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  1 / 116 MEDLINE  
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PMID:12144870
Autor:Adebiyi A; Prasad RN; Adaikan PG
Endereço:Department of Obstetrics and Gynaecology, National University of Singapore, Singapore.
Título:Effect of polyphloretin phosphate on the response of non-gravid rat uterus to folkloric and standard oxytocics in vitro.
Fonte:Prostaglandins Leukot Essent Fatty Acids; 66(5-6):499-503, 2002 May-Jun.
ISSN:0952-3278
País de publicação:Scotland
Idioma:eng
Resumo:Polyphloretin phosphate (PPP) has been reported by previous workers to be a specific antagonist of prostaglandin (PGE(1), PGE(2) & PGF(2 alpha))-induced contractions of isolated jird colon, gerbil colon, guinea pig ileum, and rabbit jejunum. In the present study, we examined the effect of PPP on uterotonic activities of crude papaya latex (a folkloric oxytocic), PGF(2 alpha), oxytocin, acetylcholine, and 5-hydroxytryptamine (standard oxytocics) on non-gravid, oestrogen-primed (50 microg/kg) rats in vitro. The effect of PPP on the oxytocics was evaluated qualitatively by incubating the tissues in PPP (25 - 400 microg/ml) for 20 min prior to the addition of a constant concentration of each oxytocic. PPP concentration dependently inhibited the contractile response of the uterine muscles to all the oxytocics. The inhibition was reversible after washing out the drugs. Results of the present study suggest that PPP is a non-specific and reversible antagonist of the response of non-gravid rat uterine smooth muscle to oxytocics in vitro. The specificity of PPP as a prostaglandin antagonist could therefore be species/tissue dependent.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Oxytocics); 0 (Prostaglandin Antagonists); 9014-72-6 (Polyphloretin Phosphate)


  2 / 116 MEDLINE  
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PMID:8750212
Autor:Blazsó G; Gábor M
Endereço:Department of Pharmacodynamics, Albert Szent-Györgyi Medical University, Szeged, Hungary.
Título:Effects of prostaglandin antagonist phloretin derivatives on mouse ear edema induced with different skin irritants.
Fonte:Prostaglandins; 50(3):161-8, 1995 Sep.
ISSN:0090-6980
País de publicação:United States
Idioma:eng
Resumo:Edema was induced in one ear of male mice of the CFLP strain with solutions of different skin irritants (croton oil 10 microL/35 micrograms, dithranol 10 microL/30 micrograms, capsaicin 10 microL/40 micrograms or arachidonic acid to 10 microL/2 mg per ear). Edema, determined by the edema-disk gravimetric technique, was inhibited in a dose-dependent manner by the intraperitoneally administered prostaglandin antagonists polyphloretin phosphate (PPP) or di-4-phloretin phosphate (DPP). With croton oil-induced mouse ear edema, DPP 10 mg/kg caused a 38% inhibition, PPP 25 mg/kg a 33% inhibition. With dithranol-induced edema DPP 0.5 mg/kg caused a 57% inhibition, while PPP 25 mg/kg was needed to exert a similar effect. Doses of DPP and PPP needed to cause a > 40% inhibition of edema were 10 mg/kg and 25 mg/kg, respectively, for capsaicin, and 25 mg/kg and 100 mg/kg for arachidonic acid. The inhibition of the ear edema by the phloretin derivatives was: dithranol > croton oil > capsaicin > arachidonic acid. This probably reflects the different contributions of prostaglandins to the inflammation.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Irritants); 0 (Prostaglandin Antagonists); 27YG812J1I (Arachidonic Acid); 39201-04-2 (diphloretin phosphate); 8001-28-3 (Croton Oil); 9014-72-6 (Polyphloretin Phosphate); S07O44R1ZM (Capsaicin); U8CJK0JH5M (Anthralin)


  3 / 116 MEDLINE  
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PMID:7954342
Autor:Zhang SZ; Fulton AM
Endereço:University of Maryland Cancer Center, University of Maryland School of Medicine, Baltimore 21201.
Título:Modulation of integrin-laminin receptor function on mammary tumor cells by prostaglandin E2 receptor antagonism.
Fonte:Cancer Lett; 85(2):233-8, 1994 Oct 14.
ISSN:0304-3835
País de publicação:Ireland
Idioma:eng
Resumo:Our previous studies indicate that prostaglandin E2 (PGE2) receptors play a role in tumor metastasis. We asked if PGE2 receptor antagonism would affect murine mammary tumor cell attachment to immobilized laminin, a critical step in metastasis. The PGE2 receptor antagonist, LEO101, at a concentration of 20 micrograms/ml, inhibited tumor cell attachment to laminin and the laminin-peptide PA-22 by 41 and 82%, respectively. Immunoprecipitation studies identified the beta 1 integrin subunit as well as the alpha 3 subunit as major membrane components of these cells, whereas little or no alpha 1, alpha 5 or alpha 6 was detected. Antibody blocking studies confirmed that these cells use beta 1, but not the alpha 6 subunit, to attach to laminin. Immunoprecipitation studies of untreated or LEO101-treated cells indicate that the expression of the alpha 3 integrin, but not other integrins, was decreased by LEO101.
Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, P.H.S.
Nome de substância:0 (Integrins); 0 (Peptides); 0 (Receptors, Laminin); 0 (Receptors, Prostaglandin E); 9014-72-6 (Polyphloretin Phosphate)


  4 / 116 MEDLINE  
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PMID:8388118
Autor:Tamaoki J; Chiyotani A; Takeyama K; Yamauchi F; Tagaya E; Konno K
Endereço:First Department of Medicine, Tokyo Women's Medical College, Japan.
Título:Relaxation and inhibition of contractile response to electrical field stimulation by Beraprost sodium in canine airway smooth muscle.
Fonte:Prostaglandins; 45(4):363-73, 1993 Apr.
ISSN:0090-6980
País de publicação:United States
Idioma:eng
Resumo:To elucidate the effect of Beraprost, a stable prostaglandin (PG) I2 analogue, on airway smooth muscle functions and its mechanism of action, we studied canine bronchial segments under isometric conditions in vitro. Addition of PGI2 and its analogues dose-dependently relaxed bronchial smooth muscle precontracted with acetylcholine, with the rank order of potency being Beraprost (1) > or = Hoprost (0.65) > PGI2 (0.04), accompanied by the corresponding increase in intracellular cyclic AMP levels. The Beraprost- and PGI2-induced muscle relaxations were significantly inhibited by each of the PG antagonist diphloretin phosphate, the adenylate cyclase inhibitor SQ 22,536, and the Na(+)-K(+)-ATPase inhibitor ouabain. Beraprost and PGI2 at concentrations insufficient to cause muscle relaxation reduced the contractile responses to electrical field stimulation, whereas they were without effect on those to exogenous acetylcholine. These results suggest that Beraprost not only potently relaxes airway smooth muscle through cyclic AMP production and the subsequent stimulation of Na(+)-K(+)-ATPase but also reduces neurally mediated contraction by inhibiting the release of acetylcholine from the cholinergic nerve terminals.
Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
Nome de substância:0 (Adenylyl Cyclase Inhibitors); 0 (Prostaglandin Antagonists); 17318-31-9 (9-(tetrahydro-2-furyl)-adenine); 35E3NJJ4O6 (beraprost); 39201-04-2 (diphloretin phosphate); 5ACL011P69 (Ouabain); 660YQ98I10 (Potassium Chloride); 9014-72-6 (Polyphloretin Phosphate); DCR9Z582X0 (Epoprostenol); EC 3.6.3.9 (Sodium-Potassium-Exchanging ATPase); JAC85A2161 (Adenine); N9YNS0M02X (Acetylcholine)


  5 / 116 MEDLINE  
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PMID:1511609
Autor:Ratnasooriya WD; Premakumara GA
Endereço:Department of Zoology, University of Colombo, Sri Lanka.
Título:Effects of the prostanoid receptor antagonist, di-4-phloretin phosphate, upon human sperm motility.
Fonte:Contraception; 45(3):239-48, 1992 Mar.
ISSN:0010-7824
País de publicação:United States
Idioma:eng
Resumo:The inhibitory effects of the prostanoid receptor antagonist, di-4-phloretin phosphate (DPP), upon washed human sperm motility were determined in vitro (up to 60 min of incubation). Concentrations tested were: 0.001, 0.01, 0.1, 0.25, 0.5, 2.5, 5.0 and 10.0 mM. All concentrations of DPP investigated caused cessation of sperm movement (percentage motility and average forward velocity) and the antimotility effect was essentially irreversible. The concentrations producing 50% inhibition were: percentage motility--1.31 +/- 0.56 mM (mean +/- SEM) and average forward velocity--1.95 +/- 0.68 mM. The mode of antimotility action appears to be multi-faceted. At high (10 mM) and intermediate (2.5 mM) concentrations, changes in fluidity of sperm plasmalemma (hypoosmotic swelling test) and loss of viability (nigrosin-eosin stain technique) constitute the primary means by which motility was disrupted. In contrast, these two parameters of motility remained unaltered at a lower concentration (0.25 mM) of DPP, and the mechanism precipitating the antimotility effect may involve mobilization of stored calcium ions and modulation of cyclic AMP levels.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Prostaglandin Antagonists); 39201-04-2 (diphloretin phosphate); 3G6A5W338E (Caffeine); 9014-72-6 (Polyphloretin Phosphate); EC 2.6.1.1 (Aspartate Aminotransferases); SY7Q814VUP (Calcium)


  6 / 116 MEDLINE  
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PMID:1467826
Autor:Okamura T; Matsumoto T; Ikemoto F; Toda N
Endereço:Department of Pharmacology, Shiga University of Medical Sciences, Ohtsu, Japan.
Título:Mechanisms of the biphasic responses to endothelin-3 in dog coronary arteries.
Fonte:Br J Pharmacol; 107(4):1037-41, 1992 Dec.
ISSN:0007-1188
País de publicação:England
Idioma:eng
Resumo:1. Endothelin-3 (ET-3) elicited relaxations at low concentrations (up to 10(-8) M) and contractions at higher concentrations in dog isolated coronary arteries precontracted with prostaglandin F2 alpha (PGF2 alpha). The relaxation by ET-3 was not affected by endothelium denudation nor treatment with NG-nitro-L-arginine, but was abolished or reversed to a contraction by treatment with indomethacin and markedly suppressed by tranylcypromine, a PGI2 synthetase inhibitor, or diphloretin phosphate, a prostaglandin receptor antagonist. ET-1 produced only concentration-dependent contractions. 2. BQ-123, a new selective ETA receptor antagonist, caused relaxation of the strips contracted with ET-3 in a dose-dependent manner and prevented the ET-3-induced contraction but did not affect the contraction produced by PGF2 alpha. The relaxation caused by ET-3 was enhanced by treatment with BQ-123. 3. It is concluded that the relaxations elicited by ET-3 in dog coronary arteries are mediated via liberation of PGI2 by activation of non-ETA receptors, located in subendothelial tissues, possibly smooth muscle cells, whereas the peptide-induced contractions are mediated via ETA receptors.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Endothelins); 0 (Peptides, Cyclic); 2149-70-4 (Nitroarginine); 39201-04-2 (diphloretin phosphate); 3E3V44J4Z9 (Tranylcypromine); 9014-72-6 (Polyphloretin Phosphate); 94ZLA3W45F (Arginine); B7IN85G1HY (Dinoprost); DCR9Z582X0 (Epoprostenol); S2A8YZM151 (cyclo(Trp-Asp-Pro-Val-Leu))


  7 / 116 MEDLINE  
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PMID:1361677
Autor:Vassilev P; Radomirov R
Endereço:Department of Experimental Pharmacology, Bulgarian Academy of Sciences, Sofia.
Título:Contractile effects of prostaglandin E2 in rat rectum: sensitivity to the prostaglandin antagonists diphloretin phosphate and SC 19220.
Fonte:Prostaglandins; 44(5):471-83, 1992 Nov.
ISSN:0090-6980
País de publicação:United States
Idioma:eng
Resumo:Prostaglandin E2 (PGE2) applied cumulatively (1 nM-1 microM) induced concentration-dependent tonic contractions in the longitudinal muscle of isolated rat rectum. The PGE2 effects were not altered by guanethidine (50 microM), whereas atropine (3 microM), guanethidine plus atropine or tetrodotoxin (0.1 microM) reduced them to an almost equal extent and increased the EC50 values for PGE2. The after-contractions following electrical stimulation were enhanced by PGE2 (10 nM) and inhibited by atropine. Diphloretin phosphate (DPP, 100 microM) shifted the regression lines for PGE2 to the right in both untreated and tetrodotoxin-treated preparations, and thereby increased the EC50 values. Slopes of the concentration-effect lines for PGE2 before and after DPP differed in the presence of tetrodotoxin. The regression line for PGE2 with SC 19220 (100 microM) in tetrodotoxin-treated preparations was shifted to the right in a parallel fashion. It is concluded that PGE2 exerted both a neural (cholinergic) and a smooth muscle effect. There may be a competitive antagonism between SC 19220 and PGE2 but the block by DPP may be nonselective.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:19395-87-0 (Dibenz(b,f)(1,4)oxazepine-10(11H)-carboxylic acid, 8-chloro-, 2-acetylhydrazide); 39201-04-2 (diphloretin phosphate); 4368-28-9 (Tetrodotoxin); 7C0697DR9I (Atropine); 9014-72-6 (Polyphloretin Phosphate); K7Q1JQR04M (Dinoprostone); ZTI6C33Q2Q (Guanethidine)


  8 / 116 MEDLINE  
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PMID:1331278
Autor:Fulton AM; Chong YC
Endereço:University of Maryland Cancer Center, Baltimore.
Título:Prostaglandin E2 receptor activity and susceptibility to natural killer cells.
Fonte:J Leukoc Biol; 51(2):176-80, 1992 Feb.
ISSN:0741-5400
País de publicação:United States
Idioma:eng
Resumo:We have described a high-affinity receptor for prostaglandin E2 (PGE2) present on metastatic murine mammary tumor cells. Pharmacologic antagonism of this receptor increases metastatic potential. In the present study, we have asked whether the binding activity of PGE on tumor target cells plays a role in natural killer (NK)-target cell interactions. We have used three unrelated PGE-receptor antagonists, SC19220, LEO101, and AH6809, to show inhibition of [3H]PGE2 binding to YAC-1 cells and inhibition of PGE2-mediated elevation of intracellular cyclic AMP (cAMP). Addition of any of these three receptor antagonists to standard 4-h 51Cr-release assays inhibits YAC-1 lysis by NK-enriched populations from murine spleen. This is the first report that antagonism of PGE binding affects NK activity. Our studies demonstrate that these effects are mediated through inhibition of target-effector cell conjugate formation. Studies in which effector and target cells were pretreated separately indicate that the PGE-mediated effects are expressed at the target cell level.
Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, U.S. GOV'T, P.H.S.
Nome de substância:0 (Receptors, Prostaglandin); 0 (Receptors, Prostaglandin E); 9014-72-6 (Polyphloretin Phosphate); E0399OZS9N (Cyclic AMP); XXE1CET956 (Indomethacin)


  9 / 116 MEDLINE  
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PMID:1755324
Autor:Gábor M; Rázga Z
Endereço:Department of Pharmacodynamics, Albert-Szent Györgyi University Medical School, Hungary.
Título:Effect of benzopyrone derivatives on simultaneously induced croton oil ear oedema and carrageenin paw oedema in rats.
Fonte:Acta Physiol Hung; 77(3-4):197-207, 1991.
ISSN:0231-424X
País de publicação:Hungary
Idioma:eng
Resumo:Carrageenin paw oedema and croton oil ear oedema induced simultaneously in rats are inhibited in a dose-dependent manner and to statistically significant degrees by lipoxygenase- and cyclooxygenase-blocker flavonoids (diosmin, fisetin, quercetin, myricetin, galangin, sophoricoside, hesperidin-methylchalcone, oligomeric procyanidin, anthocyanidins (delphinidin, pelargonidin], and the prostaglandin antagonist polyphloretin phosphate and di-4-phloretin phosphate. Outstanding anti-inflammatory effects are displayed by myricetin and delphinidin, which contain vicinal hydroxy groups in ring B. The results confirm the importance of hydroxy group substitution in ring B. The most effective of the examined substances proved to be the prostaglandin antagonist di-4-phloretin phosphate.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Flavonoids); 0 (Prostaglandin Antagonists); 39201-04-2 (diphloretin phosphate); 8001-28-3 (Croton Oil); 9000-07-1 (Carrageenan); 9014-72-6 (Polyphloretin Phosphate)


  10 / 116 MEDLINE  
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PMID:1720068
Autor:Rhaleb NE; Rouissi N; Drapeau G; Jukic D; Regoli D
Endereço:Department of Pharmacology, Faculty of Medicine, University of Sherbrook, Qué., Canada.
Título:Characterization of bradykinin receptors in peripheral organs.
Fonte:Can J Physiol Pharmacol; 69(7):938-43, 1991 Jul.
ISSN:0008-4212
País de publicação:Canada
Idioma:eng
Resumo:Bradykinin (BK) and related kinins are potent stimulants of the rabbit jugular vein, the hamster urinary bladder, and the guinea pig trachea. The characterization of kinin receptors in these tissues was made with agonists and antagonists. Results obtained with agonists indicate that bradykinin and kallidin are much more active than des-Arg9-BK and suggest the presence of B2 receptors in the three organs. Some new agonists were also tested and the BK analogue, [Hyp3,Tyr(Me)8]BK, was found to be a potent and selective stimulant of the three preparations, with pD2 values of 8.56, 8.00, and 8.39, respectively, but inactive on the rabbit aorta (a B1-receptor system). Contractile effects of kinins in the rabbit jugular vein and hamster urinary bladder were reduced or eliminated by B2-receptor antagonists but at different concentration levels; e.g., acetyl-D-Arg[Hyp3,D-Phe7]BK showed pA2 values of 7.78 on the rabbit jugular vein but only 5.72 on hamster urinary bladder. This compound contracted the guinea-pig trachea and was found to be inactive as an antagonist on this preparation. Contractions of the hamster urinary bladder and the guinea-pig trachea in response to bradykinin were markedly reduced or eliminated by indomethacin and by BW 755C, while those of the rabbit jugular vein were not modified. The present findings indicate that the myotropic effect of kinins on the rabbit jugular vein depends on the activation of B2 receptors and suggest that B2 receptors are largely responsible also for the response of the hamster urinary bladder. B2 receptors and (or) a nonreceptor mechanism appear to be involved in the stimulant effects of the kinin agonists and some antagonists in the guinea-pig trachea.
Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
Nome de substância:0 (Leukotriene Antagonists); 0 (Methacholine Compounds); 0 (Prostaglandin Antagonists); 0 (Quinolines); 0 (Receptors, Bradykinin); 0 (Receptors, Neurotransmitter); 105350-26-3 (SR 2640); 33507-63-0 (Substance P); 39201-04-2 (diphloretin phosphate); 66000-40-6 (4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyrazol-3-amine); 86933-74-6 (Neurokinin A); 9014-72-6 (Polyphloretin Phosphate); S8TIM42R2W (Bradykinin); XXE1CET956 (Indomethacin)



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