposed to phenolic acids in the concentration range of 1 to 50 microM as well as to tannic acid in the presence of Cu2+ ions (5 microM). On the basis of the obtained results we can conclude that among the tested acids, gallic acid did not contribute to the change in AMP-deaminase activity, whereas ellagic acid diminished its activity at the highest concentration (50 microM). Tannic acid caused a significant decrease in the enzyme activity in comparison to control for all used concentrations. Cu2+ ions alone reduced the activity of AMP-deaminase for all studied concentrations. A combined action of a chosen Cu2+ ions concentration (5 microM) with tannic acid at the concentration higher than 2 microM resulted in a decrease in the enzyme activity, but for lower tannic acid concentration of 1 microM the activity of AMP-deaminase was stimulated. These experiments showed that tannic acid may stop free radical chain reactions only at low concentrations (1 microM) in the presence of Cu2+ ions (5 microM).

AMP Deaminase↗
PubMed2005

Phenolic acids in neem (Azadirachta indica): a major pre-existing secondary metabolites.

High Performance Liquid Chromatographic (HPLC) analyses of various parts (fresh and dry bark of stem, mature and tender leaves, flower and different parts of fruit, i.e., raw and ripe fruit epicarp, mesocarp and seed) of neem (Azadirachta indica), which occupies an important place in socio-cultural-religious life in Indian communities, indicate that neem is rich in pre-existing secondary metabolites (phenolic acids). Dry bark showed only tannic acid but in fresh bark three phenolic acids were observed, i.e., gallic, tannic, and ferulic acids. In tender leaves only gallic and ferulic acids were detected, but the levels of these phenolic acids in mature leaves were about three times and fifty times greater, respectively. Flowers had only two phenolic acids in which gallic acid was maximum followed by chlorogenic acid. The level of phenolic acid was maximum in seeds followed by epicarp and pulp. In raw and ripe fruit seeds four phenolic acids were detected. Raw fruit seeds were rich in phenolic acids than ripe fruit seeds. Fruit epicarp was relatively richer than seed, seed pulp and flowers of the plants. Neem flowers were also rich in gallic and chlorogenic acids.

Azadirachta↗
PubMed2005

Polyphenol levels in human urine after intake of six different polyphenol-rich beverages.

Dietary polyphenols are suggested to participate in the prevention of CVD and cancer. It is essential for epidemiological studies to be able to compare intake of the main dietary polyphenols in populations. The present paper describes a fast method suitable for the analysis of polyphenols in urine, selected as potential biomarkers of intake. This method is applied to the estimation of polyphenol recovery after ingestion of six different polyphenol-rich beverages. Fifteen polyphenols including mammalian lignans (enterodiol and enterolactone), several phenolic acids (chlorogenic, caffeic, m-coumaric, gallic, and 4-O-methylgallic acids), phloretin and various flavonoids (catechin, epicatechin, quercetin, isorhamnetin, kaempferol, hesperetin, and naringenin) were simultaneously quantified in human urine by HPLC coupled with electrospray ionisation mass-MS (HPLC-electrospray-tandem mass spectrometry) with a run time of 6 min per sample. The method has been validated with regard to linearity, precision, and accuracy in intra- and inter-day assays. It was applied to urine samples collected from nine volunteers in the 24 h following consumption of either green tea, a grape-skin extract, cocoa beverage, coffee, grapefruit juice or orange juice. Levels of urinary excretion suggest that chlorogenic acid, gallic acid, epicatechin, naringenin or hesperetin could be used as specific biomarkers to evaluate the consumption of coffee, wine, tea or cocoa, and citrus juices respectively.

Adult↗
PubMed1995

Granule exocytosis in a cultured human natural killer cell-rich population induced by K562 target cells and by PMA/A23187.

Granule exocytosis in natural killer (NK) cells induced by K562 target cells and by PMA/A23187 was examined by measuring N-benzyloxycarboxy-L-lysine esterase activity. We obtained a cultured human NK cell-rich population containing around 90% of CD16+ cells by culturing peripheral blood mononuclear cells with mitomycin C-treated Daudi cells in the presence of IL-2. Granule exocytosis in the cultured NK cells was induced by K562 cells in a target/effector cell ratio-dependent manner. The granule exocytosis induced by K562 cells was inhibited neither by EGTA nor by TMB-8, an intracellular calcium antagonist, nor by a combination of these two reagents, while the exocytosis induced by PMA/A23187 was inhibited in a dose-dependent manner both by EGTA and by TMB-8. However, the cytotoxic activity of the cultured NK cells was inhibited by EGTA, suggesting that calcium is required not for the induction of granule exocytosis but for other steps including its requirement for the exertion of perforin activity.

Cells, Cultured↗
PubMed1984

Activation of the human neutrophil secretory process with 5(S),12(R)-dihydroxy-6,14-cis-8,10-trans-eicosatetraenoic acid.

Exposure of human neutrophils to 5(S),12(R)-dihydroxy-6,14-cis-8,10-trans-eicosatetraenoic acid (leukotriene B4, LTB4) resulted in a time- and concentration- (10(-9)-10(-6) M) dependent extracellular release of granule-associated lysozyme and myeloperoxidase (MPO). Enzyme extrusion was negligible if cells were not pretreated with cytochalasin B prior to exposure to LTB4. A time-dependent deactivation of granule exocytosis was observed in neutrophils which were stimulated with LTB4 prior to contact with cytochalasin B. LTB4-induced enzyme release was markedly enhanced in the presence of extracellular calcium. Nevertheless, significant enzyme discharge occurred in the absence of extracellular calcium, and the percent of total activity released was not altered in the presence of EGTA. The calmodulin antagonist, trifluoperazine (TFP), and the intracellular calcium antagonist, 8-(N,N-diethylamino)-octyl-(3,4,5-trimethoxy)benzoate hydrochloride (TMB-8), caused a dose-related inhibition of enzyme release from LTB4-stimulated neutrophils. Degranulation was suppressed by the glycolytic inhibitor, 2-deoxy-D-glucose (2-DG), and the sulfhydryl reagents iodoacetic acid (IA) and N-ethylmaleimide (NEM). Sodium cyanide was inactive. Two inhibitors of transmethylation, 3-deazaadenosine (3-DZA) and L-homocysteine thiolactone (HCTL), alone or in combination, had no effect on LTB4-elicited degranulation. The protein synthesis inhibitor, cycloheximide, was inactive. Neutrophils pretreated with LTB4 or 5(S),12(R),20-trihydroxy-6,14-cis-8,10-trans-eicosatetraenoic acid (20-OH-LTB4, an omega-oxidation metabolite of LTB4) were desensitized to the subsequent exposure to LTB4. Cross-desensitization was also demonstrated between LTB4 and 20-OH-LTB4. The stimulus specific nature of LTB4-induced desensitization of neutrophil degranulation was demonstrated by the fact that cells exposed to 1-O-hexadecyl/octadecyl-2-O-acetyl-sn-glyceryl-3-phosphorylcholine (AGEPC) or N-formyl-methionyl-leucyl-phenylalanine (FMLP) were capable of inducing granule exocytosis from LTB4-pretreated neutrophils. Enzyme release from LTB4-treated cells was suppressed with the phospholipase inhibitor, 4-bromophenacyl bromide (4-BPB), the cyclooxygenase/lipoxygenase inhibitor, ETYA, and the 5-lipoxygenase inhibitor, U-60, 257. However, the cyclooxygenase inhibitor, flurbiprofen, exerted a weak suppressive effect on LTB4-induced degranulation.

Arachidonic Acid↗
PubMed1985

Effects of calcium antagonists and calmodulin inhibitors on angiotensin II-induced prostaglandin productions in the isolated dog renal arteries.

Angiotensin II markedly potentiated both PGE2 and PGI2 productions in the isolated dog renal arteries. This angiotensin II-induced response was significantly reduced by the treatments of EGTA and calcium antagonists such as verapamil, nifedipine and 8-(N,N'-diethylamino)-octyl-3,4,5,-trimethoxybenzoate (TMB-8). Calmodulin inhibitors, trifluoperazine and W-7 also inhibited the angiotensin II-induced PG productions while an inactive analogue of W-7, W-5 did not have any effect. The results suggest that angiotensin II may enhance the intracellular Ca2+ level through the influx of extracellular Ca2+ and then, calmodulin activated with Ca2+ will stimulate both PGE2 and PGI2 productions via its activation of phospholipase A2 in the dog renal arteries.

6-Ketoprostaglandin F1 alpha↗
PubMed1988

Effects of 8-N,N-diethylamino-octyl-3,4,5-trimethoxybenzoate (TMB-8) HCl and verapamil on the metabolism of free fatty acid by hepatocytes.

The influence of calcium antagonists on hepatic lipid metabolism was investigated in freshly dispersed rat hepatocytes incubated with [1-14C]oleate and verapamil or 8-N,N-diethylamino-octyl-3,4,5-trimethoxybenzoate (TMB-8). Synthesis of triglyceride was calculated from the specific radioactivity of [1-14C]oleate in extracted total lipid, after separation of each lipid class by thin-layer chromatography. Ketogenesis was measured enzymatically or as the amount of radioactivity incorporated into neutralized acid-soluble extracts. Neither verapamil nor TMB-8 affected triglyceride synthesis. In contrast, TMB-8 and verapamil exerted a concentration-dependent inhibition of ketogenesis, with TMB-8 being more potent than verapamil (inhibition by 50 microM TMB-8 was 73 +/- 9% versus 38 +/- 2% inhibition by 50 microM verapamil). Increasing the concentrations of calcium (0 to 4.2 mM) or oleate (0 to 2.0 mM) increased the rate of ketogenesis but did not alter the antiketogenic potency of TMB-8 or verapamil, indicating that inhibition of ketogenesis by these drugs was not calcium dependent. Since the calcium antagonists did not affect ketogenesis from octanoic acid, and since carnitine stimulated ketogenesis from [1-14C]oleate by 25% and reversed the antiketogenic effects of TMB-8 and verapamil, it appeared that the two calcium antagonists inhibited ketogenesis by interfering with the activity of the outer mitochondrial carnitine palmitoyltransferase. In assays of the outer carnitine palmitoyltransferase in isolated mitochondria, both TMB-8 and verapamil were inhibitory. TMB-8 was the more potent inhibitor of this enzyme, and carnitine was able to overcome inhibition by each of the inhibitors. These results suggest that verapamil and TMB-8 may inhibit ketogenesis by mechanisms independent of their well known effects on cellular calcium concentrations, and that inhibition may be competitive with respect to carnitine concentration. However, direct inhibition of carnitine palmitoyltransferase may not explain completely the inhibition of ketogenesis by these drugs, since concentrations required for enzyme inhibition were greater than those required for inhibition of ketogenesis in isolated hepatocytes.

Animals↗