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Academic literature on the topic 'Prostaglandins Antagonists'

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Published: 10 December 2022
Last updated: 29 January 2023

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Journal articles on the topic "Prostaglandins Antagonists"

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Vanner, S., M. M. Jiang, and A. Surprenant. "Mucosal stimulation evokes vasodilation in submucosal arterioles by neuronal and nonneuronal mechanisms." American Journal of Physiology-Gastrointestinal and Liver Physiology 264, no. 2 (February 1, 1993): G202—G212. http://dx.doi.org/10.1152/ajpgi.1993.264.2.g202.

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The effects of mechanical stimulation of intestinal mucosa on submucosal arterioles of guinea pig ileum were examined using video microscopy of in vitro preparations consisting of submucosal plexus with adjacently attached mucosa. Mucosal stimulation did not alter the diameter of relaxed vessels but dilated arterioles preconstricted with phenylephrine or the prostaglandin analogue U-46619. Tetrodotoxin (TTX) or muscarinic receptor antagonists inhibited the vasodilation evoked by mucosal stimulation in 60% of preparations examined from normal and extrinsically denervated animals. The TTX-sensitive vasodilation to mucosa stimulation was partially inhibited by the 5-hydroxytryptamine3 (5-HT3) receptor antagonist ICS 205930. The TTX-insensitive vasodilation was largely prevented when the histamine receptor antagonists cimetidine and pyrilamine and the prostaglandin synthesis inhibitor indomethacin were applied. This study has demonstrated a reflex vasodilation to mucosal stimulation in an isolated submucosal plexus preparation that involves both neuronal and nonneuronal pathways. The neuronal pathway converges on cholinergic vasodilator neurons in the submucosal ganglia. The nonneuronal pathway involves the release of 5-HT, histamine, and prostaglandins from mucosal elements; 5-HT excites cholinergic vasodilator neurons, whereas histamine and prostaglandins dilate submucosal arterioles directly.
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Banks, R. O., and E. D. Jacobson. "Renal vasodilation with ureteral occlusion and prostaglandins: attenuation by histamine H1 antagonists." American Journal of Physiology-Renal Physiology 249, no. 6 (December 1, 1985): F851—F857. http://dx.doi.org/10.1152/ajprenal.1985.249.6.f851.

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We evaluated the effects of histamine receptor antagonists on the renal vasodilatory responses to ureteral occlusion (UO), to the intrarenal infusion of prostaglandins E2, I2, A2, D2 and E1, and to bradykinin. We also determined the effects of meclofenamic acid, a cyclooxygenase inhibitor, on histamine-induced renal vasodilation and the effects of 2-methylhistamine (2-MeH), and H1 agonist, on glomerular filtration rate (GFR) and renal blood flow (RBF). Experiments were performed on adult mongrel dogs anesthetized with pentobarbital sodium. RBF was measured with an electromagnetic flow probe. Neither UO-induced nor prostaglandin- (PG) induced renal vasodilation was affected by infusion of the histamine H2 receptor antagonist cimetidine into the renal artery at 10(-5) M/min. On the other hand, renal artery infusion of the H1 receptor antagonist chlorpheniramine (CP) at 10(-5) M/min blocked UO-induced renal vasodilation [RBF increased 34 +/- 4% (SE) prior to but only 2 +/- 2% during infusion of CP) and markedly attenuated PGI2-, PGA2-, and PGE2-induced increases in RBF (CP inhibited 64 +/- 9% of the PGE2-induced renal vasodilation). CP had less effect on the renal vasodilation associated with infusion of PGD2 or PGE1 and had no effect on the vasodilation induced by bradykinin. Infusion of exogenous histamine (1 micrograms X kg-1 X min-1) into the renal artery prior to ureteral occlusion resulted in a typical H1 + H2-mediated vasodilatory response (RBF increased 53 +/- 7%).(ABSTRACT TRUNCATED AT 250 WORDS)
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Lonardoni, Maria Valdrinez Campana, Momtchillo Russo, and Sonia Jancar. "Essential Role of Platelet-Activating Factor in Control of Leishmania (Leishmania)amazonensis Infection." Infection and Immunity 68, no. 11 (November 1, 2000): 6355–61. http://dx.doi.org/10.1128/iai.68.11.6355-6361.2000.

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ABSTRACT In the present study we investigated the role of platelet-activating factor (PAF) and prostaglandins in experimental Leishmania (Leishmania)amazonensis infection and the relationship between these mediators and nitric oxide (NO) production. Mouse peritoneal macrophages elicited with thioglicolate were infected with leishmania amastigotes, and the infection index determined 48 h later. The course of infection was monitored for 5 weeks in mice infected in the footpad with promastigotes by measuring the footpad swelling and parasite load in regional lymph nodes and spleen. The addition of PAF to C57BL/6 mouse macrophages significantly inhibited parasite growth and induced NO production. Treatment of macrophages with a selective PAF antagonist, WEB2086, increased the infection, indicating that endogenously produced PAF regulates macrophage ability to control leishmania infection. This effect of PAF was abolished by addition of the inhibitor of NO synthesis, L-NAME, to the cultures. The addition of prostaglandin E2 significantly increased the infection and NO production. Treatment with cyclo-oxygenase inhibitor, indomethacin, reduced the infection and PAF-induced release of NO. Thus, the increased NO production induced by PAF seems to be mediated by prostaglandins. The more-selective inhibitors of cyclo-oxygenase 2, nimesulide and NS-398, had no significant effect. Thus, antileishmanial activity correlates better with the presence of PAF or absence of prostaglandins than with NO production. In vivo treatment with PAF antagonists significantly increased leishmania lesions, as well as the parasite load, in regional lymph nodes and spleens. These findings indicate that PAF is essential for the control of leishmania infection.
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Ye, Yao, Peng Lin, Junyan Zhu, Udo Jeschke, and Viktoria von Schönfeldt. "Multiple Roles of Prostaglandin E2 Receptors in Female Reproduction." Endocrines 1, no. 1 (May 6, 2020): 22–34. http://dx.doi.org/10.3390/endocrines1010003.

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Among prostaglandins, Prostaglandin E2 (PGE2) (PGE2) is considered especially important for decidualization, ovulation, implantation and pregnancy. Four major PGE2 receptor subtypes, EP1, EP2, EP3, EP4, as well as peroxisome proliferator-activated receptors (PPARs), mediate various PGE2 effects via their coupling to distinct signaling pathways. This review summarizes up-to-date literatures on the role of prostaglandin E2 receptors in female reproduction, which could provide a broad perspective to guide further research in this field. PGE2 plays an indispensable role in decidualization, ovulation, implantation and pregnancy. However, the precise mechanism of Prostaglandin E2 (EP) receptors in the female reproductive system is still limited. More investigations should be performed on the mechanism of EP receptors in the pathological states, and the possibility of EP agonists or antagonists clinically used in improving reproductive disorders.
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Ribeiro-Junior, Jerônimo Aparecido, Marcelo Franchin, Miriam Elias Cavallini, Carina Denny, Severino Matias de Alencar, Masaharu Ikegaki, and Pedro Luiz Rosalen. "Gastroprotective Effect of Geopropolis fromMelipona scutellarisIs Dependent on Production of Nitric Oxide and Prostaglandin." Evidence-Based Complementary and Alternative Medicine 2015 (2015): 1–5. http://dx.doi.org/10.1155/2015/459846.

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The aim of this study was to evaluate the gastroprotective activity of ethanolic extract of geopropolis (EEGP) fromMelipona scutellarisand to investigate the possible mechanisms of action. The gastroprotective activity of the EEGP was evaluated using model ulcer induced by ethanol. To elucidate the possible mechanisms of action, we investigated the involvement of the nonprotein sulfhydryl (NP-SH) groups, nitric oxide and prostaglandins. In addition, the antisecretory activity of EEGP was also evaluated by pylorus ligated model. The EEGP orally administrated (300 mg/kg) reduced the ulcerative lesions induced by the ethanol (P<0.05). Regarding the mechanism of action, the prior administration of nitric oxide and prostaglandins antagonists suppressed the activity of gastroprotective EEGP (P<0.05). On the other hand the gastroprotective activity of EEGP was kept in the group pretreated with the antagonist of the NP-SH groups; furthermore the antisecretory activity was not significant (P>0.05). These results support the alternative medicine use of geopropolis as gastroprotective and the activities observed show to be related to nitric oxide and prostaglandins production.
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Healy, DL. "Progesterone receptor antagonists and prostaglandins in human fertility regulation: a clinical review." Reproduction, Fertility and Development 2, no. 5 (1990): 477. http://dx.doi.org/10.1071/rd9900477.

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Progesterone receptor antagonists have been developed by substitutions at the 11-beta and 17 side-chain positions of the progestagen norethisterone. The most studied progesterone receptor antagonists are mifepristone (Mifegyne; Roussel-UCLAF; RU486) and ZK98734 and ZK98299 (Schering AG). These compounds bind avidly to the progesterone receptor and glucocorticoid receptor but have essentially no binding to the mineralocortocoid, oestrogen or androgen receptors. Mifepristone also binds avidly to albumin, resulting in a half-life of approximately 24 h after oral administration. Progesterone receptor antagonists can induce menstruation by a direct action upon the endometrium. They have also been shown to exert weak progesterone agonist actions in certain circumstances and to modulate pituitary hormone secretion by antagonizing the feedback actions of progesterone. Moreover, they release prostaglandin F2 alpha and E2 from human endometrium or early pregnancy decidua and reduce the metabolism of these eicosanoids. Clinically, progesterone receptor antagonists have been used in trials of menstrual regulation, abortion and induction of labour, and during treatment of breast or ovarian cancer, some forms of hypertension and meningioma. Progesterone receptor antagonists have been administered to approximately 70,000 women in 18 countries as medical abortifacients. They have been proven, especially when combined with prostaglandin analogues, to be as effective as surgical methods of termination of pregnancy. Progesterone receptor antagonists have focussed international attention on menstrual regulation, abortion and the rights of women to regulate their fertility.
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Healy, David L. "Prostaglandins and Progesterone Receptor Antagonists in Human Fertility Regulation." Australian and New Zealand Journal of Obstetrics and Gynaecology 34, no. 3 (June 1994): 357–60. http://dx.doi.org/10.1111/j.1479-828x.1994.tb01089.x.

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Knauss, T., and H. E. Abboud. "Effect of serotonin on prostaglandin synthesis in rat cultured mesangial cells." American Journal of Physiology-Renal Physiology 251, no. 5 (November 1, 1986): F844—F850. http://dx.doi.org/10.1152/ajprenal.1986.251.5.f844.

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Serotonin (5-hydroxytryptamine) (5-HT) is a potent vasoactive amine that reduces renal blood flow and glomerular filtration rate. Vasodilator prostaglandins (PGs) modulate the effects of several vasoconstrictors on the renal circulation. Since mesangial cells are smooth muscle-like cells that may regulate glomerular hemodynamics, we studied the effect of 5-HT on PGs synthesis in rat cultured mesangial cells. 5-HT (10(-6)-10(-3) M) resulted in progressive stimulation of prostaglandin E2 (PGE2) synthesis. Significant stimulation in response to 10(-4) M 5-HT started after 2 min of incubation and progressively increased for at least 30 min. This effect was structurally specific for the 5-HT receptor since indole-containing precursors and metabolites of 5-HT as well as the aminergic compounds, adenosine, and dopamine were without effect. Moreover, 5-HT receptor antagonists, but not histaminergic or beta-adrenergic antagonists, abolished 5-HT-stimulated PGE2 synthesis. 5-HT also stimulated prostacyclin (measured as 6-ketoprostaglandin F1 alpha) but not thromboxane synthesis in the same cell cultures. 5-HT-stimulated PGE2 synthesis was not affected by extracellular calcium depletion but was abolished by preincubating the cells with the intracellular calcium antagonist 8-(N,N-diethylamine)-octyl-3,4-5 trimethoxybenzoate (10(-5) M). These studies show that 5-HT stimulates PGE2 and prostacyclin (PGI2) synthesis in mesangial cells via a mechanism dependent on intracellular calcium. These vasodilator PGs may modulate the effect of 5-HT on renal and specifically glomerular hemodynamics.
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Gulla, Surendra, Dakshayani Lomada, Anusha Lade, Reddanna Pallu, and Madhava C. Reddy. "Role of Prostaglandins in Multiple Sclerosis." Current Pharmaceutical Design 26, no. 7 (March 25, 2020): 730–42. http://dx.doi.org/10.2174/1381612826666200107141328.

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: Multiple sclerosis (MS) is an autoimmune demyelinating disorder with chronic inflammation in the central nervous system, manifested by both physical and cognitive disability. Neuroinflammation and neurodegeneration are the phenomena that appear in the central nervous system associated with various neurodegenerative disorders, including MS, Alzheimer’s diseases, amyotrophic lateral sclerosis and Parkinson’s disease. Prostaglandins are one of the major mediators of inflammation that exhibit an important function in enhancing neuroinflammatory and neurodegenerative processes. These mediators would help understand the pathophysiology of MS as the combination of antagonists or agonists of prostaglandins receptors could be beneficial during the treatment of MS. The present review focuses on the role played by different prostaglandins and the enzymes which produced them in the etiopathogenesis of MS.
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Fattahi, Mohammad Javad, and Abbas Mirshafiey. "Prostaglandins and Rheumatoid Arthritis." Arthritis 2012 (November 7, 2012): 1–7. http://dx.doi.org/10.1155/2012/239310.

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Rheumatoid arthritis (RA) is a chronic, autoimmune, and complex inflammatory disease leading to bone and cartilage destruction, whose cause remains obscure. Accumulation of genetic susceptibility, environmental factors, and dysregulated immune responses are necessary for mounting this self-reacting disease. Inflamed joints are infiltrated by a heterogeneous population of cellular and soluble mediators of the immune system, such as T cells, B cells, macrophages, cytokines, and prostaglandins (PGs). Prostaglandins are lipid inflammatory mediators derived from the arachidonic acid by multienzymatic reactions. They both sustain homeostatic mechanisms and mediate pathogenic processes, including the inflammatory reaction. They play both beneficial and harmful roles during inflammation, according to their site of action and the etiology of the inflammatory response. With respect to the role of PGs in inflammation, they can be effective mediators in the pathophysiology of RA. Thus the use of agonists or antagonists of PG receptors may be considered as a new therapeutic protocol in RA. In this paper, we try to elucidate the role of PGs in the immunopathology of RA.
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Dissertations / Theses on the topic "Prostaglandins Antagonists"

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Ratzlaff, Viviane. "Padronização e validação de um novo modelo de febre induzida pela injeção intratecal de prostaglandina e2 em ratos jovens." Universidade Federal de Santa Maria, 2006. http://repositorio.ufsm.br/handle/1/11148.

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The fever response, besides being part of host defense response to infection or inflammation, is associated with discomfort and anxiety and may constitute a risk for febrile seizures in children. Therefore, antipyretic therapy is routinely prescribed for febrile patients. The animal models of fever using the systemic injection of lipopolysaccharide (LPS) and Baker yeast, described in the literature, are suitable for screening of novel antipyretics, but they do not provide information regarding the mechanism of action of these compounds. Therefore, the present study aimed to describe and validate a model of fever induction by prostaglandin (PG) E2, the final mediator of febrile response in the central nervous system, in young male Wistar rats (25-30 days of age). In this protocol, PGE2 was injected intrathecally without implantation of cannula. Rectal temperature (TR) was recorded every thirty minutes for three hours after PGE2 injection (08:00 11:00 h). The intrathecal (i.t.) injection of PGE2 10 ηg in 100 μL/animal induced fever in the animals, which was prevented by administration of EP1 and EP3 receptors antagonists, but did not by antagonist of EP4 receptor. In addition, the classic antipyretics dipyrone and acetaminophen, at doses that had no effect per se on TR of animals, did not revert the fever induced by i.t. injection of PGE2. This model seems suitable to investigate whether the action of antipyretics occurs upstream or downstream the prostaglandin coupling in EP receptors. In addition, this protocol is advantageous from the technical, ethical and economical point of view compared to others PGE2-induced fever protocols described in the literature, because trepanation for cannula implantation is not required, reducing the inflammatory response, animals suffering and experimental costs.
A febre, apesar de fazer parte da resposta de defesa do hospedeiro à infecção ou inflamação, está associada com desconforto e ansiedade, além de representar um risco iminente de convulsões febris em crianças. Por isso, terapia antipirética é rotineiramente prescrita a pacientes febris. Os modelos animais de febre empregando a injeção sistêmica de lipopolissacarídeo (LPS) e fermento de padeiro, descritos na literatura, são úteis para a triagem de novos antipiréticos, mas não fornecem informações a respeito do mecanismo de ação desses compostos. Diante disso, o presente estudo objetivou padronizar e validar um modelo de indução de febre por prostaglandina (PG) E2, o mediador final da resposta febril no sistema nervoso central, em ratos machos jovens da raça Wistar (25-30 dias). Neste protocolo, a PGE2 foi injetada pela via intratecal (i.t.), não necessitando a implantação de cânula. A temperatura retal (TR) foi registrada a cada trinta minutos durante três horas após a injeção da PGE2 (08:00-11:00 h). A injeção i.t. de PGE2 10 ηg em 100 μL/animal induziu febre nos animais, a qual foi prevenida pela administração de antagonistas dos receptores EP1 e EP3, mas não por antagonista do receptor EP4. Além disso, os antipiréticos clássicos dipirona e paracetamol, em doses que não tiveram efeito per se na TR dos animais, não reverteram a febre induzida por PGE2 i.t. Este modelo parece útil para investigar se a ação dos antipiréticos ocorre antes ou depois da ligação da PGE2 em seus receptores EP. Além disso, este protocolo é vantajoso do ponto de vista técnico, ético e econômico em relação aos outros protocolos de indução de febre por PGE2 descritos na literatura, porque a trepanação para implantação de cânula não é necessária, reduzindo a resposta inflamatória, o sofrimento dos animais e os custos experimentais.
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Perrin, Véronique. "Synthèse et caractérisation pharmacologique de nouveaux antagonistes potentiels des récepteurs du thromboxane A2." Lyon 1, 1996. http://www.theses.fr/1996LYO10314.

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Le thromboxane a#2 est un puissant constricteur des muscles lisses vasculaires et respiratoires ainsi qu'un agent de l'agregation plaquettaire. Il est implique dans des pathologies respiratoires, cardiovasculaires et renales. Compte tenu de l'etude des caracteristiques communes a de nombreux antagonistes connus, notre but etait de preparer des antagonistes des recepteurs du thromboxane a#2 possedant une structure 2-azanorbornane et ayant une fonction sulfone sur l'atome d'azote, ainsi que la chaine superieure, plus ou moins modifiee, des prostaglandines. Les differentes molecules obtenues ont ensuite ete soumises a des tests pharmacologiques in vivo sur les recepteurs vasculaires chez le rat conscient et in vitro sur les recepteurs plaquettaires chez le cobaye ; alors que les tests in vitro se sont averes en majorite negatifs, les tests in vivo ont permis de mettre en evidence une activite antagoniste sur les recepteurs vasculaires
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Eckert, David. "The Prostaglandin E2 Receptor 1 (EP1) Antagonizes AngII in the Collecting Duct." Thesis, Université d'Ottawa / University of Ottawa, 2017. http://hdl.handle.net/10393/36196.

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Prostaglandin E2 (PGE2), a metabolite of arachidonic acid, plays a role in water and sodium reabsorption in the collecting duct of the kidney. The collecting duct is responsible for the fine tuning of water and electrolytes. Only a small fraction of the filtered water and sodium is reabsorbed in the collecting duct, a fraction crucial to the regulation of water and electrolyte balance. This current study addresses the role of EP1, one of four PGE2 receptors, in the collecting duct. It is well documented that PGE2 inhibits sodium and water reabsorption in the collecting duct, however the exact mechanism is still debated. To determine whether the EP1 receptor mitigates AngII renal effects, an in vivo study was performed with EP1-/- mice. Global EP1-/- knockout mice were crossed with a renin overexpressing mouse line (herein denoted as “Ren”) and subjected to a high salt (HS) and low salt (LS) diet. Ren mice displayed an 11mmHg increase in systolic blood pressure (BP) on a HS diet and a decrease in BP of 14mmHg on a LS diet compared to the normal salt (NS) diet. Ren EP1-/- mice did not display a significant increase or decrease in BP on a HS or LS diet. On a LS diet, Ren EP1-/- displayed a drop in urine osmolarity (1641 mOsm/ kgH2O) vs. wild type (WT) mice (2107 mOsm/ kgH2O), consistent with increased sodium reabsorption. Narrowing in on the collecting duct, Ren EP1-/- mice had enhanced αENaC levels compared to Ren mice. In ex vivo microperfusion experiments, EP1-/- tubules show no response to PGE2 in the presence of AVP, whereas PGE2 inhibits AVP induced water reabsorption in WT mice. An increase in αENaC membrane accumulation due to EP1 gene ablation results in increased sodium reabsorption subsequently leading to a rise in BP. This contributes to the lack of salt sensitivity in EP1-/- mice. Overall, the EP1 receptor in the collecting duct represents a potential therapeutic target for the treatment of hypertension.
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Fukuda, Miyuki. "Exacerbation of Intracranial Aneurysm and Aortic Dissection in Hypertensive Rat Treated With the Prostaglandin F-Receptor Antagonist AS604872." Kyoto University, 2016. http://hdl.handle.net/2433/204574.

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Riveron, Véronique. "Synthèse et étude de nouveaux antagonistes potentiels du thromboxane A2 et de la prostaglandine H2 faisant intervenir un squelette 2-azanorbornane." Lyon 1, 1993. http://www.theses.fr/1993LYO10293.

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Le thromboxane a2 est un puissant agent constricteur des muscles lisses et un agregant des plaquettes sanguines. Il intervient dans des pathologies cardiovasculaires et respiratoires. Au vu de la litterature, notre but etait d'obtenir des antagonistes des recepteurs du thromboxane a2 ayant un squelette 2-azanorbornane et incluant une fonction sulfonee sur l'azote, ainsi que la chaine alpha des prostaglandines (6 ou 7 atomes de carbone). La molecule finale comportant la chaine 5-hexenoique, a ete testee sur les recepteurs vasculaires chez le rat conscient normo-tendu, par observation des reponses du u 46619, agoniste connu des memes recepteurs: il s'est avere presenter une activite partielle et fugace a la dose de 50 mg/kg
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Traversa, Christel. "Synthèse et étude de nouveaux antagonistes potentiels du thromboxane A2 à partir d'aza-7-norbornadiènes." Lyon 1, 1994. http://www.theses.fr/1994LYO10305.

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Le thromboxane a#2 est un puissant agent constructeur des muscles lisses et un agregant plaquettaire implique dans l'hypertension arterielle, l'infarctus du myocarde, l'asthme et des maladies renales. Nous basant sur des caracteristiques communes a un grand nombre d'antagonistes connus, nous avons synthetise des molecules presentant comme structure de base un squelette 7-azanorbornane et la chaine superieure, complete ou non, des prostaglandines. Le squelette est obtenu par une reaction de diels-alder thermique entre le pyrrole 1-carboxylate de tertiobutyle et l'acetylene dicarboxylate de methyle. Le cycloadduit obtenu a pu etre transforme en aldehyde-ester sature selon deux voies. La premiere, apres l'hydrure de lithium et d'aluminium ; cependant, l'aldehyde est obtenu en melange d'isomeres. La seconde voie donne, par saponification, hydrogenation puis reduction selective de l'acide, un isomere pur. Cet aldehyde nous a alors permis, par reaction de wittig, d'introduire la chaine superieure de prostaglandines a six atomes de carbone. La chaine complete a pu etre obtenue par homologation de l'aldehyde puis condensation de wittig. Apres modification du substituant de l'azote, les molecules obtenues ont ete biologiquement testees soit in vitro sur des plaquettes de cobaye, soit in vivo sur des rats conscients. D'autres etudes ont ete menees en parallele pour eliminer la fonction ester restante sur le cycle de base et pour introduire une seconde fonction azotee dans la molecule. Ces dernieres voies n'ont pu encore aboutir
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ÁVILA, Roberta Marques Dias de. "Planejamento, síntese e avaliação farmacológica de derivados indano-hidrazônicos, candidatos a protótipos de fármacos anti-inflamatórios." Universidade Federal de Alfenas, 2010. https://bdtd.unifal-mg.edu.br:8443/handle/tede/375.

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Os AINEs constituem uma importante classe de fármacos com aplicações terapêuticas que já têm sido utilizadas por mais de um século. A evolução do tratamento de doenças inflamatórias crônicas, tais como artrite reumatóide e a osteoartrite tem seu marco a partir da indometacina, um dos representantes dos AINEs tradicionais, para posterior ascensão e mais recentemente o desuso de inibidores com grande seletividade para PGHS-2. O esforço para a descoberta de um fármaco mais seguro e eficaz continua a ser um desafio e a busca por novos agentes antiinflamatórios e analgésicos tem levado ao planejamento e a obtenção de inúmeras acil e arilidrazonas ativas de diversos padrões estruturais. Existem vários ligantes ativos capazes de atuar sobre a cascata do ácido araquidônico cujos resultados identificaram as subunidades acil e arilidrazônicos como grupo farmacofórico importante para inibição do processo inflamatório. Apesar da racionalização dos resultados obtidos e de estudos da relação estrutura-atividade no perfil biológico das subunidades acil e arilidrazonas, não foi possível até o momento identificar de fato o mecanismo de ação de tais grupamentos. O safrol, que é um alilbenzeno de distribuição ampla no reino vegetal, possui propriedades físico-químicas interessantes para ser utilizado como um produto de partida para a síntese das novas moléculas planejadas, sendo amplamente empregado em projetos de pesquisas no Laboratório de Fitoquímica e Química Medicinal (LFQM) na Universidade Federal de Alfenas (Unifal- MG). Este trabalho descreve o planejamento e síntese de novos derivados indanohidrazônicos candidatos a protótipos de fármacos anti-inflamatórios. A rota sintética foi planejada em três etapas, utilizando reagentes de baixo custo e metodologias relativamente simples. Os compostos planejados e obtidos foram avaliados com o intuito de se observar o efeito anti-inflamatório a partir de ensaios preliminares (número de contorções abdominais induzidas por ácido acético) realizadas no Instituto Biomédico da Universidade Federal Fluminense – UFF. Foi possível identificar que todos os congêneres apresentaram inibição sendo que os mais ativos da série das moléculas sintetizadas foram os derivados (1c) e (1e) com 51,0% e 48,6% de inibição das contorções abdominais induzidas por ácido acético, respectivamente.
NSAIDs are an important class of drugs with therapeutic applications that have already been used by more than a century. The evolution of treatment of chronic inflammatory diseases such as rheumatoid arthritis and osteoarthritis has its mark from indomethacin, one of the representatives of traditional NSAIDS for later rise and more recently the disuse of inhibitors with high selectivity for PGHS-2. The effort to discover safer and more effective drug remains a challenge and the search for new anti-inflammatory agents and analgesics have led to the planning and the discovery of numerous active acyl and aryl-hydrazones. And there are several active ligands able to act on the arachidonic acid cascade results identified subunits acyl and aryl-hydrazones as important pharmacophore for inhibition of the inflammatory process. Despite the rationalization of the results and studies of structure-activity relationship in the biological profile of the subunits acyl and aryl-hydrazones, we could not yet identify because of the mechanism of action of such groups. Safrole, which is a allylbenzene wide distribution in the plant kingdom, has interesting physical and chemical properties for use as a starting product for the synthesis of new molecules designed and is widely used in research projects at the Laboratory of Phytochemistry and Medicinal Chemistry . This paper describes the design and synthesis of new indane-hydrazone candidates prototype antiinflammatory drugs. The synthetic route was planned in three stages, using reagents of low cost and relatively simple methods. The compounds obtained were planned and evaluated in order to observe the anti-inflammatory effect from preliminary tests (number of writhing induced by acetic acid) held in the Biomedical Institute of Universidade Federal Fluminense - UFF. It was possible to identify all congeners showed that inhibition was the most active of the series of synthesized molecules was derived (1c) and (1e) with 51.0% and 48.6% inhibition of writhing induced by acetic acid.
Coordenação de Aperfeiçoamento de Pessoal de Nível Superior - CAPES
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Günther, Jan [Verfasser]. "Prostaglandin-EP3-Rezeptor-vermittelte Hemmung der Monoamin-Freisetzung in Nagergewebe : Beweis mit dem kompetitiven Antagonisten L 826266 / Jan Günther." Bonn : Universitäts- und Landesbibliothek Bonn, 2015. http://d-nb.info/1080592016/34.

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Wisehart, Veronica. "An antagonist of the prostaglandin F2α receptor (FP)- Gaq-dependent respone, biases FP into mitogen-activated protein kinase (MAPK) signalling through epidermal growth factor receptor (EGFR) transactivation." Thesis, McGill University, 2011. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=96903.

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The F prostanoid receptor (FP receptor) is a GPCR that, upon binding of prostaglandin F2alpha (PGF2alpha), mediates IP3 production and PKC-dependent MAPK activation. We report that AL-8810, a characterized antagonist for PGF2alpha-dependent IP3 production, potently activates ERK1/2 in a PKC-independent manner, since PGF2alpha induced PKCbeta1-GFP translocation, while AL-8810 did not. AL-8810, though, induced EGFR phosphorylation, and the resultant ERK1/2 activation was inhibited by an EGFR antagonist, which suggested a transactivation signalling pathway. Batimastat, a matrix metalloprotease (MMP) inhibitor abolished both AL-8810- and PGF2alpha-induced ERK1/2, and therefore PGF2alpha may also signal through EGFR-independent transactivation. In osteoblasts, both PGF2alpha and AL-8810 activated MAPK in an EGFR-dependent manner, though PKC remained essential for PGF2alpha, as IL-6 and cell proliferation (known PKC effects) were induced by PGF2alpha but not AL-8810. Here, we highlight the biased signalling of AL-8810 on FP receptor produced MAPK through EGFR-MMP-mediated transactivation and also suggest a novel PGF2alpha-induced PKC-MMP, EGFR-independent, pathway.
Le récepteur F-prostanoïde (FP) est un récepteur de la famille des RCPG (récepteurs couplés aux protéines G), qui, une fois lié par son ligand naturel, la prostaglandine F2alpha (PGF2alpha), induit la production d'IP3, menant à l'activation de la protéine kinase C (PKC) suivie de l'activation des MAP kinases ERK1/2. Dans ce manuscrit, nous démontrons que l'AL-8810, étant reconnu comme un antagoniste de la production d'IP3 induite par le PGF2alpha, est capable d'activer la voie des ERK1/2 d'une manière indépendante à la PKC. En effet, nous démontrons que la PKCbeta1-GFP transloque à la membrane plasmique suite au traitement avec la PGF2alpha, alors que l'AL-8810 n'induit aucune translocation. Cependant, l'AL-8810, contrairement à la PGF2alpha, est capable d'induire la phosphorylation du récepteur à l'EGF (EGFR), menant à l'activation de ERK1/2. La phosphorylation de l'EGFR induite par l'AL-8810 est blocable par une antagoniste de l'EGFR, suggérant un mécanisme de transactivation de ce dernier. De plus, le batimastat, un inhibiteur non-spécifique des métalloprotéases matricielles (MMP) abolit l'induction des ERK1/2 par la PGF2alpha ainsi que par l'AL-8810, suggérant que la PGF2alpha signale probablement par un mécanisme indépendant de la transactivation de l'EGFR. Dans des cellules ostéoblastes, la PGF2alpha et l'AL-8810 activent ERK1/2 d'une manière dépendante au EGFR, même si la PKC demeure essentielle pour l'activation des voies en aval de la PGF2alpha, puisque l'interleukine-6 et la prolifération cellulaire (tous deux dépendants de la PKC) sont induits seulement par la PGF2alpha. En conclusion, nous montrons l'activation biaisée du FP par l'AL-8810 menant à l'activation de ERK1/2 via un mécanisme de transactivation par la voie EGFR-MMP. Ces résultats suggèrent aussi un nouveau mécanisme d'activation de ERK1/2 indépendant du EGFR et induit par la voie PKC-MMP.
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Khalid, Saifudin. "Inhalational cough challenges in the assessment of cough." Thesis, University of Manchester, 2013. https://www.research.manchester.ac.uk/portal/en/theses/inhalational-cough-challenges-in-the-assessment-of-cough(8788e20e-3f76-4600-bdc1-e9bee31b5c01).html.

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Introduction: Cough is the commonest reason for which medical advice is sought. In assessment of chronic cough and in developing anti-tussive medications, inhalational cough challenges with capsaicin and citric acid are commonly employed. However the ability of these inhalational cough challenges to distinguish health and disease is not clear and it is not known which end point is best in making such assessments. Methods: Subjects belonging to five different categories (healthy volunteers, subjects with COPD, asthma, healthy current smokers and chronic cough) were compared with each another by using the standard cough challenges employing Capsaicin and Citric acid and also by using newer inhalational cough challenge agents such as prostaglandin E2 and bradykinin. In addition adaptation to repeated inhalations of tussive agents was also assessed. The relationship between the cough reflex sensitivity as gauged by using inhalational cough challenge tests and objective cough recording was explored in all five groups. Finally the change in C5 in Capsaicin evoked cough by using a substance to block TRPV1 channel and its effect on objective cough recording was assessed in subjects with chronic cough. Results: Different tussive agents have different abilities to distinguish between different diagnostic categories and a combination of inhalational cough challenge tests have a better accuracy of predicting diagnostic groups as compared to one on its own. There are significant differences in the rates of adaptation to repeated inhalations of PGE2 and there is a significant reduction in cough response over period of time in all disease groups. Using the TRPV1 antagonist resulted in a modest increase in the Log C5 concentration of capsaicin but this was not matched by a change in objective cough recording or CQLQ scores. Conclusions: The different abilities of tussive agents to distinguish between different diagnostic categories suggest that the information conveyed by the one inhalational cough challenge test is different from that by another test. The choice of the inhalational cough challenge test should therefore depend on which groups are included in the study. There was no significant difference in the rate of adaptation to prolonged challenge with citric acid or capsaicin and no significant correlation of the magnitude of adaptation with objective cough recording suggesting that this is unlikely to be responsible for the increased cough rates seen in diseases such as chronic cough, COPD or asthma. The TRPV1 antagonist did not result in a significant change in objective cough recording or CQLQ scores. The change in C5 with the TRPV1 antagonist was however modest and this may be reason for this study failing to show a relationship between these different measures.
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Books on the topic "Prostaglandins Antagonists"

1

NATO Advanced Study Institute on Prostanoids and Drugs (1988 Erice, Italy). Prostanoids and drugs. New York: Plenum Press, 1989.

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Karim, Sultan M. M. Practical Applications of Prostaglandins and their Synthesis Inhibitors. Springer, 2012.

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Marc, Bygdeman, Berger Gary S, and Keith Louis G, eds. Prostaglandins and their inhibitors in clinical obstetrics and gynaecology. Lancaster: MTP Press, 1986.

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Bygdeman, Marc. Prostaglandins and their Inhibitors in Clinical Obstetrics and Gynaecology. Springer, 2012.

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Marc, Bydgeman, Berger Gary S, and Keith Louis G, eds. Prostaglandins and their inhibitors in clinical obstetrics and gynaecology. Lancaster: MTP Press, 1986.

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Prostanoids and Drugs. Springer, 1990.

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Samuelson, B. Prostanoids and Drugs. Springer, 2012.

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Samuelson, B. Prostanoids and Drugs. Springer, 2012.

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1934-, Harris Jules E., Braun Donald P, and Anderson Kenning M, eds. Prostaglandin inhibitors in tumor immunology and immunotherapy. Boca Raton: CRC Press, 1994.

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Iversen, Leslie. Endocannabinoids. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780190846848.003.0004.

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The endocannabinoids are part of a large family of lipid signaling molecules derived from arachidonic acid, including the prostaglandins and leukotrienes, which are important mediators of inflammation. Far less is known about the newer members of the endocannabinoid group, and it remains unclear whether they all play important functional roles. This chapter reviews the multiple members of this family and their biosynthesis and inactivation. Physiological functions, including retrograde synaptic signaling, control of energy metabolism, regulation of pain sensitivity, and cardiovascular control, are discussed. In addition, the chapter reports the synthesis of novel agonists, antagonists, and compounds inhibiting endocannabinoid inactivation as novel medicines.
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Book chapters on the topic "Prostaglandins Antagonists"

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Ford-Hutchinson, A. W. "Therapeutic Aspects of Leukotriene Antagonists and Inhibitors." In Prostaglandins, Leukotrienes, Lipoxins, and PAF, 431–37. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4899-0727-1_41.

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Ford-Hutchinson, A. W. "Novel Leukotriene D4 Receptor Antagonists and 5-Lipoxygenase Inhibitors: Implications in Human Disease." In Prostaglandins and Leukotrienes in Gastrointestinal Diseases, 50–54. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73316-1_11.

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Ruppin, H. "Ulcer Healing Drugs and Endogenous Prostaglandins: Carbenoxolone, Antacids, Sucralfate, Bismuth, and H2-Receptor Antagonists." In Prostaglandins and Leukotrienes in Gastrointestinal Diseases, 213–22. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73316-1_43.

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Mest, H. J., T. Rein, A. Riedel, W. Köpernik, and C. Brequet. "Effect of BN 52256 and Other Mediator Antagonists on Ouabain-Induced Ventricular Fibrillation in Sensitized Guinea-Pigs and on Ischemia-Induced Fibrillation in Rats." In Prostaglandins in the Cardiovascular System, 228–34. Basel: Birkhäuser Basel, 1992. http://dx.doi.org/10.1007/978-3-0348-7262-1_32.

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Fritsch, W. P. "Benefits and Risks of Long-term Medical Therapy with Histamine H2-receptor Antagonists in Ulcer Disease — A Physician’s View." In Prostaglandins and Leukotrienes in Gastrointestinal Diseases, 291–95. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73316-1_58.

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Schumpelick, V., G. Arlt, and G. Winkeltau. "Benefits and Risks of Long-term Medical Therapy with Histamine H2-Receptor Antagonists in Ulcer Disease: A Surgeon’s View." In Prostaglandins and Leukotrienes in Gastrointestinal Diseases, 296–301. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73316-1_59.

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Pill, J., J. Metz, K. Stegmeier, and F. Hartig. "Effects of Daltroban, a Thromboxane (TX) A2 Receptor Antagonist, on Lipid Metabolism and Atherosclerosis." In Prostaglandins in the Cardiovascular System, 107–13. Basel: Birkhäuser Basel, 1992. http://dx.doi.org/10.1007/978-3-0348-7262-1_16.

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Darius, Harald, Jutta Michael-Hepp, and Jürgen Meyer. "Receptor Binding Properties of the New and Specific Thromboxane Receptor Antagonist Bay U 3405." In Prostaglandins in the Cardiovascular System, 157–61. Basel: Birkhäuser Basel, 1992. http://dx.doi.org/10.1007/978-3-0348-7262-1_21.

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Pettipher, Roy, and Trevor T. Hansel. "Antagonists of the prostaglandin D2 receptor CRTH2." In New Drugs and Targets for Asthma and COPD, 193–98. Basel: KARGER, 2010. http://dx.doi.org/10.1159/000320819.

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Benetos, Athanassios, Haralambos Gavras, John M. Stewart, Raymond Vavrek, Simon Hatinoglou, and Irene Gavras. "The Antihypertensive Contribution of Bradykinin as Assessed by a Specific Bradykinin Antagonist." In Vasodepressor Hormones in Hypertension: Prostaglandins and Kallikrein-Kinins, 355–64. Basel: Birkhäuser Basel, 1987. http://dx.doi.org/10.1007/978-3-0348-9299-5_37.

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Conference papers on the topic "Prostaglandins Antagonists"

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Van Nueten, J. M., W. J. Janssens, and F. De Clerck. "VASOCONSTRICTION IN RESPONSE TO HUMAN PLATELET-VESSEL WALL INTERACTIONS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644598.

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Human blood platelets, stimulated with thrombin, induced contractions of isolated basilar artery segments of the dog. These platelet-mediated vascular contractions were inhibited in a concentration-dependent way by flunarizine, a Ca2+-entry blocker, selective for vascular tissues. This inhibition increased gradually as a function of time after contact with flunarizine to reach its maximum after 60-90 min. Biochemical and pharmacological analyses, using the 5-HT2-serotonergic antagonist ritanserin, the thromboxane A2/prostaglandin endo-peroxide antagonist BM 13.177 and the fatty acid cyclo-oxygenase inhibitor suprofen, showed that 5-hydroxytryptamine and prostanoids (thromboxane A2, prostaglandine endoperoxides) were the main mediators involved. They further suggested amplification between 5-hydroxytryptamine and prostanoids at the vascular level.(1) Incubation period; (2) Inhibition of platelet-mediated vascular contractions.This study demonstrates that 5-hydroxytryptamine, acting in concert with thromboxane A2 and/or prostaglandine-endoper-oxides, is responsible for the vasoconstrictor effects of aggregating platelets. It further indicates that influx of calcium ions is involved in these vasoconstrictor responses.
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Van Diest, M. J., T. J. Verbeuren, and A. G. Herman. "RELAXATIONS INDUCED BY LIPOXYGENASE METABOLITES OF ARACHI-DONIC ACID IN SPLENIC ARTERIES OF THE DOG." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643796.

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The lipoxygenase metabolites of arachidonic acid, 15 hydroperoxyeicosatetraenoic acid (15HPETE) and its hydroxy derivative (15HETE) evoke contractions in a variety of isolated blood vessels. We recently were able to show that thromboxane A2 (TXA2)-receptor antagonists BM13177 and BM13505 suppress the contractions induced by lipoxygenase metabolites in canine splenic arteries, and that these compounds also inhibit the contractile effects of PGF2α and of the TXA2-mimetic U46619. We also reported that 15HETE and 15HPETE cause relaxations of isolated dog arteries when the tissues are contracted with prostaglandin F2α (PGF2α) or with U46619 and suggested that lipoxygenase metabolites may act as endogenous antagonists towards prostaglandin receptors. The present study was designed to investigate the effects of lipoxygenase metabolites of arachidonic acid in isolated splenic arteries in which the tone is raised by various agonists.Segments of canine splenic arteries with or without endothelium were placed in organ chambers filled with Krebs-Ringer solution at 37°C for isometric tension recording. Responses to 15HPETE were obtained in segments which were contracted with serotonin, K+, PGF2α or noradrenaline (the latter with or without BM13505); concentrations causing comparable levels of contraction were selected. HPETE evoked relaxations in segments with and without endothelium, during the contractions evoked by K+, PGF2α and noradrenaline (with or without BM13505). At higher concentrations, 15HPETE caused relaxations only during contractions induced by PGF2α and noradrenaline with BM13505. Our results suggest that 15HPETE can cause relaxations by two different mechanisms :(1) 15HPETE may act as an antagonist to PGF2α, which causes its contraction via the TXA2-receptor and,(2) in presence of BM13505, it suppresses the contractions to noradrenaline via an endothelium independent mechanism.
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Hatmi, M., A. Del Maschio, J. Lefort, G. De Gaetano, B. B. Varqaftiq, and C. Cerletti. "EFFECTS OF SULFINPYRAZONE AND ITS METABOLITE G25671 ON PLATELET ACTIVATION AND DESENSITIZATION AND ON BRONCHOCONSTRICTION INDUCED BY THE PROSTAGLANDIN ENDOPEROXIDE ANALOGUE U46619." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643854.

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In previous studies we have found (Br. 3. Pharmac. 85, 849, 1985) that a) human platelets pre-exposed to arachidonic acid or to the endoperoxide analogue, U46619 and then washed and resuspended, fail to respond to a second challenge by both arachidonic acid and U46619; b) desensitization by arachidonic acid and U46619 occurs at a site sensitive to endoperoxides / thromboxane (Tx) receptor antagonists; c) the desensitizing effects of U46619 are direct, whereas those of arachidonic acid are mediated by a cyclooxygenase-dependent metabolite. Sulfinpyrazone (100 μM) and its thioether metabolite G25671 (50 μM) are known to suppress arachidonic acid-induced platelet aggregation and TxB2 formation (Eur. 3. Pharmac, 101, 209, 1984). We now demonstrate that the presence of sulfinpyrazone or G25671 during platelet exposure to arachidonic acid or U46619 prevents desensitization. Platelet activation by the endoperoxide analogue U46619 is also prevented by sulfinpyrazone or G25671 (0.3-1 mM). The threshold aggregating concentrations of arachidonic acid and U46619 in healthy subjects before and after oral treatment with sulfinpyrazone were elevated by 2-3 fold and a good correlation between ex vivo and in vitro findings was established. We finally examined the actions of sulfinpyrazone and G25671 on the bronchoconstriction in vivo and parenchymal lung strip contraction in vitro induced by U46619. Neither drug had any preventive effect.Our results demonstrate that sulfinpyrazone and its metabolite G25671 are not only cyclooxygenase inhibitors but can also act as endoperoxide/Tx antagonists and indicate clearly that antagonism of U46619 by both drugs is selective for platelets.
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Nonomura, Kazuhiko, Katsuyoshi Miyama, Kiyoshi Kanazawa, Takako Okumura, Yoshiyuki Okumura, Masanobu Oshima, Satoru Takahashi, and Yukinori Take. "Abstract 893: Anticancer effect and mechanism of prostaglandin E2 receptor EP4 antagonist." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-893.

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Chen, Wentao, Rowie Borst, Jian Luo, Mohammad M. Chizari, Luisa Chocarro De Erauso, Veit J. Erpenbeck, Shamsah Kazani, David A. Sandham, and Luzheng Xue. "Fevipiprant antagonises prostaglandin D2-induced activation of type-2 CD8 T cells (Tc2)." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.oa4953.

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Szczeklik, A., R. J. Gryglewski, and M. Wandzilak. "THE EFFECT OF SIX PROSTAGLANDINS, PROSTACYCLIN AND ILOPROST ON GENERATION OF SUPEROXIDE ANIONS (0J) BY HUMAN NEUTROPHILS (PMNs) ACTIVATED BY ZYMOSAN OR FMLP." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643160.

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Human PMNs in a suspension (2.5 - 3.5 × 106 cells/ml of PBS) were activated by opsonized zymosan (2.5 mg/ml) or by FMLP (22 jjg/ml) in presence or absence of prostaglandins (PG) E1 E2, D2, 6-keto-F2α, 6-keto-E1 prostacyclin and Iloprost (3nM -30 pM). The generation of superoxide anions was measured as a SOD-sensitive reduction of ferrocytochrome c. In FMLP-stimulated PMNs an average production of 0- 2 of 18 ± 3.2 nmoles/10- 2 PMNs/10 min was suppressed by 25% at following concentrations of PGD2, PGE2, PGE1s 6-keto-PGE! and PGF2 : 0.1, 0.2, 0.5, 0.8 and>30.0 pM, respectively. No significant inhibition occurred in the presence of prostacyclin, 6-keto-PGF2 and Iloprost at concentrations as high as 30 pM. In zymosan-stimulated PMNs prostaglandins of E series were less potent inhibitors than in FMLP-stimulated PMNs by following factors: PGE2 - 20, 6-keto-PGE2 - 13, PGE1 - 4, whereas PGD2 was equally potent inhibitor in FMLP- and zymosan-stimulated PMNs. It is concluded that PGE2 is an antagonist of FMLP-receptor-mediated events which are responsible for the generation of superoxide anions in PMNs, whereas its isomer PGD2 has another mechanism of the 0- 2-suppressive action. Perhaps, PGD2 is a direct inhibitor of membrane-bound NADPH-oxidase or an antagonist of oxygen activation by leukotrienes and lipoxins or a promotor of scavenging of 0- 2 by mitochondrial membranes. The latter mechanism has been proposed recently by Gryglewski as explanation for cytoprotective action of stable biologically active metabolites of prostacyclin. Mechanisms of anti-0- 2 action of PGE1 and 6-keto-PGE1 in PMNs are likely to be intermediate between these proposed for PGE2 and PGD2.
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Ma, Xinrong, Namita Kundu, Peter Collin, and Amy M. Fulton. "Abstract 609: Frondoside antagonizes the prostaglandin E receptor EP4 and inhibits breast tumor metastasis." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-609.

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Shirakami, Yohei, Hiroyasu Sakai, Takahiro Kochi, Takayasu Ideta, Tsuneyuki Miyazaki, Masahito Shimizu, and Mitsuru Seishima. "Abstract 2805: Preventive effect of a prostaglandin E receptor EP4 antagonist RQ-00015986 on rat colon tumorigenesis." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-2805.

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Taylor Meadows, K., S. Sahdeo, S. Murphy, G. J. Opiteck, H. Ortega, L. Carter, and L. Salter-Cid. "GB001 Is a Differentiated Potent Prostaglandin D2 Antagonist with Long Receptor Residence Time and Extended Pharmacodynamic Efficacy." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a7417.

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Opiteck, Gregory, Kristen Taylor Meadows, Eric Butz, Scott Sugden, Richard Aranda, and Hector Ortega. "GB001, a selective prostaglandin D2 receptor 2 antagonist, blocks signaling in the peripheral blood of healthy subjects." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.1421.

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