Дисертації з теми "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.
Повний текст джерелаA 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.
Perrin, Véronique. "Synthèse et caractérisation pharmacologique de nouveaux antagonistes potentiels des récepteurs du thromboxane A2." Lyon 1, 1996. http://www.theses.fr/1996LYO10314.
Повний текст джерелаEckert, 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.
Повний текст джерелаFukuda, 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.
Повний текст джерелаRiveron, 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.
Повний текст джерелаTraversa, 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.
Повний текст джерелаÁVILA, 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.
Повний текст джерелаNSAIDs 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
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.
Повний текст джерелаWisehart, 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.
Повний текст джерелаLe 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.
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.
Повний текст джерелаTran-Drouin, Simon. "Sélectivité fonctionnelle de ligands orthostériques du récepteur FP de la PGF[indice inférieur 2alpha]." Mémoire, Université de Sherbrooke, 2010. http://savoirs.usherbrooke.ca/handle/11143/4054.
Повний текст джерелаSantos, Fabio Pereira Mesquita dos. "PGD2 e inflamação eosinofílica: mecanismos moleculares e potencial como alvo terapêutico." reponame:Repositório Institucional da FIOCRUZ, 2011. https://www.arca.fiocruz.br/handle/icict/5909.
Повний текст джерелаMade available in DSpace on 2012-11-30T11:59:08Z (GMT). No. of bitstreams: 1 fabio_p_m_santos_ioc_bcm_0037_2011.pdf: 10305796 bytes, checksum: 74de5b830c8354cd532f74bd40993c6a (MD5) Previous issue date: 2011
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Rio de Janeiro, RJ, Brasil.
Durante a resposta alérgica, dentre os vários mediadores inflamatórios de natureza lipídica, a prostaglandina D2 (PGD2) é considerada um mediador-chave. Em adição aos seus conhecidos efeitos quimiotáticos para eosinófilos, recentemente, foi descrito que a PGD2 é também capaz de promover a ativação dos eosinófilos, induzindo a biogênese de corpúsculos lipídicos e a síntese de leucotrieno C4 (LTC4) nessas organelas recém-formadas. Esses efeitos são atribuídos a ação da PGD2 sobre seus 2 receptores – DP1 e DP2 – os quais encontram-se expressos de maneira constitutiva na membrana dos eosinófilos. Então, o objetivo principal do estudo foi identificar o receptor específico da PGD2 envolvido no mecanismo de síntese de LTC4 por eosinófilos estimulados com PGD2. In vivo, num modelo murino de pleurisia alérgica e induzida por PGD2, a utilização dos antagonistas seletivos do receptor DP1 (BW A868c) ou do receptor DP2 (CAY10471) inibiu a síntese de LTC4 nessas respostas inflamatórias. No entanto, somente BWA868C foi capaz de inibir a biogênese de corpúsculos lipídicos nos eosinófilos recrutados para o sítio inflamatório; enquanto que o tratamento com o CAY10471, diminuiu o número de eosinófilos infiltrantes na cavidade pleural, mas não inibiu a biogênese de corpúsculos lipídicos nessas poucas células recrutadas. In vitro, eosinófilos humanos purificados estimulados com PGD2 tiveram a síntese de LTC4 inibida tanto pelo pré-tratamento com BWA868c, quanto pelo prétratamento com CAY10471. Além disso, a ativação do receptor DP1, com seu agonista seletivo (BW245c) e a ativação do receptor DP2 com o agonista seletivo do receptor DP2 (DK-PGD2) corroborou a observação de que no processo de síntese de LTC4 nos eosinófilos, ambos os receptores são necessáior, pois somente quando ambos os receptores foram ativados simultaneamente foi observada síntese de LTC4 nos corpúsculos lipídicos recém-formados (Eicosacell). Além disso, caracterizamos que uma das vias de sinalização intracelular envolvida na formação de corpúsculos lipídicos é depende da ativação de proteína quinase A (PKA). Em um outro grupo de ensaios, investigamos a PGD2 como potencial alvo terapêutico em doenças alérgicas. Recentemente, foi descrito que o extrato aquoso de C. sympodialis e a warafteína (alcalóide isolado) têm propriedades antialérgicas, visto que não somente reduzem a eosinofilia, mas também, a biogênese de corpúsculos lipídicos, assim como a produção de leucotrienos cisteinados. Dessa forma, aqui demonstramos que os pré-tratamentos tanto com o extrato quanto com o alcalóide isolado, foram capazes de inibir a produção de PGD2 ocorrida durante a resposta alérgica. In vitro, embora a warafteína não tenha inibido a biogênese de corpúsculos lipídicos em eosinófilos induzida por PGD2, observamos que é capaz de bloquear a liberação de PGD2 por mastócitos ativados – mas, não a produção de PGE2 por macrófagos ativados com A23187 – demonstrando que o mecanismo de ação dos seus efeitos antiinflamatórios não parecem envolver antagonismo de receptores em eosinófilos, e sim inibição da síntese da PGD2 em sítios alérgicos.
During allergic response, among several lipid mediators produced, prostaglandin D2 (PGD2) has emerged as key mediator. In addition to its known eosinophilotatics effects, recently PGD2 was described to be able to promote eosinophil activation, inducing lipid bodies biogenesis and LTC4 synthesis within these newly formed organelles. These effects are attributed to the action of PGD2 on its 2 receptors – DP1 e DP2 – which are expressed constituvely on eosinophil cell membranes. So, the main objective of this study was to identify the PGD2 specific receptor involved in LTC4 synthesis mechanism by stimulated eosinophils with PGD2. In vivo, in a murine allergic model of pleurisy and in a pleurisy induced by PGD2, the use of selective DP1 receptor (BWA868c) and DP2 receptor (CAY10471) antagonists showed us that both treatments inhibited LTC4 synthesis during these inflammatory responses. However, only BWA868C treatment was able to inhibit lipid bodies biogenesis within recruited eosinophils to the inflammatory sites, while CAY10471, decreased the number of infiltrated eosinophils in the pleural cavity, but did not inhibit lipid bodies biogenesis within these low number of recruited cells. In vitro, pre-treatment with BWA868c or CAY10471 inhibited LTC4 synthesis by human eosinophils stimulated with PGD2. Moreover, the activation of DP1 receptor with its selective agonist (BW245c) and DP2 activation with DP2 selective agonist (DK-PGD2) reinforced the observation that during LTC4 synthesis within eosinophils, activation of both receptors are necessary, because only simultaneous activation of DP1 and DP2, induced LTC4 synthesis within eosinophilic lipid bodies (Eicosacell). Moreover, we observed that the pathway of cellular signaling involved on lipid bodies biogenesis induced by DP1 activation is dependent on protein kinase A (PKA). In another set of experiments, we investigated PGD2 as a therapeutical target of allergic diseases. Recently, it was described that aqueous extract of C.sympodialis and warafteine (isolated alkaloid) have antiallergic properties, because of its effects on the reduction of eosinophils recruitment, lipid bodies biogenesis and cysteinyl leukotrienes synthesis. Here, we demonstrated that pre-treatments with extract and its alkaloid were able to inhibit PGD2 production during allergic response. In vitro, warafteine did not inhibit eosinophil lipid bodies biogenesis induced by PGD2, but it was capable to inhibit PGD2 release by activated mast cells – otherwise fail to blockade PGE2 production by A23187- activated macrophages – suggesting that the action mechanism of its antiinflammatory effects could occur through PGD2 synthesis inhibition in allergic sites.
"Synthetic studies of prostacyclin receptor antagonists." Chinese University of Hong Kong, 1993. http://library.cuhk.edu.hk/record=b5887737.
Повний текст джерелаThesis (M.Phil.)--Chinese University of Hong Kong, 1993.
Includes bibliographical references (leaves 85-95).
Chapter I. --- Introduction --- p.1
Chapter II. --- Our Approach --- p.9
Chapter III. --- Results and Discussion - Synthetic Strategy --- p.29
Chapter IV. --- Results and Discussion - Pharmacological Activity --- p.44
Chapter V. --- Conclusion --- p.49
Chapter VI. --- Further Development --- p.53
Chapter VII. --- Experimental Section --- p.55
Chapter VIII. --- References --- p.85
Chapter IX. --- Supplementary Materials --- p.96
"Synthesis of potential prostacyclin receptor antagonist." 1997. http://library.cuhk.edu.hk/record=b6073126.
Повний текст джерелаThesis (Ph.D.)--Chinese University of Hong Kong, 1997.
Includes bibliographical references (p. [254]-271).
Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Mode of access: World Wide Web.
Abstract in Chinese.
Roper, David Allen. "Pregnancy retention of bovine recipients following transfer of embryos exposed to a prostaglandin F₂[alpha] receptor antagonist." 2009. http://etd.utk.edu/2009/May2009Theses/RoperDavidAllen.pdf.
Повний текст джерелаTitle from title page screen (viewed on Oct. 22, 2009). Thesis advisor: F. Neal Schrick. [Alpha] in title is subscript. Vita. Includes bibliographical references.
Lu, Bo-Sen, and 盧柏先. "Effects of calcium antagonist on the prostaglandin D2 and leukotriene C4/D4/E4 biosynthesis of peritoneal mast cell." Thesis, 1997. http://ndltd.ncl.edu.tw/handle/46021028863843812622.
Повний текст джерела高雄醫學院
醫學研究所
85
In this study, we examined the pharmacological action of five calcium channel blockers (amlodipine, diltiazem, flunarizine, nifedipine, verapamil) oncompound 48/80 induced prostaglandin D2 and leukotriene C4/D4/E4 biosynthesisof peritoneal mast cell. Our data have indicated that preincubation of fivecalcium channel blockers possessed variant inhibitory effects on compound48/80 induced leukotrienes C4/D4/E4 and prostaglandin D2 biosynthesis from mastcells. In comparison, the inhibitory effect of amlodipine on leukotrienesC4/D4/E4 biosynthesis is more significant. And flunarizine inhibit prostaglandinD2 biosynthesis is more significant. In order to determine the role of calcium channel blockers on mediated secretion, the intracellular c-AMP and c-GMP levels of mast cell were measure by Amersham EIA kit. Calcium channel blockers exhibited concentration-dependentmanner to increase of these intracellular secondary messengers. Among fivecalcium channel blockers, flunarizine has shown a potent effect in the increaseof intracellular c-GMP level. And amlodipine exhibit a significant effect inthe increase of intracellular c-AMP level. And the modification of IP3 levelwas determined by Du- Pont RIA kit. Calcium channel blockers exhibited dose-dependent inhibitory effect on IP3 generation. In comparison, amlodipine and nifedipine possess a more significant inhibitory effect on the IP3 generation.In this study, we further characterized the mechanisms that regulate theactivation of rat mast cells response to calcium channel blocker. We suggestedthat calcium channel blockers may through modulate intracellular secondarymessenger (IP3, c-AMP, c-GMP) pathway to influence leukotrienes C4/D4/E4 andprostaglandin D2 biosynthesis on rat peritoneal mast cell.
Lu, Bo-Xian, and 盧柏先. "Effects of calcium antagonist on the prostaglandin D2 and leukotriene C4/D4/E4 biosynthesis of peritoneal mast cell." Thesis, 1997. http://ndltd.ncl.edu.tw/handle/70288898007882898788.
Повний текст джерелаGoga, Anver. "A comparative study evaluating the role of a prostaglandin (ripoprostil) and a H2 antagonist ranitidine in oesophageal mucosal protection against reflux induced oesophagitis." Thesis, 1997. http://hdl.handle.net/10413/7452.
Повний текст джерелаJohnson, Drew Leland. "Effects of hormonal, cytokine, lymphokine and paracrine agonists or antagonists on luteal and caruncular endometrial progesterone or prostaglandin sythesis in the ewe." Thesis, 2008. http://hdl.handle.net/10125/20391.
Повний текст джерелаKhidhir, K. G., D. F. Woodward, N. P. Farjo, B. K. Farjo, E. S. Tang, J. W. Wang, S. M. Picksley, and V. A. Randall. "The prostamide-related glaucoma therapy, bimatoprost, offers a novel approach for treating scalp alopecias." 2013. http://hdl.handle.net/10454/6050.
Повний текст джерела