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At least 991 records · Page 55Linked to original sources
PubMed2005

Acetoxy drug: protein transacetylase catalyzed activation of human platelet nitric oxide synthase by polyphenolic peracetates.

An enhanced intracellular level of Nitric oxide (NO) is essential to ameliorate several pathological conditions of heart and vasculature necessitating the activation of NOS. We have projected in this report the acetylation of eNOS by polyphenolic peracetates (PA) catalyzed by the novel enzyme acetoxy drug: protein transacetylase (TAase) discovered in our laboratory as an unambiguous way of activating NOS which results in the manifestation of physiological action. The human platelet was chosen as the experimental system in order to validate the aforementioned proposition. PA caused profound irreversible activation of platelet NADPH cytochrome c reductase mediated by TAase. The convincing biochemical evidences are presented to show that PA could cause acetylation of the reductase domain of NOS leading to the activation of eNOS in tune with their specificities to platelet TAase. As a result, the enhanced level of NO due to activation of platelet eNOS by PA was found to inhibit the ADP-induced platelet aggregation. The present studies highlight for the first time the role of PA as the novel potent agent for enhancing the intracellular NO levels.

Acetates↗
PubMed2004

Green tea polyphenol (-)-epigallocatechin gallate attenuates the neuronal NADPH-d/nNOS expression in the nodose ganglion of acute hypoxic rats.

Recent studies have shown that (-)-epigallocatechin gallate (EGCG), one of the green tea polyphenols, has a potent antioxidant property. Nitric oxide (NO) plays an important role in the neuropathogenesis induced by brain ischemia/reperfusion and hypoxia. This study aimed to explore the potential neuroprotective effect of EGCG on the ganglionic neurons of the nodose ganglion (NG) in acute hypoxic rats. Thus, the young adult rats were pretreated with EGCG (10, 25, or 50 mg/kg, i.p.) 30 min before they were exposed to the altitude chamber at 10,000 m with the partial pressure of oxygen set at the level of 0.27 atm (pO2=43 Torr) for 4 h. All the animals examined were allowed to survive for 3, 7, and 14 successive days, respectively, except for those animals sacrificed immediately following hypoxic exposure. Nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) histochemistry and neuronal nitric oxide synthase (nNOS) immunohistochemistry were carried out to detect the neuronal NADPH-d/nNOS expression in the NG. The present results show a significant increase in the expression of NADPH-d/nNOS reactivity in neurons of the NG at various time intervals following hypoxia. However, the hypoxia-induced increase in NADPH-d/nNOS expression was significantly depressed only in the hypoxic rats treated with high dosages of EGCG (25 or 50 mg/kg). These data suggest that EGCG may attenuate the oxidative stress following acute hypoxia.

Animals↗
PubMed2005

Water-soluble polymeric polyphenols from cinnamon inhibit proliferation and alter cell cycle distribution patterns of hematologic tumor cell lines.

To explore possible anti-cancer properties of water-soluble, polymeric polyphenols from cinnamon, three myeloid cell lines (Jurkat, Wurzburg, and U937) were exposed to increasing concentrations of an aqueous extract prepared from cinnamon (CE) for 24 h. Cell growth and cell cycle distribution patterns responded in a dose-dependent manner to CE. That is, an increase in the percentage of cells distributed in G2/M was observed in all three cell lines as the amount of CE increased. At the highest dose of CE, the percentage of Wurzburg cells in G2/M was 1.5- and 2.0-fold higher than those observed for Jurkat and U937 cells, respectively. Wurzburg cells lack the CD45 phosphatase and may be more sensitive to imbalances in signaling through kinase/phosphatase networks that promote growth. The results suggest the potential of CE to interact with phosphorylation/dephosphorylation signaling activities to reduce cellular proliferation in tandem with a block at the G2/M phase of the cell cycle.

Cell Cycle↗
PubMed2006

Dietary polyphenols: good, bad, or indifferent for your health?

Flavonoids and other polyphenolic compounds have powerful antioxidant effects in vitro in many test systems, but can act as pro-oxidants in some others. Whether pro-oxidant, antioxidant, or any of the many other biological effects potentially exerted by flavonoids account for or contribute to the health benefits of diets rich in plant-derived foods and beverages is uncertain. Phenolic compounds may help to protect the gastrointestinal tract against damage by reactive species present in foods or generated within the stomach and intestines. The overall health benefit of flavonoids is uncertain, and consumption of large quantities of them in fortified foods or supplements should not yet be encouraged.

Animals↗
PubMed2004

Therapeutic efficacy of green tea polyphenols on cellular thiols in 4-Nitroquinoline 1-oxide-induced oral carcinogenesis.

In cancer, a high flux of oxidants not only depletes the cellular thiols, but damages the whole cell as well. Epidemiological studies suggest green tea may mitigate cancers in human and animal models for which several mechanisms have been proposed. In the present investigation, the levels of cellular thiols such as reduced glutathione (GSH), oxidised glutathione (GSSG), protein thiols (PSH), total thiols, lipid peroxidation product conjugated dienes and the activity of gamma glutamyl transferase (GGT) were assessed in tongue and oral cavity. In 4-Nitroquinoline 1-oxide- (4-NQO) induced rats, there was a decrease in the levels of GSH, PSH and total thiols and an increase in the levels of GSSG, conjugated dienes and the activity of GGT. On supplementation of green tea polyphenols (GTP) for 30 days (200 mg/kg) for the oral cancer-induced rats, there was a moderate increase in the levels of GSH, PSH and total thiols and a decrease in the levels of GSSG, conjugated dienes and the activity of GGT. Thus, GTP reduces the oxidant production thereby maintains the endogenous low molecular weight cellular thiols in oral cancer-induced rats. From the results, it can be concluded that GTP supplementation enhances the cellular thiol status thereby mitigate oral cancer.

4-Nitroquinoline-1-oxide↗
PubMed2006

Modulatory efficacy of green tea polyphenols on glycoconjugates and immunological markers in 4-Nitroquinoline 1-oxide-induced oral carcinogenesis-A therapeutic approach.

Green tea polyphenols (GTP) has been used as a chemopreventive agent world wide against chemically induced cancer. The present study is aimed to understand the therapeutic action of GTP on glycoconjugates and immunological markers in 4-Nitroquinoline 1-oxide (4-NQO)-induced oral cancer over a period of 30 days at 200mg/kg, p.o., Oral cancer was induced by painting 4-NQO for 8 weeks followed by administration of GTP after 22 weeks, for 30 days. Glycoconjugates such as hexose, hexosamine, sialicacid, fucose and mucoprotein were analysed. Expression of glycoconjugates was examined through histology and SDS-PAGE. Immunological markers such as circulating immune complex and mast cell density were studied. Oral cancer-induced animals showed a significant increase in levels of glycoconjugates and its expression, similar to that observed for immunological markers. Treatment with GTP altered the expression of glycoconjugates as well as immunological markers. The results suggest that GTP modulates both the expression of glycoconjugates and immunological markers resulting in regression of oral cancer.

4-Nitroquinoline-1-oxide↗
PubMed2005

Resveratrol, a polyphenolic compound in red wine, protects against oxidized LDL-induced cytotoxicity in endothelial cells.

BACKGROUND: Resveratrol, a polyphenolic constituent of red wine, has antioxidant effects. However, its protective effects against oxLDL-induced endothelial injury remained unclarified. METHODS: Primary human umbilical vein endothelial cell cultures (HUVECs) treated with oxLDL (200 microg/ml) were used to explore the protective effect of resveratrol. Cytotoxicity of oxLDL on HUVECs was studied by measuring lactate dehydrogenase (LDH) release, methylthiazol tetrazolium (MTT) and apoptotic cell death as characterized by terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) stain. We also measured the production of reactive oxygen species (ROS) by using the fluorescnet probe 2', 7'-dichlorofluorescein acetoxymethyl ester (DCF-AM), and observed the activity of antioxidant enzymes. Furthermore, several apoptotic signaling pathway with increased cytosolic calcium, alteration of mitochondrial membrane potential, cytochrome c release and activation of caspase 3 were also investigated. RESULTS: Resveratrol attenuated oxLDL-induced cytotoxicity, apoptotic features, generation of ROS and intracellular calcium accumulation. OxLDL-induced mitochondria membrane potential collapase, cytochrome c release and activation of caspase 3 in HUVECs were also suppressed by resveratrol pretreatment. CONCLUSIONS: Red wine intake may protect against oxLDL-induced dysfunction of endothelial cells.

Antioxidants↗
PubMed2005

Comparative study of the alkyl and peroxy radical scavenging activities of polyphenols.

The lipid antioxidative activities of polyphenols with high oxygen radical capacities need to be measured at low oxygen tensions. In this study, differences in the reactivity of catechins and resveratrols towards alkyl (R*) and peroxy (PhCOO*) radicals were observed at lower oxygen pressures. The radical scavenging activities for catechin, epicatechin, resveratrol and n-propyl gallate with or without 2-mercapto-1-methylimidazole (MMI), a thiol were investigated by differential scanning calorimetry (DSC) monitoring of the polymerization of methyl methacrylates (MMA) initiated by 2,2'-azobisisobutyronitrile (AIBN, an R* radical) or benzoyl peroxide (BPO, an PhCOO* radical) at 70 degrees C under nearly anaerobic conditions. Catechin, epicatechin and resveratrol with MMI, but not n-propyl gallate showed the less length of induction period than that for corresponding ones without MMI, probably resulting from the reaction of MMI radicals with molecular oxygen in the system. Also, the inhibitory rate of propagation (R(inh)) for catechin and resveratrol in the BPO system was much more greater than that in the AIBN system. The reactivity of catechins and resveratrol with R() or PhCOO* radical was considerably different, whereas n-propyl gallate did not different between radicals under nearly anaerobic conditions.

Anaerobiosis↗
PubMed2004

Effects of green tea polyphenols on murine transplant-reactive T cell immunity.

Green tea polyphenols (GrTP), the active ingredient of green tea, may have immunosuppressive properties, but whether and how GrTP affect transplant-reactive T cells is unknown. To address this, we tested the effects of GrTP on in vitro and in vivo transplant-reactive T cell immunity. GrTP inhibited IFNgamma secretion by cultured monoclonal T cells and by alloreactive T cells in mixed lymphocyte reactions. Oral GrTP significantly prolonged minor antigen-disparate skin graft survival and decreased the frequency of donor-reactive interferon gamma-producing T cells in recipient secondary lymphoid organs compared to controls. In contrast to other hypothesized actions, oral GrTP did not alter dendritic cell trafficking to lymph nodes or affect metalloproteinase activity in the graft. This is the first report of an immunosuppressive effect of GrTP on transplant-reactive T cell immunity. The results suggest that oral intake of green tea could act as an adjunctive therapy for prevention of transplant rejection in humans.

Adjuvants, Immunologic↗
PubMed2005

Inhibition of survival signalling by dietary polyphenols and indole-3-carbinol.

Epidemiological studies have long hinted at the possibility that what we eat greatly influences our state of health, in particular our relative risk of developing cancer. In recent years there has been an exponential increase in the number of studies investigating how individual components of the diet interact at the molecular level to determine the fate of a cell. It is now apparent that many such molecules can preferentially inhibit the growth of tumour cells, by inducing cell cycle arrest or apoptosis. The number of signalling pathways and molecular targets involved is continually expanding. Consequently, the picture is becoming ever more complicated, not least because results often appear to be cell-type specific, dose-response relationships are critical, and any one agent appears to have multiple mechanisms of action. In addition most studies have been conducted in cell culture, often with physiologically unachievable concentrations of single agents, making extrapolation to the clinical situation difficult. In this review the mechanisms of action of a few well-studied dietary polyphenols (curcumin, epigallocatechin gallate and resveratrol) and indole-3 carbinol are considered in the light of these issues.

Apoptosis↗
PubMed2005

The red wine polyphenol, resveratrol, exerts acute direct actions on guinea-pig ventricular myocytes.

Epidemiological evidence suggests that moderate consumption of red wine may be cardioprotective, although the precise mechanism(s) responsible remains poorly understood. We hypothesized that the red wine polyphenol, resveratrol, may exert direct actions on the heart and thus potentially contribute to cardioprotection. We show that resveratrol acutely decreases Ca2+ transient amplitude in isolated cardiac myocytes. Intriguingly, resveratrol simultaneously increases cell shortening in half the cells tested, while decreasing shortening in the other half. The former could be attributed to heightened myofilament Ca2+ sensitivity. This was no longer observed in myocytes that had been incubated with the oestrogen receptor antagonist, ICI 182,780, suggesting an oestrogen-receptor dependent mechanism of action. In addition, resveratrol significantly decreased action potential duration and the peak L-type Ca2+ current. Our findings provide evidence that resveratrol exerts multiple direct actions on cardiac myocytes, the net result of which is no overall change in cell contraction. The clinical significance of these results remains to be determined.

Animals↗
PubMed2006

Chronic pretreatment with American ginseng berry and its polyphenolic constituents attenuate oxidant stress in cardiomyocytes.

The acute anti-oxidant and protective effect of American ginseng berry extract (AGBE) has been demonstrated in cultured cardiomyocytes in our previous study. In the current study we evaluated if a chronic pretreatment of cultured cardiomyocytes with AGBE can alter the cellular antioxidant potential. Chick embryo cardiomyocytes were treated with AGBE (0.5-2.5 mg/ml) for up to 72 h. The treated cells were then exposed to exogenously added hydrogen peroxide (H(2)O(2); 500 microM). The oxidant-mediated injury was measured using a fluorescent probe 2',7'-dichlorofluorescin diacetate (DCFH/DA) while cell death was measured using propidium iodide (PI) staining. The non-treated (control) cells exposed to H(2)O(2) showed significant increase in DCF- and PI-mediated fluorescence suggesting significant oxidative injury and cell death. Pretreatment with AGBE demonstrated a significant attenuation of DCF fluorescence (p<0.005) with AGBE 0.5 mg/ml showing a 17% decrease, AGBE 1.0 mg/ml showing a 26% decrease, and AGBE 2.5 mg/ml showing a 49% decrease from control DCF fluorescence following a 72 h pretreatment. Cell death caused by H(2)O(2) was also significantly attenuated in AGBE-pretreated cells in a concentration- and time-dependent manner (p<0.005). We also demonstrated that active polyphenolic constituents in AGBE, caffeic acid and chlorogenic acid, appear to contribute significantly to AGBE's protective effects. Finally, catalase inhibition resulted in a significantly increased fluorescence in AGBE-treated cells compared to the control. The results suggest that pretreatment with AGBE upregulates peroxide detoxifying mechanisms, which could affect intracellular oxidant dynamics in cardiomyocytes.

Animals↗
PubMed2005

Inhibition of benzo[a]pyrene induced mutagenicity and genotoxicity by black tea polyphenols theaflavins and thearubigins in multiple test systems.

This study investigated the antimutagenic and anticlastogenic effects of black tea polyphenols, theaflavins (TF) and thearubigins (TR) in Salmonella assay in vitro and in vivo in bone marrow cells of mice as measured by chromosomal aberrations (CA) and sister chromatid exchange (SCE) against a known carcinogen, benzo[a]pyrene (B[a]P). A significant decrease in mutagenicity in Salmonella assay and both CA and SCE were observed in all the different concentrations of TF and TR plus B[a]P treated series when compared with B[a]P treated group alone. These results indicate that both TF and TR have significant antimutagenic and anticlastogenic effects.

Animals↗
PubMed2006

Distinct mechanisms underlie distinct polyphenol-induced neuroprotection.

Glutamate excitotoxicity is mediated by intracellular Ca(2+) overload, caspase-3 activation, and ROS generation. Here, we show that curcumin, tannic acid (TA) and (+)-catechin hydrate (CA) all inhibited glutamate-induced excitotoxicity. Curcumin inhibited PKC activity, and subsequent phosphorylation of NR1 of the NMDA receptor. As a result, glutamate-mediated Ca(2+) influx was reduced. TA attenuated glutamate-mediated Ca(2+) influx only when simultaneously administered, directly interfering with Ca(2+). Both curcumin and TA inhibited glutamate-induced caspase-3 activation. Although Ca(2+) influx was not attenuated by CA, caspase-3 was reduced by direct inhibition of the enzyme. All polyphenols reduced glutamate-induced generation of ROS.

Animals↗
PubMed2004

Catechin polyphenols: neurodegeneration and neuroprotection in neurodegenerative diseases.

Neurodegeneration in Parkinson's, Alzheimer's, and other neurodegenerative diseases seems to be multifactorial, in that a complex set of toxic reactions including inflammation, glutamatergic neurotoxicity, increases in iron and nitric oxide, depletion of endogenous antioxidants, reduced expression of trophic factors, dysfunction of the ubiquitin-proteasome system, and expression of proapoptotic proteins leads to the demise of neurons. Thus, the fundamental objective in neurodegeneration and neuroprotection research is to determine which of these factors constitutes the primary event, the sequence in which these events occur, and whether they act in concurrence in the pathogenic process. This has led to the current notion that drugs directed against a single target will be ineffective and rather a single drug or cocktail of drugs with pluripharmacological properties may be more suitable. Green tea catechin polyphenols, formerly thought to be simple radical scavengers, are now considered to invoke a spectrum of cellular mechanisms of action related to their neuroprotective activity. These include pharmacological activities like iron chelation, scavenging of radicals, activation of survival genes and cell signaling pathways, and regulation of mitochondrial function and possibly of the ubiquitin-proteasome system. As a consequence these compounds are receiving significant attention as therapeutic cytoprotective agents for the treatment of neurodegenerative and other diseases.

Animals↗
PubMed2005

Protective effect of green tea polyphenols on the SH-SY5Y cells against 6-OHDA induced apoptosis through ROS-NO pathway.

Green tea polyphenols (GTP) are thought to help prevent oxidative stress-related diseases, such as cancer, cardiovascular disease, neurodegenerative disease, and aging. We here investigate the protective mechanisms of GTP on SH-SY5Y cells against apoptosis induced by the pro-parkinsonian neurotoxin 6-hydroxydopamine (6-OHDA). GTP rescued the changes in condensed nuclear and apoptotic bodies, attenuated 6-OHDA-induced early apoptosis, prevented the decrease in mitochondrial membrane potential, and suppressed accumulation of reactive oxygen species (ROS) and of intracellular free Ca(2+). GTP also counteracted the 6-OHDA-induced nitric oxide increase and overexpression of nNOS and iNOS, and decreased the level of protein-bound 3-nitrotyrosine (3-NT). In addition, GTP inhibited the autooxidation of 6-OHDA and scavenged oxygen free radicals in a dose- and time-dependent manner. Our results show that the protective effects of GTP on SH-SY5Y cells are mediated, at least in part, by controlling the ROS-NO pathway.

Annexin A5↗
PubMed2005

Inhibition of sphingosine-1-phosphate- and vascular endothelial growth factor-induced endothelial cell chemotaxis by red grape skin polyphenols correlates with a decrease in early platelet-activating factor synthesis.

Vascular endothelial growth factor (VEGF) and platelet-derived lipid sphingosine-1-phosphate (S1P) are two proinflammatory mediators which contribute to angiogenesis, in part through the synthesis of platelet-activating factor (PAF). The red grape skin polyphenolic extract (SGE) both prevents and inhibits angiogenesis in the Matrigel model, decreases the basal motility of endothelial and cancer cells, and reverses the chemotactic effect of S1P and VEGF on bovine aortic endothelial cells (BAECs) as well as the chemotactic effect of conditioned medium on human HT-1080 fibrosarcoma, human U-87 glioblastoma, and human DAOY medulloblastoma cells. Inhibition of VEGF- and S1P-mediated chemotaxis by SGE is associated with a down-regulation of ERK and p38/MAPK phosphorylation and a decreased in acute PAF synthesis. Notably, as do extracellular inhibitors of PAF receptor, SGE prevents S1P-induced PAF synthesis and the resulting activation of the S1P/endothelial differentiation gene-1 cascade. Given the key role of VEGF and S1P in inflammation, angiogenesis, and tumor invasion, SGE may therefore contribute to prevent (or to delay) the development of diseases associated with angiogenesis dysregulation, including cancer. The dual inhibition of S1P- and VEGF-mediated migration of endothelial cell and of serum-stimulated migration of U-87 cells suggests a usefulness of SGE against highly invasive human glioblastoma.

Animals↗