Relevant bibliographies by topics / Prostaglandin

Academic literature on the topic 'Prostaglandin'

Author: Grafiati
Published: 4 June 2021
Last updated: 21 February 2023

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Journal articles on the topic "Prostaglandin"

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Sirchak, Yelyzaveta S., Oleksandr O. Boldizhar, Yaroslav F. Filak, Olena V. Ustych, Velentina Yu Koval, Vasyl Ye Barani, and Inna S. Borisova. "CHANGES IN PROSTAGLANDIN LEVELS IN BLOOD SERUM OF PATIENTS WITH GASTROESOPHAGEAL REFLUX DISEASE ON THE BACKGROUND OF THE OSTEOCHONDROSIS OF THE SPINE AND OBESITY." Wiadomości Lekarskie 75, no. 10 (2022): 2497–500. http://dx.doi.org/10.36740/wlek202210134.

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The aim: To study the features of changes in the level of prostaglandins (I2 and F2α) in blood serum of patients GERD on the background of OH of the cervical and thoracic spine and obesity. Materials and methods: The examined patients included 56 patients with GERD and OH of the cervical and thoracic spine. All patients had their blood serum prostaglandin (Pg) F2α and 6-keto prostaglandin F1α (blood prostacyclin – Pg I2) levels examined using the method of immunoassay analysis. Results: In all patients with GERD and OH an excessive body weight or obesity of varying degrees was found while analyzing anthropometric study results. The determination of prostaglandin F2α and prostacyclin (Pg I2) levels in blood serum in patients with GERD and OH and healthy individuals was performed. A more pronounced increase of Pg I2 and Pg F2α in blood serum in patients with GERD and OH with III degree obese was found and the smallest concentration of prostaglandines in blood serum was diagnosed in patients with excessive weight (p<0.05). Conclusions: 1. In patients with GERD and OH, an increase in levels of prostaglandins F2α and I2 in blood serum has been established. 2. The relationship between the duration of excess body weigh, obesity and the dynamics of the level of prostaglandin Pg I2 and F2α in blood serum in patients with GERD on the background of OH has been established.
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Kirchner, K. A. "Role of prostaglandins in renin suppression during acute potassium loading." American Journal of Physiology-Renal Physiology 248, no. 3 (March 1, 1985): F360—F365. http://dx.doi.org/10.1152/ajprenal.1985.248.3.f360.

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Acute K loading suppresses plasma renin activity (PRA) and may alter prostaglandin biosynthesis. To determine whether the effect of K on PRA was modulated through changes in the prostaglandin system, dietary NaCl-restricted rats were infused with prostaglandin I2. PRA was then determined before and 90 min after a KNO3 infusion. Control rats received only the prostaglandin infusion. PRA increased in rats receiving prostaglandins alone. K loading prevented the increase in PRA. To further exclude prostaglandins in PRA suppression during K loading, the effects of K on PRA were determined during prostaglandin inhibition with meclofenamate or indomethacin. K loading also suppressed PRA during prostaglandin inhibition. In neither study could the changes in PRA be attributed to changes in mean arterial pressure, glomerular filtration rate, plasma volume expansion, or urinary NaCl excretion rate. We conclude that the effects of K on PRA are independent of the prostaglandin system.
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Jara-Gutiérrez, Álvaro, and Victoriano Baladrón. "The Role of Prostaglandins in Different Types of Cancer." Cells 10, no. 6 (June 13, 2021): 1487. http://dx.doi.org/10.3390/cells10061487.

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The prostaglandins constitute a family of lipids of 20 carbon atoms that derive from polyunsaturated fatty acids such as arachidonic acid. Traditionally, prostaglandins have been linked to inflammation, female reproductive cycle, vasodilation, or bronchodilator/bronchoconstriction. Recent studies have highlighted the involvement of these lipids in cancer. In this review, existing information on the prostaglandins associated with different types of cancer and the advances related to the potential use of them in neoplasm therapies have been analyzed. We can conclude that the effect of prostaglandins depends on multiple factors, such as the target tissue, their plasma concentration, and the prostaglandin subtype, among others. Prostaglandin D2 (PGD2) seems to hinder tumor progression, while prostaglandin E2 (PGE2) and prostaglandin F2 alpha (PGF2α) seem to provide greater tumor progression and aggressiveness. However, more studies are needed to determine the role of prostaglandin I2 (PGI2) and prostaglandin J2 (PGJ2) in cancer due to the conflicting data obtained. On the other hand, the use of different NSAIDs (non-steroidal anti-inflammatory drugs), especially those selective of COX-2 (cyclooxygenase 2), could have a crucial role in the fight against different neoplasms, either as prophylaxis or as an adjuvant treatment. In addition, multiple targets, related to the action of prostaglandins on the intracellular signaling pathways that are involved in cancer, have been discovered. Thus, in depth research about the prostaglandins involved in different cancer and the different targets modulated by them, as well as their role in the tumor microenvironment and the immune response, is necessary to obtain better therapeutic tools to fight cancer.
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Martens, Matthew D., Amy S. Fernando, and Joseph W. Gordon. "A new trick for an old dog? Myocardial-specific roles for prostaglandins as mediators of ischemic injury and repair." American Journal of Physiology-Heart and Circulatory Physiology 320, no. 6 (June 1, 2021): H2169—H2184. http://dx.doi.org/10.1152/ajpheart.00872.2020.

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The small lipid-derived paracrine signaling molecules known as prostaglandins have been recognized for their ability to modulate many facets of cardiovascular physiology since their initial discovery more than 85 years ago. Although the role of prostaglandins in the vasculature has gained significant attention across time, a handful of historical studies have also directly implicated the cardiomyocyte in both prostaglandin synthesis and release. Recently, our understanding of how prostaglandin receptor modulation impacts and contributes to myocardial structure and function has gained attention while leaving most other components of myocardial prostaglandin metabolism and signaling unexplored. This mini-review highlights both the key historical studies that underpin modern prostaglandin research in the heart, while concurrently presenting the latest findings related to how prostaglandin metabolism and signaling impact myocardial injury and repair.
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Codde, James P., and Lawrence J. Beilin. "Dietary fish oil prevents dexamethasone induced hypertension in the rat." Clinical Science 69, no. 6 (December 1, 1985): 691–99. http://dx.doi.org/10.1042/cs0690691.

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1. This study was designed to examine the effect of dexamethasone treatment on tissue and urinary prostanoids, and to determine whether inhibition of prostaglandin biosynthesis by manipulation of dietary fatty acids accelerates the development of glucocorticoid hypertension. 2. Forty-eight rats were placed on either a 2-series prostaglandin ‘inhibitory’ diet (cod liver oil/linseed oil) or a control diet of saturated fat for an initial period of 4 weeks. The groups were then divided into two so that half of each received dexamethasone in their drinking water (2.5 mg/1) for 1 week whilst continuing their respective dietary regimens. 3. Rats on the cod liver oil diet incorporated eicosapentaenoic acid into tissue stores with a corresponding decrease in arachidonic acid, and significantly impaired ability to generate serum thromboxane B2 (33%), aortic 6-oxo-prostaglandin F1α (44%), renal homogenate prostaglandin E2 (45%) and 6-oxo-prostaglandin F1α (74%) and urinary prostaglandin E2 (84%) and 6-oxo-prostaglandin F1α (79%). 4. Despite the diminished levels of vasodilator 2-series prostaglandins, the cod liver oil diet prevented the development of glucocorticoid induced hypertension. 5. Relative to their respective dietary controls, dexamethasone treatment resulted in decreased serum thromboxane B2 (20%) but increased aortic 6-oxo-prostaglandin F1α (186%), renal homogenate prostaglandins (127–230%) and urinary excretion of prostaglandin E2 (640–860%) and 6-oxo-prostaglandin F1α(230–365%) in both dietary groups. 6. It therefore seems unlikely that glucocorticoid induced hypertension is a consequence of inhibition of vasodilator prostaglandin synthesis.
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Leighton, B., L. Budohoski, F. J. Lozeman, R. A. J. Challiss, and E. A. Newsholme. "The effect of prostaglandins E1, E2 and F2α and indomethacin on the sensitivity of glycolysis and glycogen synthesis to insulin in stripped soleus muscles of the rat." Biochemical Journal 227, no. 1 (April 1, 1985): 337–40. http://dx.doi.org/10.1042/bj2270337.

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Prostaglandins E1 and E2 increased the sensitivity of glycolysis to insulin in the isolated stripped soleus muscle of the rat, but prostaglandin F2 alpha had no effect. Indomethacin, which inhibits prostaglandin formation, markedly decreased the sensitivity of glycolysis to insulin. These findings suggest that prostaglandins of the E series increase the sensitivity of muscle glycolysis to insulin in vivo.
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Tiwary, Ekta, Muhan Hu, and Jeevan K. Prasain. "Sperm-Guiding Unconventional Prostaglandins in C. elegans: Synthesis and Signaling." Metabolites 11, no. 12 (December 8, 2021): 853. http://dx.doi.org/10.3390/metabo11120853.

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Prostaglandins comprise a family of lipid signaling molecules derived from polyunsaturated fatty acids and are involved in a wide array of biological processes, including fertilization. Prostaglandin-endoperoxide synthase (a.k.a. cyclooxygenase or Cox) initiates prostaglandin synthesis from 20-carbon polyunsaturated fatty acids, such as arachidonic acid. Oocytes of Caenorhabditis elegans (C. elegans) have been shown to secrete sperm-guidance cues prostaglandins, independent of Cox enzymes. Both prostaglandin synthesis and signal transduction in C. elegans are environmentally modulated pathways that regulate sperm guidance to the fertilization site. Environmental factors such as food triggers insulin and TGF-β secretion and their levels regulate tissue-specific prostaglandin synthesis in C. elegans. This novel PG pathway is abundant in mouse and human ovarian follicular fluid, where their functions, mechanism of synthesis and pathways remain to be established. Given the importance of prostaglandins in reproductive processes, a better understanding of how diets and other environmental factors influence their synthesis and function may lead to new strategies towards improving fertility in mammals.
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Nassar, Bassam A., Yung-Sheng Huang, Alan T. J. McDonald, Kenneth D. Jenkins, and David F. Horrobin. "The influence of phenelzine and tranylcypromine on the release of prostaglandins from the rat mesenteric vascular bed." Canadian Journal of Physiology and Pharmacology 66, no. 9 (September 1, 1988): 1206–9. http://dx.doi.org/10.1139/y88-198.

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We investigated the effects of phenelzine and tranylcypromine on the release of prostacyclin, thromboxane A2, prostaglandin E2, and prostaglandin E1 from the isolated perfused rat mesenteric vascular bed. Perfusion of the preparation with phenelzine in concentrations of 15, 45, and 135 μM for 150 min led to attenuated release of all four prostaglandins measured. Inhibition generally occurred with the lowest dose used and was most prominent with the highest concentration. Tranylcypromine also decreased prostaglandin formation. However, low doses were not effective in the suppression of prostacyclin release. Both drugs had an inhibitory effect on production of prostaglandin E1, which is a metabolite of dihomo-γ-linolenic acid, the precursor of arachidonic acid, but this was only shown to be significant with phenelzine. In this work we demonstrate that phenelzine and tranylcypromine have an inhibitory effect on the production of 2-series prostaglandins derived from arachidonic acid, and possibly a similar effect on prostaglandins of the 1-series derived from dihomo-γ-linolenic acid.
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Surbek, Hösli, and Holzgreve. "Current aspects of labor induction." Therapeutische Umschau 59, no. 12 (December 1, 2002): 650–54. http://dx.doi.org/10.1024/0040-5930.59.12.650.

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Die Geburtseinleitung ist eines der wichtigsten therapeutischen Interventionsmittel in der Geburtshilfe und Schwangerschaftsmedizin. Das Ziel der Einleitung ist es, das bessere «perinatale Ergebnis» für Mutter und Kind im Gegensatz zum abwartenden Vorgehen zu erreichen. Zu den verschiedenen Methoden der Geburtseinleitung gehören insbesondere die Verabreichung von Oxytocin oder Prostaglandinen, die Amniotomie, und mechanische Methoden der Zervixdilatation. Der Erfolg der Geburtseinleitung ist vorab abhängig von der Geburtsbereitschaft des Uterus und von der verwendeten Methode. Bei sehr reifer Zervix scheint die Einleitung mittels Oxytocin und Amniotomie günstig. Umgekehrt ist die lokale, intravaginale oder intrazervikale Verabreichung von Prostaglandinen bei noch unreifer Zervix erfolgsversprechender. Als Prostaglandine wurden bisher in erster Linie Prostaglandine E2 verwendet. Neuerdings wird das Prostaglandin E1-Analogon Misoprostol zunehmend verwendet. Grundsätzlich sollte die Geburtseinleitung unter stationären Bedingungen erfolgen, um die notwendige Sicherheit für Mutter und Fetus mittels entsprechender Überwachung gewährleisten zu können.
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Tsuchida, Keiichiro, Takae Ibuki, and Kiyoshi Matsumura. "Bromoenol Lactone, an Inhibitor of Calcium-Independent Phospholipase A2, Suppresses Carrageenan-Induced Prostaglandin Production and Hyperalgesia in Rat Hind Paw." Mediators of Inflammation 2015 (2015): 1–7. http://dx.doi.org/10.1155/2015/605727.

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Prostaglandin (PG) E2and PGI2are essential to hyperalgesia in inflammatory tissues. These prostaglandins are produced from arachidonic acid, which is cleaved from membrane phospholipids by the action of phospholipase A2(PLA2). Which isozyme of PLA2is responsible for the cleavage of arachidonic acid and the production of prostaglandins essential to inflammation-induced hyperalgesia is not clear. In this study, we examined the effects of two PLA2isozyme-specific inhibitors on carrageenan-induced production of PGE2and PGI2in rat hind paw and behavioral nociceptive response to radiant heat. Local administration of bromoenol lactone (BEL), an inhibitor of calcium-independent PLA2(iPLA2), significantly reduced carrageenan-induced elevation of prostaglandins in the inflamed foot pad 3 h after injection. It also ameliorated the hyperalgesic response between 1 h and 3 h after carrageenan injection. On the other hand, AACOCF3, an inhibitor of cytosolic PLA2, suppressed neither prostaglandin production nor the hyperalgesic response. BEL did not suppress the mRNA levels of iPLA2β, iPLA2γ, cyclooxygenase-2, microsomal prostaglandin E synthase, prostaglandin I synthase, or proinflammatory cytokines in the inflamed foot pad, indicating that BEL did not suppress inflammation itself. These results suggest that iPLA2is involved in the production of prostaglandins and hyperalgesia at the inflammatory loci.
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Dissertations / Theses on the topic "Prostaglandin"

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Venturin, Gabriela Lovizutto. "Efeito regulador da PGE2 na produção de TNF-α e IL-17 na atividade microbicida na leishmaniose canina. /." Araçatuba, 2019. http://hdl.handle.net/11449/183297.

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Orientador: Valéria Marçal Felix de Lima
Resumo: A leishmaniose canina (CanL) é causada pelo parasito intracelular Leishmania infantum. Devido ao alto parasitismo na pele o cão é considerado o principal reservatório urbano da L. Infantum. A prostaglandina-E2 (PGE2) possui propriedades reguladoras potentes do sistema imunológico e pode se ligar aos receptores EP1, EP2 e EP4 que geram ativação celular ou EP3 que gera inibição de resposta celular. Na CanL o papel regulador da PGE2 ainda não foi estudado, por isso, os parâmetros foram avaliados em cultura de leucócitos esplênicos de cães com CanL. Avaliando o nível de PGE2, seus receptores, e seu efeito modulador sobre a PGE2 na atividade da arginase, NO2, citocinas IL-10, IL-17 e TNF-α e carga. Para isso utilizamos seus agonistas, antagonista e inibidor. Nossos resultados mostraram que a expressão do receptor EP2 diminuiu nos leucócitos esplênicos dos cães com CanL quando comparado aos cães saudáveis. Observamos que o NO2 diminuiu quando tratados com os agonistas dos receptores de PGE2 (EP1/EP2/EP3), antagonista dos receptores de PGE2 (AH-6809) e inibidor de COX-2 (NS-398). A concentração das citocinas TNF-α e a IL-17 diminuíram quando tratadas com agonista do receptor de PGE2 (EP2), e quando estimuladas com a PGE2. A carga parasitária diminuiu na cultura de leucócitos esplênicos de cães com CanL estimulados com PGE2. Concluímos que a infecção por Leishmania modula os receptores de PGE2 em cães, e que a ligação da PGE2 aos receptores pode ativar a capacidade microbicida das cé... (Resumo completo, clicar acesso eletrônico abaixo)
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Javed, T. "Synthesis of prostaglandins and prostaglandin analogues from norbornadiene." Thesis, University of Salford, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.356170.

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Nielsch, A. S. "Effects of prostaglandins and prostaglandin synthetase inhibitors on liver toxicity." Thesis, University of Aberdeen, 1987. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU499301.

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A total of 22 non-steroidal anti-inflammatory drugs and derivatives were added to microsomes to study the denaturation of cytochrome P-450 to cytochrome P-420 in the absence of an NADPH-generating system. There was a highly significant correlation among the different compounds between the extent of denaturation of cytochrome P-450 and their surfactant potency. Endotoxin administration to rats caused a maximum decrease in hepatic microsomal enzymes after 24 hours. Significant decreases in cytochrome P-450 (40%), cytochrome b5 levels (22%), aminopyrine N-demethylase (31%) and biphenyl 4-hydroxylase (54%) activities were obtained. Concomitant intravenous injection of 16,16-DMPG F2 and 16,16-DMPG E2 prevented some of the endotoxin-induced changes in hepatic microsomal enzymes. Three days treatment with cocaine was required to obtain hepatic damage in mice. Decreases in cytochrome P-450 content (41%), aminopyrine N-demethylase (31%) and FAD-monooxygenase (35%) activities were obtained, when compared to saline treated mice. The serum enzyme activities were markedly increased (SGOT 13-fold and SOCT 44-fold). Histological changes in form of centrilobular necrosis and fatty changes were present. Repeated subcutaneous administration of iloprost or synthetic prostaglandins just before cocaine prevented some of the hepatic lesions. Iloprost was found to be a better hepatoprotective agent than synthetic prostaglandins against the cocaine mediated liver toxicity. Carbon tetrachloride administration to mice produced similar lesions to those obtained with cocaine. Administration of iloprost prevented some of the lesions caused by carbon tetrachloride, giving a partial protection to the carbon tetrachloride-induced decrease in cytochrome P-450 and the increase in SGOT. Iloprost also partially prevented the carbon tetrachloride mediated centrilobular necrosis.
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Ujjan, Safdar Ali. "Prostaglandin D2 (PGD2) signalling and male germ cell : differentiation in the mouse embryonic testis." Thesis, Montpellier 2, 2014. http://www.theses.fr/2014MON20099.

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La détermination du sexe et la différenciation des cellules germinales est un processus très organisé qui commence au stade embryonnaire et se termine à la vie adulte. Dans les gonades embryonnaires l'expression de Sry suivie par l'expression de Sox9 initie le développement testiculaire tandis que, en l'absence de l'expression de Sry, les gènes associés au sexe féminin initient le développement des ovaires. Les cellules germinales qui ont migré vers les gonades nouvellement formées continuent leur prolifération intense jusqu'à ce qu'ils s'engagent dans la voie le mâle ou femelle. La décision de devenir des cellules germinales mâle ou femelle ne dépend pas seulement du chromosome sexuel des cellules germinales, mais aussi du microenvironnement des gonades. Si les cellules germinales entrent dans la gonade femelle, ils doivent arrêter la prolifération, dépasser l'arrêt mitotique et entrer en méiose et alors s'arrêter en prophase I. Alors que si les cellules germinales entrent dans la gonade mâle, ils doivent arrêter la prolifération et entrer en arrêt de la mitose. Ici, nous montrons que, lors de la détermination du sexe embryonnaire, la prostaglandine D2 (PGD2) produite par chacune des deux enzymes: la L-PGDS et H-PGDS dans les cellules somatiques et les cellules germinales du testicule mâle participe au programme de différenciation des cellules germinales. La voie de signalisation PGD2 entraine l'arrêt de la mitose par l'activation de l'expression et de la localisation nucléaire de l'inhibiteur du cycle cellulaire p21Cip1 et en réprimant les marqueurs de pluripotence et aussi Stra8. En outre, PGD2 est responsable de l'activation du gène spécifique au mâle Nanos2. Par conséquent, ces données suggèrent que la signalisation par le récepteur de PGD2 DP2 est requise pour la différenciation correcte de la cellule germinale mâle
The sex determination and subsequent germ cell differentiation is highly ordered process that starts at embryonic stage and completes at adult life. In the embryonic gonads Sry expression followed by Sox9 expression initiates testis development while in the absence of Sry expression, genes associated to female fate initiate ovary development. The germ cells that migrated towards newly formed gonads continue extensive proliferation until they commit to the male or female pathway. The fate decision of germ cells as male or female does not depend only on germ cell chromosomal sex but also on gonadal micro-environment. If germ cells enter into female gonad, they have to stop proliferation, pass through mitotic arrest and enter into meiosis; then arrest into prophase I. While if germ cells enter into male gonad, they have to stop proliferation and enter into mitotic arrest. Here we show that during embryonic sex determination, Prostaglandin D2 (PGD2) produced by each of the two enzymes: L-Pgds and H-Pgds in somatic cells and germ cells of testis participates in male germ cell differentiation program. PGD2 signalling supports mitotic arrest by activating the expression and nuclear localization of cell cycle inhibitor P21cip1 and by repressing pluripotency markers and PGD2 has negative effects on Stra8 expression. In addition PGD2 supports activation of male specific gene Nanos2. Hence these data suggest that PGD2 signalling through DP2 receptor is required for proper male germ cell differentiation
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Gagliolo, Jean-Marie. "Rôle de la sénescence des fibroblastes dans la physiopathologie de la bronchopneumopathie chronique obstructive." Thesis, Paris Est, 2013. http://www.theses.fr/2013PEST1065.

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La sénescence, perte irréversible des capacités réplicatives des cellules associée à la sécrétion de médiateurs inflammatoires, pourrait participer au développement de l'atteinte pulmonaire dans la bronchopneumopathie chronique obstructive (BPCO) en initiant, maintenant et propageant un état inflammatoire. L'objectif de ce travail était d'évaluer les mécanismes de la sénescence impliqués dans l'induction et le maintien de l'inflammation au cours de la BPCO. Ainsi, des fibroblastes pulmonaires de témoins et de patients atteints de BPCO ont été mis en culture à long terme. Un phénotype sénescent majoré associée à un sécrétome pro-inflammatoire était détectée dans les fibroblastes de patients avec BPCO par rapport aux témoins. Par ailleurs, ces fibroblastes présentaient une expression accrue des récepteurs à la PGE2 (EP2 /4)au stade non sénescent et une production accrue de PGE2, un médiateur lipidique pro-inflammatoire, au stade sénescent. Dans cette optique, une partie du travail a consisté à déterminer si la PGE2 pouvait induire la sénescence et l'inflammation des fibroblastes pulmonaires de sujets atteints ou non de BPCO. Nous avons pu démontrer que la PGE2 synthétisée par les fibroblastes sénescents induisait, maintenait (effet autocrine) et propageait (effet paracrine) la sénescence et l'inflammation associée via une voie EP2/4 / COX-2 / oxydants / p53. L'implication des oxydants dans l'induction de la sénescence nous a conduit à étudier les effets de l'hème oxygénase (HO)-1, un système anti-oxydant et anti-inflammatoire sur la prévention de la sénescence des fibroblastes pulmonaires. Ainsi, des fibroblastes pulmonaires ont été traités chroniquement avec des substances pharmacologiques modulant l'activité d'HO-1. Des résultats préliminaires nous ont permis d'observer que l'activation de HO-1 prévenait l'induction de la sénescence chez des fibroblastes pulmonaires de témoins et de BPCO. Au total, la modulation des voies de la PGE2 et de l'HO-1 pourrait contribuer à limiter la sénescence des fibroblastes pulmonaires dans la BPCO
Cellular senescence, a state of irreversible loss of replicative capacity associated with the secretion of inflammatory mediators, could participate in the development of chronic obstructive pulmonary disease (COPD) by initiating, maintaining and propagating an inflammatory state. The aim of this PhD project was to evaluate the mechanisms involved in senescence induction in COPD lung fibroblasts. COPD fibroblasts exhibited an increased senescent phenotype as compared to control cells. In addition, COPD fibroblasts showed an increased PGE2 receptors (EP2 /4) expression at non senescent stage and PGE2 production, apro-inflammatory lipid mediator at senescent stage. In this context, one part of the study was devoted to determine whether PGE2 could induce senescence of lung fibroblasts of subjects with and without COPD. We have shown that PGE2 synthesized by senescent fibroblasts induced, maintained (autocrine effect) and propagated (paracrine effect) senescence and associated inflammation via EP2 /4 / COX-2 / oxidants / p53 pathway. The essential role of oxidants production in the induction of senescence in COPD led us to study the effects of heme oxygenase (HO)-1, an antioxidant and anti-inflammatory system on the prevention of senescence in COPD fibroblasts. Pharmacological activation of HO-1 by hemin prevented the induction of senescence in lung fibroblasts from COPD patients probably in relation with an anti -oxidant effect. The modulation of PGE2 and HO-1 pathways may contribute to attenuate fibroblasts senescence in COPD
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Pereira, Priscilla Aparecida Tartari. "Efeitos antagônicos da prostaglandina D2 e prostaglandina E2 na resposta imune durante infecção experimental por Histoplasma capsulatum." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/17/17147/tde-06012014-081806/.

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O Histoplasma capsulatum é um fungo dimórfico, patogênico e responsável por graves lesões pulmonares. A infecção é adquirida pela inalação de conídios e posterior conversão para leveduras nos alvéolos e bronquíolos, onde são fagocitadas por macrófagos alveolares residentes e leucócitos que migram para o local da infecção. Recentemente, demonstramos que animais infectados com H. capsulatum e tratados com inibidor da síntese de prostaglandinas apresentaram diminuição de carga fúngica nos pulmões e baço, aumento da produção de nitrito e da fagocitose de leveduras por macrófagos alveolares, e maior sobrevivência, quando comparados com os animais somente infectados. Porém, neste estudo não foram determinados quais subtipos de prostaglandinas participam na patogênese da histoplasmose. Vários grupos de pesquisa têm demonstrado que PGD2 e PGE2 podem ter ações biológicas distintas quanto à remoção de microrganismos no hospedeiro. Desta maneira, é fundamental o entendimento do papel da PGD2 e da PGE2 nos mecanismos efetores dos macrófagos na defesa do hospedeiro, especialmente na histoplasmose. Portanto, o objetivo deste estudo foi investigar a participação da PGD2 e PGE2 na infecção experimental por H. capsulatum. Assim, demonstramos que a PGD2 aumentou a fagocitose e mecanismos microbicidas de macrófagos alveolares infectados in vitro com H. capsulatum. Observamos ainda que a 15dPGJ2, metabólito da PGD2, aumentou somente a fagocitose, e PGE2 inibiu os mecanismos efetores do macrófago. Mostramos ainda o aumento de BLT1 em macrófagos alveolares após adição de PGD2, e a possível ligação desta ao BLT1, e de LTB4 em DP2. Além disso, caracterizamos micropartículas de PLGA contendo PGD2 (MS-PGD2), e investigamos seus efeitos. O tamanho, carga elétrica e morfologia das micropartículas foram adequados para um tratamento intranasal e para fagocitose por macrófagos alveolares. As MS-PGD2 foram fagocitadas e capazes de ativar NF-B, e consequentemente, influenciar na produção de nitrito, IL-1, TNF-, IL-6 e TGF-. Com base nestes dados, avaliamos os efeitos do tratamento da MS-PGD2 ou da MS-PGE2 em animais infectados com H. capsulatum. Estas foram administradas via intranasal em animais infectados e tratados ou não com celecoxibe. Verificamos a diminuição da carga fúngica nos pulmões e baço, diminuição do infiltrador celular no espaço broncoalveolar e de citocinas inflamatórias no pulmão após tratamento com MS-PGD2. Contrariamente, após tratamento da MS-PGE2 observamos maior carga fúngica nos pulmões e baço, e aumento da inflamação no tecido e maior produção de IL-10. Além disso, demonstramos que no 21° dia após infecção, referente ao 7° dia após o término do tratamento com MS-PGD2, a carga fúngica manteve-se reduzida nos pulmões, comprovando assim a eficácia deste tratamento. Posteriormente, utilizando inibidores específicos, HQL-79 e CAY10526, mostramos respectivamente o papel protetor da PGD2 e o deletério da PGE2 na histoplasmose. Em conjunto, nossos dados contribuíram para o entendimento das funções antagônicas da PGD2 e PGE2 nesta micose.
Histoplasma capsulatum is a pathogenic dimorphic fungus and responsible for severe pulmonary lesions. Infection is acquired by inhalation of conidia and posterior conversion to yeasts in the alveoli and bronchioles, in which they are phagocyted by resident alveolar macrophages and leukocytes that migrate to the local infection. Recently, we demonstrate that mice infected by H. capsulatum and treated with inhibitor of prostaglandins synthesis presented a decrease in fungal burden in lungs and spleen, increase in nitrite production and uptake of yeasts by alveolar macrophages, and more survival, when compared with animals only infected. However, in this study, it was not determined what subtypes of prostaglandins participate in pathogenesis of histoplasmosis. Many research groups have demonstrated that PGD2 and PGE2 can have different biological effects regarding to microorganisms elimination in the host. Thus, it is primordial the understanding about the role of PGD2 and PGE2 on effector mechanisms of macrophages in host defense, especially in histoplasmosis. Therefore, the aim of this study was to investigate the role of PGD2 and PGE2 on experimental infection by H. capsulatum. So, we verify that PGD2 increased the uptake and microbicidal mechanisms of alveolar macrophages infected in vitro by H. capsulatum. 15dPGJ2, a PGD2 metabolite, increased only the phagocytosis, and PGE2 inhibited the effector mechanisms of macrophages. Among these results, we showed an increase of BLT1 expression on alveolar macrophages after addition of PGD2, and a possible binding of this mediator to BLT1, and of LTB4 to DP2. Later, as tool of therapeutic investigation, we used PGD2 encapsulation in biodegradable polymer, PLGA, in order to preserve its stability. Size, zeta potential and morphology were adequate for a possible intranasal treatment and uptake by alveolar macrophages. MS-PGD2 were phagocyted and able to activate NF-B, and consequently, to modulate nitrite, IL-1, TNF-, IL-6 and TGF- production. In this context, we purpose a treatment of the infection with MS-PGD2, in comparison to treatment with PGE2. MS-PGD2 were administrated via intranasal in infected mice, treated or not with celecoxib. We verify a decrease of fungal burden in lungs and spleen, less cellular infiltrate and decrease of some inflammatory cytokines. In contrast, after treatment of MS-PGE2, we observed greater fungal burden in the lungs and spleen, and an increase of the tissue inflammation and production of IL-10. Furthermore, we show that on day 21 after infection, referring to the 7th day after the treatment with MS-PGD2, fungal burden remained reduced in the lungs, thus proving the effectiveness of the treatment. Subsequently, using specific inhibitors, HQL-79 and CAY10526, respectively show the protective role of PGD2 and in deleterious to PGE2 in histoplasmosis. Together, our data contribute to the understanding of the antagonistic functions of PGD2 and PGE2 in this mycosis.
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Oliveira, Milena Lopes. "Ação do 17β-estradiol na síntese de PGF2α endometrial em vacas." Universidade de São Paulo, 2017. http://www.teses.usp.br/teses/disponiveis/10/10131/tde-25082017-095013/.

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O 17β-E2 estimula a expressão de receptores endometriais, ER e OXTR. A ativação de OXTR induz a ativação da cadeia de síntese de PGF2α. A hipótese do presente estudo é que as enzimas de síntese de PGF2α são reguladas pelo 17β-E2. Objetivou-se determinar os efeitos do 17β-E2 na expressão gênica e proteica, assim como na localização de proteínas envolvidas na síntese de PGF2α. Vacas Nelore multíparas, solteiras e cíclicas foram sincronizadas por aplicação de BE e inserção de dispositivo de P4. Após 8 dias realizou-se a remoção do dispositivo de P4 e aplicação de PGF2α, seguido por 4 dias de observação de estro (D0=dia do estro). Entre D14 e D27 foram realizadas avaliações diárias da área do CL (cm2), fluxo sanguíneo (%) e concentração plasmática de progesterona (P4). No D15 as vacas foram divididas em três grupos: Controle (C; não tratado;N= 10), Placebo (P; 6mL de etanol 50%; IV; N= 21) e Estradiol (E; 3mg 17β-E2; 6mL de etanol 50%; IV;N=21). Subsequente aos tratamentos, biópsias uterinas foram coletadas nos tempos 0h (C; N=10); 4h (E4h, N=11 e P4h; N=10) ou 7h (E7h, N=10 e P7h, N=11). Amostras de sangue foram obtidas nos tempos 0h a 7h, para mensuração das concentrações PGFM no D15. O grupo E apresentou acentuada diminuição da área do CL, fluxo sanguíneo e concentração de P4 (P<0,05), comparado ao grupo P. Comparado ao grupo P, as vacas do grupo E anteciparam o dia da luteólise funcional e estrutural em 2 e 3 dias, respectivamente. O grupo E apresentou maior concentração de PGFM nos tempos 4h, 6h e 7h (P<0,05), comparado ao grupo P. A quantificação dos transcritos realizada por qPCR (N=6/grupo). Na hora 4, a abundância dos genes ESR1, ESR2, PRKCα, PRKCβ, PLA2G4, AKR1B1 e AKR1C4 foi menor nas amostras E4h, enquanto OXTR foi maior nas mesmas amostras comparando-se com as amostras P4h (P<0,05). A expressão gênica de PTGS2 não diferiu entre os grupos E4h e P4h (P>0,05). Na hora 7, as amostras E7h também apresentaram menor abundância de ESR1, PRKCα, PRKCβ, AKR1B1 e AKR1C4 (P<0,05) e houve tendência para menor expressão de ESR2, comparado às amostras P7h. Contudo, não houve diferença na abundância de OXTR, PLA2G4 e PTGS2 entre as amostras E7h e P7h (P>0,05). A abundância da enzima PKCα analisada por Western Blotting (N=3/grupo) foi diminuída tanto nas amostras E4h como nas E7h, em relação às amostras P4h e P7h, respectivamente. Na avaliação por imunohistoquímica (N=5/grupo), o grupo E4h apresentou maior imunomarcação de PGR no epitélio glandular (P< 0,05) e houve tendência para maior imunomarcação de PKCϒ no epitélio luminal, comparado ao grupo P4h (P=0,08). Houve tendência para menor imunomarcação de ERα no epitélio glandular do grupo E4h comparado ao grupo E7h (P=0,1). Concluí-se que a aplicação do 17β-E2 levou a redução da maioria dos transcritos das moléculas de síntese de PGF2α, assim como da abundância de PKCα. O possível mecanismo para a estimulação de PGFM por 17β-E2 pode incluir o aumento da ativação de enzimas que participam na cascata de síntese de PGF2α.
17β-E2 stimulates the expression of endometrial receptors, ER and OXTR. Activation of OXTR induces the activation of the synthesis of PGF2α pathway. The central hypothesis is that the enzymes involved in PGF2 synthesis are reguleted by 17β-E2. The objective of this study was to determine the effects of 17β-E2 on gene and protein expression and localization of the enzymes involved in PGF2α synthesis. Multiparous, non-lactating and cyclic Nelore cows were synchronized by BE application and P4 device insertion. After 8 days the P4 device was removed and a single dose of PGF2α applied, followed by 4 days of estrus detection (D0 = day of estrus). Daily measurements of CL area (cm2), blood flow (%), and plasma progesterone concentration (P4) were performed between D14 and D27. On D15 cows were divided into three groups: Control (C, untreated, N = 10), Placebo (P; 6mL of ethanol 50%, IV; N = 21) and Estradiol (E; 3mg 17β-E2; Ethanol 50%, IR: N = 21). After the treatments administration, uterine biopsies were collected at times 0h (C; N = 10); 4h (E4h, N = 11 and P4h, N = 10) or 7h (E7h, N = 10 and P7h, N = 11). Blood samples were obtained from time 0h to 7h for the measurement of the PGFM concentrations on D15. Group E showed a marked decrease in CL area, blood flow, and P4 concentration (P <0.05) compared to group P. Also, when compared to group P, cows from group E anticipated the day of functional and structural luteolysis in 2 and 3 days, respectively. Group E presented higher concentration of PGFM at 4h, 6h and 7h (P <0.05), compared to group P. The transcripts abundance was performed by qPCR (N = 6 / group). The transcripts abundance of ESR1, ESR2, PRKCα, PRKCβ, PLA2G4, AKR1B1, and AKR1C4 genes was lower in the E4h samples, while OXTR was higher in the same samples compared to the P4h (P <0.05) samples in the time 4h. The gene expression of PTGS2 did not differ between groups E4h and P4h (P> 0.05). At time 7h, samples E7h also had lower abundance of ESR1, PRKCα, PRKCβ, AKR1B1 and AKR1C4 (P <0.05) and there was a tendency for lower ESR2 expression, compared to samples P7h. Nevertheless, there was no difference in the abundance of OXTR, PLA2G4, and PTGS2 between samples E7h and P7h (P> 0.05). The abundance of the PKCα enzyme analyzed by Western Blotting (N = 3 / group) was decreased in both the E4h and E7h samples, relative to the samples P4h and P7h, respectively. In the evaluation by immunohistochemistry (N = 5 / group), the E4h group presented greater PGR immunostaining in the glandular epithelium (P <0.05) and there was a tendency for a greater immunostaining of PKCϒ in the luminal epithelium, compared to the P4h group (P = 0,08). There was a tendency for lower ERα immunostaining in the glandular epithelium of the E4h group compared to the E7h group (P = 0.1). It was concluded that the application of 17β-E2 led to the reduction of most of the transcripts of the PGF2α synthesis molecules, as well as the abundance of PKCα. The possible mechanism for stimulation of PGFM by 17β-E2 may include increased activation of enzymes that participate in the cascade of PGF2α synthesis.
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Feltrin, Isabella Rio. "Efeitos do 17β-estradiol na abundância de transcritos para enzimas envolvidas na síntese de PGF2α endometrial em fêmeas bovinas no final do diestro." Botucatu, 2020. http://hdl.handle.net/11449/192193.

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Orientador: Claudia Maria Bertan Membrive
Resumo: Em bovinos, o 17β-estradiol (17β-E2) estimula a expressão de receptores de estradiol (ER) e ocitocina (OXTR) no endométrio. A ativação de OXTR induz a ativação de uma complexa cascata que resulta na síntese de PGF2α. A hipótese é que o tratamento com 17β-E2, 15 dias após o estro (D15), modula a expressão gênica das proteínas quinase (PKC) e fosfolipase A2 (PLA2), ambas envolvidas na síntese de PGF2α e dependentes de cálcio. Objetivou-se neste estudo determinar os efeitos do 17β-E2 na abundância de trancritos (PKCα, PKCβ, PLA2G4, AKR1B1, AKR1C4 e PTGS2) diretamente envolvidos na síntese de PGF2α. Novilhas (N=50), não prenhes, cíclicas, foram sincronizadas pela inserção de um dispositivo de liberação intravaginal contendo 0,558g de progesterona (P4), pela administração de 1 mg de benzoato de estradiol e 0,075 mg de D-Cloprostenol, ambos intramuscular (IM). Após 6 dias, foi injetado 0,075 mg de D-Cloprostenol, IM. Após 48 horas, o dispositivo contendo P4 foi removido e 0,150 mg de D-Cloprostenol foi administrado IM. Nesta ocasião, um adesivo foi inserido na base da cauda para a identificação dos estros (Boviflag Red Estrus Detector - ABS Pecplan) e observações de estro foram realizadas nos próximos 4 dias. Participaram do experimento somente novilhas identificadas em estro (D0 = dia do estro) e que ovularam (N=46). Entre D14 e D23, a área do corpo lúteo (CL; cm2), fluxo sanguíneo (%) e as concentrações plasmáticas de progesterona (P4) foram avaliadas diariamente. No D15, as novi... (Resumo completo, clicar acesso eletrônico abaixo)
Abstract: In cattle, 17β-estradiol (17β-E2) stimulates expression of estradiol (ER) and oxytocin receptor (OXTR) in the endometrium. The activation of OXTR leads to the induction of a complex cascade of molecular activation resulting in PGF2α synthesis. The hypothesis was that 17β-E2 treatment on day 15 (D15) after estrus modulates the gene expression of protein kinase (PKC) and phospholipase A2 (PLA2), both directly involved in the synthesis of PGF2α and calcium dependent. The aim of this study was to determine the effects of 17β-E2 on the abundance of key transcripts (PKCα, PKCβ, PLA2G4, AKR1B1, AKR1C4 and PTGS2) involved in PGF2α signaling and synthesis. Nelore heifers (N=50), don't pregnant, cyclic were synchronized by insertion an intravaginal release device containing 0.558g of progesterone (P4), and by the administration of 1 mg of estradiol benzoate and 0.075 mg de D-Cloprostenol, both intramuscularly (IM). After 6 days, 0.075 mg D-Cloprostenol was injected, IM. After 48 hours the P4 device was removed and 0.150 mg D-Cloprostenol was administered IM. On this occasion, an adhesive was inserted at the base of the tail for the identification of estrus (Boviflag Red Estrus Detector - ABS Pecplan) and estrous observation were made in the next 4 days. Participated in the experiment only the heifers identified in estrus (D0 = day of estrus) that ovulated (N=46). Between D14 and D23, corpus luteum (CL) area (cm2), blood flow (%), and progesterone (P4) plasmatic concentrations were eval... (Complete abstract click electronic access below)
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Gyomorey, Sandor. "Temporal expression of prostaglandin endoperoxide H synthase type 2 and prostaglandin receptors at birth." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape10/PQDD_0023/MQ40864.pdf.

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Matthews, Jane Simone. "Characterisation of prostaglandin E receptors." Thesis, University of Edinburgh, 1993. http://hdl.handle.net/1842/19997.

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Prostaglandin (PG) E2 has been shown to act on at least three distinct receptor subtypes, designated EP1, EP2 and EP3, with recent evidence suggesting the possibility of a fourth EP-receptor subtype. Whilst good antagonists are not available, a range of PGE analogues of differing selectivity for the three receptor subtypes may be used to determine which is effective in a given system. The activity of these analogues has not yet been assessed on the putative EP4-receptor containing preparation. This research has involved the use of such compounds in an in vivo model of rabbit-skin inflammation, and biochemical studies on both platelets and cultured macrophages, to determine the subtype(s) of PGE receptor mediating the pro-inflammatory, pro-aggregatory, and anti-inflammatory effects, respectively, of PGE2. Whilst PGE2 alone had little effect on rabbit skin inflammation, potentiation of vascular permeability induced by mediators of inflammation, such as bradykinin (BK) and FMLP was observed. The potentiation has been attributed to the vasodilator activity of PGE2 which is typically mediated via the EP2-receptor subtype. However the finding that compounds with both EP2- and EP3-receptor activity were the most active, suggested that vasodilatation was not the sole mechanism of the potentiation. A comparison of the ability of PGE2 and the stable PGI2 analogue, cicaprost, to induce vasodilatation and potentiate the responses to both BK and FMLP, was consistent with this suggestion. It has since been proposed that there is an initial EP3-receptor mediated, dilatation-independent component to the potentiation of BK by PGE2.
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Books on the topic "Prostaglandin"

1

Javed, Tariq. Synthesis of prostaglandins and prostaglandin analogues from norbornadiene. Salford: University of Salford, 1985.

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Diehm, Curt, Helmut Sinzinger, and Waltraud Rogatti, eds. Prostaglandin E1. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-76910-8.

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Heidrich, H., H. Böhme, and Waltraud Rogatti, eds. Prostaglandin E1. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73943-9.

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Sinzinger, Helmut, and Waltraud Rogatti, eds. Prostaglandin E1 in Atherosclerosis. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71679-9.

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Wasinger, Thomas. Prostaglandin receptors and prostaglandin metabolism in the terminal vascular bed of the brain. Wien: Facultas Universitätsverlag, 1989.

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Gyomorey, Sandor. Temporal expression of prostaglandin endoperoxide H synthase type 2 and prostaglandin receptors at birth. Ottawa: National Library of Canada, 1998.

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Samuelsson, Bengt, R. Paoletti, Giancarlo C. Folco, E. Granström, and S. Nicosia, eds. Advances in Prostaglandin and Leukotriene Research. Dordrecht: Springer Netherlands, 2001. http://dx.doi.org/10.1007/978-94-015-9721-0.

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Taipei Conference on Prostaglandin and Leukotriene Research (1988). Taipei Conference on Prostaglandin and Leukotriene Research. Edited by Samuelsson Bengt, Wong Patrick Y. -K, and Sun Frank F. New York: Raven, 1988.

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Walden, Thomas L., and Haywood N. Hughes, eds. Prostaglandin and Lipid Metabolism in Radiation Injury. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-5457-4.

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L, Walden Thomas, and Hughes Haywood N, eds. Prostaglandin and lipid metabolism in radiation injury. New York: Plenum Press, 1987.

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Book chapters on the topic "Prostaglandin"

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Donato, Dominique M., Steven K. Hanks, Kenneth A. Jacobson, M. P. Suresh Jayasekara, Zhan-Guo Gao, Francesca Deflorian, John Papaconstantinou, et al. "Prostaglandin." In Encyclopedia of Signaling Molecules, 1478. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_101094.

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Gooch, Jan W. "Prostaglandin." In Encyclopedic Dictionary of Polymers, 917. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_14584.

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Giangiacomo, Annette. "Prostaglandin Analogues." In Encyclopedia of Ophthalmology, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-35951-4_121-2.

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Hubl, W. "Prostaglandin E2." In Lexikon der Medizinischen Laboratoriumsdiagnostik, 1–2. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-49054-9_2394-1.

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Degen, Gisela H., Christoph Vogel, and Josef Abel. "Prostaglandin Synthases." In Enzyme Systems that Metabolise Drugs and Other Xenobiotics, 189–229. Chichester, UK: John Wiley & Sons, Ltd, 2002. http://dx.doi.org/10.1002/0470846305.ch6.

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Giangiacomo, Annette. "Prostaglandin Analogues." In Encyclopedia of Ophthalmology, 1451. Berlin, Heidelberg: Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-540-69000-9_121.

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Hubl, W. "Prostaglandin E2." In Springer Reference Medizin, 1966–67. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_2394.

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Wilson, John Fawcett. "Prostaglandin D2." In The Immunoassay Kit Directory, 1799–800. Dordrecht: Springer Netherlands, 1995. http://dx.doi.org/10.1007/978-94-011-0679-5_85.

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Wilson, John Fawcett. "Prostaglandin E2." In The Immunoassay Kit Directory, 1801–8. Dordrecht: Springer Netherlands, 1995. http://dx.doi.org/10.1007/978-94-011-0679-5_86.

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Wilson, John Fawcett. "Prostaglandin F2α." In The Immunoassay Kit Directory, 1809–12. Dordrecht: Springer Netherlands, 1995. http://dx.doi.org/10.1007/978-94-011-0679-5_87.

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Conference papers on the topic "Prostaglandin"

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Maher, SA, MA Birrell, and MG Belvisi. "Prostaglandin E2Mediates Cough Via the EP3Receptor." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a6056.

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Zhou, Kaile. "Prostaglandin activity in established cell lines." In 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.108381.

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Konya, Viktoria, Eva M. Sturm, Petra Luschnig-Schratl, and Akos Heinemann. "Endothelial Prostaglandin I2 Restrains Eosinophil Trafficking." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a6401.

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Sheehan, S. J., A. B. Latif, S. R. Bibby, R. C. Kester, and S. M. Rajah. "THE RECOVERY OF ENDOTHELIAL CELL AND PLATELET PROSTAGLANDIN SYNTHESES AFTER ADMINISTRATION OF ASPIRIN AND INDOBUFEN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643389.

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Suppression of endothelial prostacyclin (PGI2) by cyclooxygenase inhibition may contribute to the formation of neointimal hyperplasia. While aspirin (ASA) inhibits platelet function for several days, it returns to normal within 24 hours after indobufen (IDB), a reversible cyclooxygenase inhibitor, suggesting that prostacyclin may recover at an even faster rate. In a randomised, controlled study, recovery of platelet and endothelial cell prostaglandin synthesis was compared in 49 New Zealand white rabbits following indobufen (3.5 mg/kg) or aspirin (5 mg/kg). Prostacyclin in arterial incubates and platelet thromboxane A2 (TXA2) production in serum were measured by radioimmunoassay of their meta-bolities, 6Keto PGF1 and thromboxane B2. Platelet prostaglandin synthesis was also monitored by changes in serum malondiealdehyde (MDA).At one hour, both ASA and IDB significantly inhibited PGI2 (p<0.005). TXA2 (p<0.005), and MDA (p<0.02). After IDB, TXA2 and MDA levels returned to normal by 24 hours while inhibition continued in the ASA group (p<0.01). PGI2 synthesis following IDB recovered at 8 hours against 24 hours in the ASA group. We conclude that while both drugs inhibit platelet and endothelial prostaglandins, the earlier recovery of prostacyclin synthesis following indobufen may allow the endothelium to resume its physiological function.
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Spears, Mark, Rekha Chaudhuri, Charles McSharry, Lisa Jolly, Joyce Thompson, Jane Lafferty, Iona Donnelly, Doug Miller, and N. Thomson. "Elevated Sputum Prostaglandin D2 (PGD2) Concentrations In Asthma." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a4448.

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Poskitt, K. R., J. T. C. Irwin, C. M. Backhouse, and C. N. McCollum. "MICROEMBOLISATION DURING SURGICAL SHOCK: EFFECT OF PROSTAGLANDIN E1." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643450.

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Embolisation of microaggregates following major surgery may be a cause of pulmonary arterio-venous shunt and postoperative respiratory failure (1). Prostaglandin E1 may prevent intravascular aggregation and we studied this possibility in a pig model of surgical shock.Following autologous platelet labelling with Indium, 16 pigs (20-30kg) were randomised to receive a perioperative infusion of PGE1 (100ng/kg/min) or placebo. Arterial and Swann Ganz catheters were inserted under anaesthesia prior to surgery consisting of midline laparotomy, exteriorisation of small bowel 1.5 hours of aortic clamping and 1 hour of hypotension. On induction, during shock and at 3 days in survivors platelet and leucocyte count, blood radioactivity, venous aggregates (SFP), lung platelet uptake (LPU), pulmonary vascular resistance (PVR) and alveolar-arterial p02 difference (A-ad02) were measured.All results mean ± sem *p <0.05 Mann Whitney U-testDuring surgical shock, the formation of venous aggregates, the fall in circulating radiolabelled platelets and their accumulation in lungs were reduced by PGE1 (p< 0.05). BP, CVP and PWP were all lower on PGE1 and at 3 days the improvement in A-ad02 in PGE1 pigs failed to reach significance.PGE1 reduced platelet aggregate formation and their subsequent pulmonary microembolisation despite worsening shock due to vasodilation.1. McCollum CN, Campbell IT. The value of measuring intravascular platelet aggregation in the prediction of postoperative pulmonary dysfunction. Br J Surg 1979: 66; 703-707
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Perelman, Juliy M., Eduard V. Nekrasov, Anna G. Prikhodko, and Galina A. Makarova. "A metabolite of prostaglandin D2, 15-deoxy-?12,14-prostaglandin J2 (15d-PGJ2), in exhaled breath condensate (EBC) of asthma patients." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa4946.

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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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Kock, Anna, Karin Larsson, Linda Ljungblad, Helena Idborg, Marina Korotkova, Lotta Elfman, John-Inge Johnsen, Per-Johan Jakobsson, and Per Kogner. "Abstract 3986: Characterization of prostaglandin signaling in primary neuroblastoma." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-3986.

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Oga, Toru, Daiji Sakata, Kiminobu Tanizawa, Yoshio Taguchi, Michiaki Mishima, Kazuo Chin, Takao Shimizu, and Shuh Narumiya. "Prostaglandin F2±-FP Signaling Facilitates Bleomycin-induced Pulmonary Fibrosis." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a1967.

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Reports on the topic "Prostaglandin"

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Moreno, Jacqueline. Vitamin D-Prostaglandin Interactions and Effects on Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2005. http://dx.doi.org/10.21236/ada446263.

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Moreno, Jacqueline. Vitamin D-Prostaglandin Interactions and Effects in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2006. http://dx.doi.org/10.21236/ada463443.

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Naseem, Syed M., K. A. Mereish, Rikki Solow, and Harry Hines. Toxin-Induced Activation of Rat Hepatocyte Prostaglandin Synthesis and Phospholipid Metabolism. Fort Belvoir, VA: Defense Technical Information Center, April 1990. http://dx.doi.org/10.21236/ada221157.

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Liebert, Monica. Increase in Breast Cancer Stem Cells in Response to Prostaglandin E2. Revision. Fort Belvoir, VA: Defense Technical Information Center, October 2010. http://dx.doi.org/10.21236/ada583511.

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Kim, Sangmi. Urinary Level of Prostaglandin E2 Metabolite and Risk of Incident Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, January 2012. http://dx.doi.org/10.21236/ada559390.

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Fields, Michael, Mordechai Shemesh, Philip A. Fields, Anna-Riitta Fuchs, and Michael Diskin. Bovine Relaxin: A Placental Source and Effects on Prostaglandin and Steroid Metabolism. United States Department of Agriculture, January 1988. http://dx.doi.org/10.32747/1988.7568097.bard.

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Fields, Michael, Mordechai Shemesh, and Phillip A. Fields. Bovine Relaxin: A Placental Source and Effects on Prostaglandin and Steroid Metabolism. United States Department of Agriculture, December 1991. http://dx.doi.org/10.32747/1991.7594379.bard.

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Will, James A., Ricardo Saban, and Nian-Ji Li. Pharmacologic Studies on the In Vitro Bronchodilating Vasoactive Actions of Oligo-PGB (Prostaglandin B). Fort Belvoir, VA: Defense Technical Information Center, January 1988. http://dx.doi.org/10.21236/ada193138.

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McDonagh, Marian, Andrea C. Skelly, Amy Hermesch, Ellen Tilden, Erika D. Brodt, Tracy Dana, Shaun Ramirez, et al. Cervical Ripening in the Outpatient Setting. Agency for Healthcare Research and Quality (AHRQ), March 2021. http://dx.doi.org/10.23970/ahrqepccer238.

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Objectives. To assess the comparative effectiveness and potential harms of cervical ripening in the outpatient setting (vs. inpatient, vs. other outpatient intervention) and of fetal surveillance when a prostaglandin is used for cervical ripening. Data sources. Electronic databases (Ovid® MEDLINE®, Embase®, CINAHL®, Cochrane Central Register of Controlled Trials, and Cochrane Database of Systematic Reviews) to July 2020; reference lists; and a Federal Register notice. Review methods. Using predefined criteria and dual review, we selected randomized controlled trials (RCTs) and cohort studies of cervical ripening comparing prostaglandins and mechanical methods in outpatient versus inpatient settings; one outpatient method versus another (including placebo or expectant management); and different methods/protocols for fetal surveillance in cervical ripening using prostaglandins. When data from similar study designs, populations, and outcomes were available, random effects using profile likelihood meta-analyses were conducted. Inconsistency (using I2) and small sample size bias (publication bias, if ≥10 studies) were assessed. Strength of evidence (SOE) was assessed. All review methods followed Agency for Healthcare Research and Quality Evidence-based Practice Center methods guidance. Results. We included 30 RCTs and 10 cohort studies (73% fair quality) involving 9,618 women. The evidence is most applicable to women aged 25 to 30 years with singleton, vertex presentation and low-risk pregnancies. No studies on fetal surveillance were found. The frequency of cesarean delivery (2 RCTs, 4 cohort studies) or suspected neonatal sepsis (2 RCTs) was not significantly different using outpatient versus inpatient dinoprostone for cervical ripening (SOE: low). In comparisons of outpatient versus inpatient single-balloon catheters (3 RCTs, 2 cohort studies), differences between groups on cesarean delivery, birth trauma (e.g., cephalohematoma), and uterine infection were small and not statistically significant (SOE: low), and while shoulder dystocia occurred less frequently in the outpatient group (1 RCT; 3% vs. 11%), the difference was not statistically significant (SOE: low). In comparing outpatient catheters and inpatient dinoprostone (1 double-balloon and 1 single-balloon RCT), the difference between groups for both cesarean delivery and postpartum hemorrhage was small and not statistically significant (SOE: low). Evidence on other outcomes in these comparisons and for misoprostol, double-balloon catheters, and hygroscopic dilators was insufficient to draw conclusions. In head to head comparisons in the outpatient setting, the frequency of cesarean delivery was not significantly different between 2.5 mg and 5 mg dinoprostone gel, or latex and silicone single-balloon catheters (1 RCT each, SOE: low). Differences between prostaglandins and placebo for cervical ripening were small and not significantly different for cesarean delivery (12 RCTs), shoulder dystocia (3 RCTs), or uterine infection (7 RCTs) (SOE: low). These findings did not change according to the specific prostaglandin, route of administration, study quality, or gestational age. Small, nonsignificant differences in the frequency of cesarean delivery (6 RCTs) and uterine infection (3 RCTs) were also found between dinoprostone and either membrane sweeping or expectant management (SOE: low). These findings did not change according to the specific prostaglandin or study quality. Evidence on other comparisons (e.g., single-balloon catheter vs. dinoprostone) or other outcomes was insufficient. For all comparisons, there was insufficient evidence on other important outcomes such as perinatal mortality and time from admission to vaginal birth. Limitations of the evidence include the quantity, quality, and sample sizes of trials for specific interventions, particularly rare harm outcomes. Conclusions. In women with low-risk pregnancies, the risk of cesarean delivery and fetal, neonatal, or maternal harms using either dinoprostone or single-balloon catheters was not significantly different for cervical ripening in the outpatient versus inpatient setting, and similar when compared with placebo, expectant management, or membrane sweeping in the outpatient setting. This evidence is low strength, and future studies are needed to confirm these findings.
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Eck, Stephen L. The Role of Breast Cancer Derived Prostaglandin E2 in the Elaboration of a Therapeutic Immune Response. Fort Belvoir, VA: Defense Technical Information Center, July 2001. http://dx.doi.org/10.21236/ada409420.

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