Journal articles on the topic 'Prostaglandin'
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1
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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Mitchell, MD, RJ Romero, SS Edwin, and MS Trautman. "Prostaglandins and parturition." Reproduction, Fertility and Development 7, no. 3 (1995): 623. http://dx.doi.org/10.1071/rd9950623.
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It seems likely that prostaglandins play a significant part in the mechanisms of parturition both at term and preterm. Concentrations of prostaglandins are increased in the blood, urine and amniotic fluid during labour. There are differences in the concentrations of prostaglandins in amniotic fluid from the forebag and hindbag. Nevertheless, if liquor is sampled only from the hindbag a highly significant increase in prostaglandin concentrations occurs throughout labour. Furthermore, we now have evidence that prostaglandin concentrations in amniotic fluid increase before the onset of labour. Prostaglandins are synthesized by uterine tissues and increased rates of production occur during labour. The amnion, chorion and decidua all contain mRNA for the newly-discovered inducible form of prostaglandin H synthase (PGHS-2) as well as mRNA for the constitutive form (PGHS-1). Using the reverse transcription polymerase chain reaction (RT-PCR) both mRNAs can be detected during late pregnancy whether women are in labour or not. PGHS-2 protein is detected by Western blot analysis in cells derived from all three tissues. There is regulation of PGHS-2 protein amounts by cytokines, phorbol esters and growth factors. For example, in amnion cells interleukin-1 beta induces a rapid increase in PGHS-2 mRNA levels followed by a decrease to undetectable levels within 4 h of treatment; PGHS-2 protein amounts are also elevated by this treatment. Administration of prostaglandins will induce labour and delivery, whereas inhibition of prostaglandin biosynthesis will delay labour and delivery. Hence, increased prostaglandin production is likely to be a key determinant of the onset and progression of the parturient process.
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Watson, John, and Siew Yeam Chuah. "Technique for the primary culture of human breast cancer cells and measurement of their prostaglandin secretion." Clinical Science 83, no. 3 (September 1, 1992): 347–52. http://dx.doi.org/10.1042/cs0830347.
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1. A method is described for the primary culture of human breast tumour cells on feeder layers of the STO mouse embryo fibroblast cell line. 2. The secretion of the prostaglandins E2 and F2α from the cells was measured and the results indicate that the secretion of both prostaglandins was dependent on oestrogen-receptor status, with cells from oestrogen-receptor-positive tumours secreting significantly more prostaglandin than cells from oestrogen-receptor-negative tumours. 3. Postaglandin E2, but not prostaglandin F2α, secretion was also significantly greater from cells of tumours from postmenopausal women than from cells of tumours from premenopausal women. Small (< 3 cm) tumours secreted significantly more prostaglandin than large (> 3 cm) tumours, and increased levels of prostaglandin were secreted with advancing clinical stage (T1-T4). 4. Additional evidence for increased prostaglandin metabolism in oestrogen-receptor-positive tumours compared with oestrogen-receptor-negative tumours was obtained from studies on the uptake of [14C]arachidonic acid from the cultures. Significantly more labelled arachidonic acid was incorporated into cells from oestrogen-receptor-positive tumours compared with oestrogen-receptor-negative tumours, with the subsequent release of more prostaglandin in response to various stimuli.
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Madar, R. John, Tim J. D. Donaldson, and Stewart Hunter. "Prostaglandins in congenital heart disease—potential for confusion." Cardiology in the Young 5, no. 2 (April 1995): 202–3. http://dx.doi.org/10.1017/s1047951100011859.
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the use of prostaglandians in maintaining the patency of the arterial duct in congenital heart disease is well established. Intravenous1-3 and ora12–4 administration has been used, although for acute use intravenous and possibly intraosseous5 routes are favored. Both prostaglandin E1 (alprostadil—ProstinVR: Upjohn)1,4 and prostaglandin E2 (dinoprostone—Prostin E2: Upjohn)2,3 are used for this purpose, although only prostaglandin E1 is licensed for this indication in the United Kingdom. Prostaglandin E1 costs approximately 8 times more than prostaglandin E2 (£56.96 versus £7.43 per vial).
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Sahmay, S., A. Coke, N. Hekim, and T. Atasu. "Maternal, Umbilical, Uterine and Amniotic Prostaglandin E and F2α Levels in Labour." Journal of International Medical Research 16, no. 4 (July 1988): 280–85. http://dx.doi.org/10.1177/030006058801600405.
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This paper confirms the important role played by prostaglandins in the induction of uterine contractions and the initiation of human labour, although the exact mechanism of action in labour remains unclear. Seventeen pregnant women at term were studied. Of these nine were in labour and the remainder underwent elective section. Prostaglandin E and F2α levels were measured in maternal, umbilical and uterine plasma and amniotic fluid by radioimmunoassay. Levels of prostaglandin E were generally higher than prostaglandin F2α but they were significantly lower in maternal and uterine plasma. Levels of prostaglandin F2α were significantly higher in maternal plasma during labour. The highest levels of prostaglandin were found in amniotic fluid. Measurements indicate that the decreasing ratio of prostaglandin E/F2α is more important in the initiation of labour than absolute levels of either prostaglandin.
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Scott, I. M., R. H. Fertel, and J. A. Boulant. "Leukocytic pyrogen effects on prostaglandins in hypothalamic tissue slices." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 253, no. 1 (July 1, 1987): R71—R76. http://dx.doi.org/10.1152/ajpregu.1987.253.1.r71.
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Some studies suggest that leukocytic pyrogen (LP) increase hypothalamic prostaglandins which, in turn, affect hypothalamic thermoregulatory neurons to produce fever. The present study used radioimmunoassays to quantitate the ability of guinea pig hypothalamic tissue slices to produce prostaglandin E2 (PGE2), prostaglandin F2 alpha (PGF2 alpha), 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), and thromboxane B2 (TxB2). Dose- and time-dependent prostaglandin increases occurred when these slices were perfused with LP media. Steady-state levels of tissue release were reached at 0-3 min for 6-keto-PGF1 alpha, at 6-9 min for PGE2 and PGF2 alpha, and at 12-15 min for TxB2. With the exception of 6-keto-PGF1 alpha, all substances showed continuous dose-response relationships for concentrations ranging from 0.001 to 0.25 LP dilutions. Tissue PGE2, for example, was 0.7 pg X min-1 X mg-1 with the 0.001 LP dilution and 8.7 pg X min-1 X mg-1 with the 0.25 LP dilution. Indomethacin blocked much of the LP-induced prostaglandin increase. Although there is a relationship between hypothalamic LP and prostaglandins in response to physiological LP levels, tissue prostaglandins are several orders of magnitude lower than concentrations necessary to produce fever by hypothalamic microinjection. This suggests that prostanoids, such as PGE2, may not be the sole mediators of fever induced by leukocytic pyrogen.
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Lijnen, P., J. Staessen, R. Fagard, and A. Amery. "Effect of prostaglandin inhibition by indomethacin on plasma active and inactive renin concentration in men." Canadian Journal of Physiology and Pharmacology 69, no. 9 (September 1, 1991): 1355–59. http://dx.doi.org/10.1139/y91-200.
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The effect of inhibition of prostaglandin synthesis by indomethacin on active renin and on acid-activable inactive renin was studied in nine healthy, sodium-replete men, both at rest and exercise. These volunteers were investigated after pretreatment with placebo or indomethacin, 150 mg daily for 3 days. Indomethacin induced a decrease in active (p = 0.004), total (p < 0.001), and inactive (p = 0.02) renin at rest recumbent on average by 42, 19, and 8%, respectively, and at rest sitting on average by 45, 15, and 3%, respectively. Inhibition of prostaglandins with indomethacin reduced (p < 0.001) active and total renin at each level of work load but not (p = 0.32) inactive renin. However, the exercise-induced stimulation (p < 0.05) of active and total renin still occur during indomethacin. Indomethacin reduced (p < 0.001) at rest sitting and at maximal exercise the plasma concentrations of immunoreactive prostaglandins E2 by 50 and 54%, respectively, prostaglandin F2α by 36 and 39%, respectively, and 13,14-dihydro-15-keto-prostaglandin Fα by 38 and 60%, respectively. The urinary excretion of immunoreactive prostaglandin E2 and F2α was also reduced.Key words: indomethacin, prorenin, active renin, prostaglandins.
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Bandali, Karim S., and Uwe Ackermann. "Are prostaglandins involved in atrial natriuretic peptide mechanisms of cardiovascular control?" Canadian Journal of Physiology and Pharmacology 77, no. 3 (March 1, 1999): 211–15. http://dx.doi.org/10.1139/y99-004.
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Atrial natriuretic peptide (ANP) can excite cardiac nerve endings and invoke a decrease in arterial blood pressure and a reduction in renal sympathetic nerve activity. Our laboratory has previously demonstrated that this renal depressor reflex was invoked by systemic injection of ANP and not by the direct application of ANP to the epicardium, a major locus for vagal afferents. We now examine whether inhibition of prostaglandin synthesis impairs reflex responses that are normally associated with ANP injections. Renal sympathetic nerve activity, arterial blood pressure, and heart rate were recorded in anesthetized rats. Indomethacin was used to inhibit prostaglandin synthesis through the cyclooxygenase pathway. The ANP-mediated decrease in arterial blood pressure and renal sympathetic nerve activity, observed when prostaglandin synthesis was inhibited, did not differ significantly from the decreases observed in these parameters when prostaglandin synthesis was not inhibited. Heart rate remained unchanged. Our results suggest that the sympatho-inhibitory effects of ANP do not require prostaglandins as intermediary compounds.Key words: sympathetic nervous system, renal nerves, prostaglandins.
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Dongre, Veena, R. C. Dabhade, and A. M. Khurad. "Effect of prostaglandin on reproduction in relation to pituitary gonadal axis in the fish, Cyprinus carpio (L.)." Journal of Applied and Natural Science 4, no. 2 (December 1, 2012): 192–95. http://dx.doi.org/10.31018/jans.v4i2.247.
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Prostaglandins are a class of fatty acids which are “traditionally” associated with a variety of autocrine and paracrine functions in the vertebrate body. In many fishes, however, F prostaglandins also function as a hormone that stimulates sexual behavior. In the present study, F prostaglandin was used to assess the efficacy on reproductive behavior and spawning in relation to pituitary gonadal axis in the fish, Cyprinus carpio by administering different doses. Early maturity was observed in fish leading to courtship and spawning. The histological study of olfactory lobe, pituitary gland and gonads showed that the prostaglandin is also functioning as potent olfactory stimulants with sex pheromonal activity of the fish. F prostaglandin was metabolized and released into the water where it functions as a sex pheromone, stimulating male and female sexual behavior resulting into spawning. It was concluded that F prostaglandin acts as an inducer for successful breeding in the fish, C. carpio.
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Thore, C. R., M. Nam, and D. Busija. "Phorbol ester-induced prostaglandin production in piglet cortical astroglia." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 267, no. 1 (July 1, 1994): R34—R37. http://dx.doi.org/10.1152/ajpregu.1994.267.1.r34.
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We examined effects of phorbol 12,13-dibutyrate (PDB), which activates protein kinase C (PKC), on prostaglandin and leukotriene production in piglet cultured glia derived from cerebral cortex and white matter. Levels of prostaglandins were determined using enzyme immunoassay. Baseline levels in media for prostaglandin F2 alpha (PGF2 alpha) were 730 +/- 116 pg/ml and increased to 1,551 +/- 196 pg/ml at 10(-8) M PDB (P < 0.05) and to 2,182 +/- 190 pg/ml at 10(-6) M PDB (P < 0.05) (n = 16). Little or no 6-keto-prostaglandin F1 alpha, prostaglandin E2, or leukotrienes C4/D4 were produced. PGF2 alpha levels in media did not increase in the presence of the vehicle for PDB (dimethyl sulfoxide) or 4 alpha-phorbol 12,13-didecanoate (PDD; a phorbol ester that does not activate protein kinase C) or when indomethacin (10 micrograms/ml), quinacrine (10(-6) M), or isoquinolinylsulfonylmethyl piperazine (10(-4) M) (an inhibitor of PKC activation) was coadministered with PDB. We conclude that glia can be important contributors of prostaglandins to extracellular-cerebrospinal fluids where they could influence cerebrovascular tone, and that PDB probably increases prostaglandin production via liberation of arachidonic acid by PKC-induced activation of phospholipase A2.
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Asrina, Andi, Arsyad Aryadi, and Nilawati Andi. "Kadar Prostaglandin dan Endorfin pada Remaja dengan Dismenore Primer yang diberi Hidroterapi Hangat dan Dingin." Jurnal Riset Kesehatan Poltekkes Depkes Bandung 12, no. 1 (May 30, 2020): 115–21. http://dx.doi.org/10.34011/juriskesbdg.v12i1.841.
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This study aims to determine the comparison of prostaglandin and endorphin levels in adolescents with primary dysmenorrhea with and without warm (37-40oC) and cold (18-20oC) hydrotherapy. This quasi-experimental study with a post-test only controls group design was carried out in Islamic Boarding Schools with a sample of 36 young girls divided into 3 groups: 12 teens given warm hydrotherapy, 12 teens given cold hydrotherapy and 12 teens not given intervention (control). Blood plasma is taken after an intervention is given on the first day of menstruation. Examination of prostaglandin and endorphins levels using the enzyme-linked immunosorbent assay (ELISA) kit method. After cold hydrotherapy, the mean levels of prostaglandins in the cold hydrotherapy group were twice higher (569 pg/ml) compared to controls (394 pg/ml). The mean prostaglandin level in the warm hydrotherapy group also showed an increase prostaglandin (437 pg/ml) compared to the control (394 pg/ml). In addition to increasing levels of prostaglandins, increased levels of endorphins also occurred in the group given warm hydrotherapy (154 pg/ml) and the group was given cold hydrotherapy (187 pg/ml) compared to the control (119 pg/ml) p = 0.001. The conclusion in this study is that warm and cold hydrotherapy can increase levels of prostaglandins and endorphins in adolescents with primary dysmenorrhea. However, cold hydrotherapy increases endorphin levels higher than warm hydrotherapy.
Key words: Prostaglandin, Endorphin, Hydrotherapy, Primary Dismenorrhea.
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Hsu, Ho-Wei, Ting-Yi Lin, Yi-Ching Liu, Jwu-Lai Yeh, and Jong-Hau Hsu. "Molecular Mechanisms Underlying Remodeling of Ductus Arteriosus: Looking beyond the Prostaglandin Pathway." International Journal of Molecular Sciences 22, no. 6 (March 22, 2021): 3238. http://dx.doi.org/10.3390/ijms22063238.
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The ductus arteriosus (DA) is a physiologic vessel crucial for fetal circulation. As a major regulating factor, the prostaglandin pathway has long been the target for DA patency maintenance or closure. However, the adverse effect of prostaglandins and their inhibitors has been a major unsolved clinical problem. Furthermore, a significant portion of patients with patent DA fail to respond to cyclooxygenase inhibitors that target the prostaglandin pathway. These unresponsive medical patients ultimately require surgical intervention and highlight the importance of exploring pathways independent from this well-recognized prostaglandin pathway. The clinical limitations of prostaglandin-targeting therapeutics prompted us to investigate molecules beyond the prostaglandin pathway. Thus, this article introduces molecules independent from the prostaglandin pathway based on their correlating mechanisms contributing to vascular remodeling. These molecules may serve as potential targets for future DA patency clinical management.
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Bedrick, A. D., M. A. Wells, D. L. Ford, and O. Koldovsky. "Intact biliary excretion of gastrically administered prostaglandin F2 alpha in rats: developmental differences." American Journal of Physiology-Gastrointestinal and Liver Physiology 253, no. 6 (December 1, 1987): G787—G792. http://dx.doi.org/10.1152/ajpgi.1987.253.6.g787.
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Tritium-labeled prostaglandin F2 alpha was administered via orogastric tube to bile duct-cannulated suckling and weanling rats to determine if maturational differences were present in the biliary excretion of prostaglandin F2 alpha and metabolites. Animals were killed 2 h after radioactivity administration. Characterization of radioactivity present in bile revealed age-related differences in biliary prostaglandin F2 alpha excretion. Suckling rats had a greater proportion of radioactivity migrating in chromatographic regions of greater polarity than prostaglandin F2 alpha. Compared with the weanling, a significantly greater amount of radioactivity cochromatographed with intact, unmetabolized prostaglandin F2 alpha (33.08 +/- 1.99 vs. 21.38 +/- 1.46). These results indicate that orogastrically administered prostaglandin F2 alpha can be absorbed from the gastrointestinal tract, transported to the liver, and subsequently excreted into bile and detected in an unmetabolized form in suckling and weanling rats. The enterohepatic circulation of milk-derived prostaglandin present in bile may contribute to the overall content of intestinal prostaglandins.
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Ajuebor, Maureen N., Anita Singh, and John L. Wallace. "Cyclooxygenase-2-derived prostaglandin D2 is an early anti-inflammatory signal in experimental colitis." American Journal of Physiology-Gastrointestinal and Liver Physiology 279, no. 1 (July 1, 2000): G238—G244. http://dx.doi.org/10.1152/ajpgi.2000.279.1.g238.
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The ability of nonsteroidal anti-inflammatory drugs and cyclooxygenase-2 inhibitors to exacerbate inflammatory bowel disease suggests that prostaglandins are important anti-inflammatory mediators in this context. Prostaglandin D2 has been suggested to exert anti-inflammatory effects. We investigated the possibility that prostaglandin D2 derived from cyclooxygenase-2 plays an important role in downregulating colonic inflammation in rats. Colitis was induced by intracolonic administration of trinitrobenzene sulfonic acid. At various times thereafter (from 1 h to 7 days), colonic prostaglandin synthesis and myeloperoxidase activity (index of granulocyte infiltration) were measured. Prostaglandin D2synthesis was elevated >4-fold above controls within 1–3 h of induction of colitis, preceding significant granulocyte infiltration. Treatment with a selective cyclooxygenase-2 inhibitor abolished the increase in prostaglandin D2 synthesis and caused a doubling of granulocyte infiltration. Colonic granulocyte infiltration was significantly reduced by administration of prostaglandin D2 or a DP receptor agonist (BW-245C). These results demonstrate that induction of colitis results in a rapid increase in prostaglandin D2 synthesis via cyclooxygenase-2. Prostaglandin D2 downregulates granulocyte infiltration into the colonic mucosa, probably through the DP receptor.
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Srivastava, R. C., A. Tandon, A. N. Nagappa, and R. K. Sharma. "Liquid membrane phenomena in prostaglandins: Studies on prostaglandin E1 and prostaglandin F2α." Journal of Colloid and Interface Science 117, no. 2 (June 1987): 375–83. http://dx.doi.org/10.1016/0021-9797(87)90396-1.
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Mikkelsen, Ulla Ramer, Ida Carøe Helmark, Michael Kjær, and Henning Langberg. "Prostaglandin synthesis can be inhibited locally by infusion of NSAIDS through microdialysis catheters in human skeletal muscle." Journal of Applied Physiology 104, no. 2 (February 2008): 534–37. http://dx.doi.org/10.1152/japplphysiol.01016.2007.
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Prostaglandins are known to be involved in the regulation of local blood flow within human skeletal muscles during exercise, and the concentration of prostaglandins increases locally and systemically in response to exercise. The systemic release of prostaglandins can be inhibited by oral intake of nonsteroidal anti-inflammatory drugs (NSAIDs). However, to study the local role of prostaglandins, the formation of prostaglandins within the tissue must be controlled. Microdialysis enables determination of local concentrations of water-soluble substances within the tissue. In the present study, the microdialysis method was used to infuse NSAIDs locally into human skeletal muscles producing a local block of prostaglandin formation. In addition, the graded blockade at various distances from the infusion site within the muscle during rest, exercise and recovery was determined. Microdialysis was performed in thigh muscles (vastus lateralis muscle) in six healthy men. One of the microdialysis catheters was used to block prostaglandin synthesis by infusion of the NSAID indomethacin. Additional catheters were placed 1 and 4 cm away from the infusion and in the contralateral leg (working control). Following 2 h of rest, the subjects performed 200 maximal eccentric contractions with each leg followed by 3 h of rest. The study revealed that infusion of NSAID reduced local prostaglandin E2 concentration by ∼30–50% (4 cm away from the infusion) and 85% (1 cm away from the infusion) compared with the contralateral (unblocked) thigh muscle. In conclusion, the present study shows that infusion of NSAIDs into human muscle via microdialysis catheters results in a graded blockade of prostaglandin synthesis.
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Tsang, B. K., M. T. Domingo, J. E. H. Spence, P. R. Garner, D. K. Dudley, and H. Oxorn. "Endometrial prostaglandins and menorrhagia: influence of a prostaglandin synthetase inhibitor in vivo." Canadian Journal of Physiology and Pharmacology 65, no. 10 (October 1, 1987): 2081–84. http://dx.doi.org/10.1139/y87-326.
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Prostaglandin levels in the human endometrium were determined on day 2 of the menstrual cycle in eumenorrheic subjects and in patients with menorrhagia, dysmenorrhea, or both. Menorrhagic subjects had significantly higher levels of endometrial prostaglandins of the E and F series when compared with eumenorrheics. Prostaglandin E levels were markedly higher than prostaglandin F. In 10 menorrhagic subjects who completed a double-blind clinical study on the effectiveness of mefenamic acid in lowering menstrual blood loss, 9 exhibited statistically significant reduction in endometrial prostaglandin levels. A decrease in menstrual blood loss was also noted during mefenamic acid treatment in these patients. These findings are consistent with the concept that abnormally high uterine prostaglandin levels may be an important etiologic factor in menorrhagia and support the notion that one of the mechanisms of action of nonsteroidal anti-inflammatory agents in the treatment of this menstrual disorder is inhibition of endometrial prostaglandin production.
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Beierwaltes, W. H. "Prostaglandin independence of kinin-stimulated renin release." American Journal of Physiology-Renal Physiology 252, no. 5 (May 1, 1987): F794—F799. http://dx.doi.org/10.1152/ajprenal.1987.252.5.f794.
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Bradykinin can increase prostaglandin synthesis and also stimulate renin release in vitro. Because prostaglandins also stimulate renin, studies were performed to determine whether bradykinin stimulation of renin is a function of prostaglandin synthesis. Isolated glomeruli with attendant arteriolar attachments were harvested from rat kidneys and superfused. The effluent was analyzed for renin, prostaglandins E2 and I2 (6-keto-PGF1 alpha). Bradykinin (10(-5) M) increased renin by 50% with a concomitant increase in prostacyclin (PGI2) but not in prostaglandin E2 (PGE2). The cyclooxygenase inhibitor meclofenamate (1.6 X 10(-5) M) inhibited bradykinin-induced PGI2 synthesis but not the concurrent increase in renin release. Additionally, neither the phospholipase inhibitor quinacrine (10(-2) M) nor the prostacyclin synthetase inhibitor 9,11-azoprosta-5,13-dienoic acid (Azo analogue-1) (5.67 X 10(-6) M) eliminated bradykinin-induced renin release. Superfusion with calcium-free media and EDTA increased basal renin release 2.5-fold, and bradykinin stimulated a twofold increase in renin release. Neither a high (10(-2) M) media calcium nor the calcium channel blocker nifedipine (10(-6) M) eliminated bradykinin stimulation of renin. These results suggest that bradykinin stimulation of renin is at least partially independent of prostaglandin synthesis and that bradykinin must act by some prostaglandin-independent pathway to induce renin release from isolated glomeruli.
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Adachi, Hisanobu, Takehiro Suzuki, Michiaki Abe, Naoki Asano, Hiroya Mizutamari, Masayuki Tanemoto, Toshiyuki Nishio, et al. "Molecular characterization of human and rat organic anion transporter OATP-D." American Journal of Physiology-Renal Physiology 285, no. 6 (December 2003): F1188—F1197. http://dx.doi.org/10.1152/ajprenal.00402.2002.
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We have isolated and characterized a novel human and rat organic anion transporter subtype, OATP-D. The isolated cDNA from human brain encodes a polypeptide of 710 amino acids ( Mr 76,534) with 12 predicted transmembrane domains. The rat clone encodes 710 amino acids ( Mr 76,821) with 97.6% amino acid sequence homology with human OATP-D. Human and rat OATP-D have moderate amino acid sequence homology with LST-1/rlst-1, the rat oatp family, the prostaglandin transporter, and moat1/MOAT1/KIAA0880/OATP-B. Phylogenetic tree analysis revealed that OATP-D is branched in a different position from all known organic anion transporters. OATP-D transports prostaglandin E1 ( Km 48.5 nM), prostaglandin E2 ( Km 55.5 nM), and prostaglandin F2α, suggesting that, functionally, OATP-D encodes a protein that has similar characteristics to those of the prostaglandin transporter. Rat OATP-D also transports prostaglandins. The expression pattern of OATP-D mRNA was abundant mainly in the heart, testis, brain, and some cancer cells. Immunohistochemical analysis further revealed that rat OATP-D is widely expressed in the vascular, renal, and reproductive system at the protein level. These results suggest that OATP-D plays an important role in translocating prostaglandins in specialized tissues and cells.
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Gibb, William, and Jean-Claude Lavoie. "Effects of glucocorticoids on prostaglandin formation by human amnion." Canadian Journal of Physiology and Pharmacology 68, no. 6 (June 1, 1990): 671–76. http://dx.doi.org/10.1139/y90-101.
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The human amnion may be an important source of prostaglandins involved in the onset of human labor and therefore it is important to define the factors that regulate their formation in this tissue. In the present study we demonstrate that glucocorticoids inhibit prostaglandin production by freshly isolated amnion cells. The inhibitory action of the glucocorticoids, however, changes to a stimulatory action when the cells are maintained in primary culture for a few days. For both inhibition and stimulation, concentrations of 10−8 M dexamethasone or greater were required to give significant effects, and estradiol and progesterone had no effect on the prostaglandin output of the cells. Epidermal growth factor (EGF), which has previously been found to stimulate prostaglandin output by confluent amnion cells, did not alter prostaglandin output of cells initially placed in culture. Furthermore, the stimulatory action of EGF and dexamethasone appeared additive. The calcium ionophore A23187 stimulated prostaglandin output in freshly isolated cells and accentuated the inhibitory effect of dexamethasone. These studies indicate that prostaglandin formation by human amnion during pregnancy could be regulated by glucocorticoids. These steroids are easily available to the amnion by way of cortisone conversion to Cortisol by the maternal decidua. The results also indicate that amnion is capable of responding to glucocorticoids in both a stimulatory and inhibitory fashion and whether one or both actions are of importance in vivo is a question that is as yet unresolved.Key words: prostaglandins, amnion, fetal membranes, glucocorticoids, labor, pregnancy.
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Goetz, F. W. "Compartmentalization of prostaglandin synthesis within the fish ovary." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 260, no. 5 (May 1, 1991): R862—R865. http://dx.doi.org/10.1152/ajpregu.1991.260.5.r862.
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Numerous studies have shown that the follicle walls surrounding mature vertebrate oocytes are capable of producing primary prostaglandins. However, very few studies have looked at the prostaglandin synthetic potential of other ovarian tissue components. In brook trout (Salvelinus fontinalis) and goldfish (Carassius auratus), mature follicle walls can produce prostaglandins E and F (PGE and PGF, respectively); however, it is apparent that several other tissues within the fish ovary also produce specific primary PGs. Incubation of stroma or connective tissue from brook trout and goldfish ovaries with [14C]-arachidonic acid resulted in a very significant production of PGE2, whereas small immature oocytes of both species produced primarily PGF2 alpha. While the function of the primary prostaglandins produced by tissues external to the mature oocytes is unknown, it is important to recognize that multiple sites for prostaglandin synthesis are present within the fish ovary.
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Kulsum, Syeda Ummay, Sabera Khatun, and SM Shahnawaz Bin Tabib. "Use of Misoprostol in Pregnancy- A Review Article." Medicine Today 22, no. 2 (October 31, 2012): 94–98. http://dx.doi.org/10.3329/medtoday.v22i2.12443.
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Prostaglandins are the pharmacological agents used for induction of labour and augmentation of labour. Prostaglandin E2 gel is used for cervical ripening and induction of labour. These are however, costly and need to be stored in a refrigerator at a temperature of 2 - 8°C, half life 18 months. The Tablet form of prostaglandin E2 is not available in Bangladesh. Misoprostol, a synthetic prostaglandin (PG) E1 analogue is used orally for the treatment of gastric and duodenal ulcer and used as a cytoprotective agent. It was first used for labour induction in 1987. Prostaglandin can be used in several gynaecological and obstetric conditions. It can be given through several routes. This article will elaborately delinate the role of misoprostol, a prostaglandin in obstetrics and gynaecological conditions. Medicine Today 2010 Volume 22 Number 02 Page 94-98 DOI: http://dx.doi.org/10.3329/medtoday.v22i2.12443
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Kutyrev, Olennikov, Kaschenko, and Mazur. "DYNAMICS OF SECRETION OF PROSTAGLANDINS E2 AND D2 WITH DIBOTHRIOCHEPHALLUS DENDRITICUS (CESTODA) PLEROCERCOIDS IN RESPONSE TO EXPOSURE OF BLOOD SERUM OF BAIKAL CISCO, THE HOST." THEORY AND PRACTICE OF PARASITIC DISEASE CONTROL, no. 21 (May 29, 2020): 180–86. http://dx.doi.org/10.31016/978-5-9902341-5-4.2020.21.180-186.
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Parasites regulate host immune response via secretion of soluble mediators which interact in a certain way with cells and molecules of the immune system. The aim of the study was to determine changes of prostaglandins E2 и D2 content in Dibothriochephallus dendriticus plerocercoids and also in the incubation media during incubation of tapeworms with addition of blood serum from the intermediate host – Baikal cisco. D. dendriticus plerocercoids were retrieved from the host body cavity, ashed in the physiological solution and placed in incubation media. Microcolumn high-performance liquid chromatography was used to detect prostaglandins. Concentration of prostaglandins in the plerocercoid organism increased insignificantly after incubation in the Hanks’ solution with addition of blood serum, when compared with incubation in the Hanks’ solution only. Concentration of prostaglandin E2 increased significantly in the incubation media after incubation of plerocercoids in the Hanks’ solution with addition of blood serum. Prostaglandin D2 was also identified in high concentrations after 12 h and 24 h of incubation, whereas prostaglandin D2 was not quite detected during incubation in Hanks’ solution only.
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Hartuti, Noviyani, and Asyima Asyima. "Hubungan prostaglandin terhadap kejadian premenstrual syndrome (PMS) pada remaja putri." Holistik Jurnal Kesehatan 15, no. 4 (April 20, 2022): 713–19. http://dx.doi.org/10.33024/hjk.v15i4.5307.
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Background: Young women and middle-aged women during the luteal phase of the menstrual cycle will experience emotional and physical problems called premenstrual syndrome (PMS).Purpose: To determine the relationship of prostaglandins to the incidence of premenstrual syndrome in young women at the Pelamonia Midwifery Academy.Method: A Cross-Sectional Study with a population was the student of nursing academy Pelamonia Makassar. The sampling technique used a total sampling technique with a sample of 50 respondents. The research instrument used a daily note sheet (LCH), questionnaire data collection which included identity and symptoms or complaints of premenstrual syndrome. Prostaglandin examination using the Prostaglandin Enzyme-Linked ImmunoSorbent Assay (ELISA) kitResults: Showed that of the 26 respondents with mild PMS, 23 respondents (46%) had prostaglandin F2α levels <420.6 pg / mL and 3 respondents (6%) had prostaglandin F2α levels> 420.6 pg / mL. Meanwhile, of the 24 respondents who had severe PMS, 15 respondents (30%) had prostaglandin F2α levels <420.6 pg / mL and 9 respondents (18%) had prostaglandin F2α levels> 420.6 pg / mL. The results of the Chi-Square statistical test for the relationship of prostaglandins to the incidence of premenstrual syndrome in adolescent girls at the 0.05 level indicate that p value = 0.047, so p value ≤ α so that Ha is accepted and H0 is rejected.Conclusion: The study was a prostaglandin relationship to the incidence of premenstrual syndrome at the Pelamonia Midwifery Academy in Makassar in 2020.Keywords: Adolescents; Pre Menstrual Syndrome; ProstaglandinsPendahuluan: Remaja putri dan wanita setengah baya selama fase luteal pada siklus menstruasi akan mengalami gangguan emosional dan gangguan fisik yang dinamakan dengan premenstrual syndrome (PMS).Tujuan: Diketahui hubungan prostaglandin terhadap kejadian premenstrual syndrome pada remaja putri di akademi kebidanan pelamonia.Metode: Cross Sectional Study dengan populasinya mahasiswi Akbid Pelamonia Makassar. Teknik pengambilan Sampel menggunakan teknik total sampling dengan didapatkan sampel berjumlah 50 responden. Instrumen penelitian menggunakan lembar catatan harian (LCH), kuisioner pengumpulan data yang meliputi identitas serta gejala ataupun keluhan dari premenstrual syndrome. Pemeriksaan prostaglandin menggunakan prostaglandin Enzim Linked Immuno Sorbent Assay (ELISA) kit.Hasil: Didapatkan bahwa dari 26 responden yang PMS Ringan terdapat 23 responden (46%) memiliki kadar prostaglandin F2α <420,6 pg/mL dan 3 responden (6%) memiliki kadar prostaglandin F2α >420,6 pg/mL. Sedangkan, dari 24 responden yang PMS Berat terdapat 15 responden (30%) memiliki kadar prostaglandin F2α <420,6 pg/mL dan 9 responden (18%) memiliki kadar prostaglandin F2α >420,6 pg/mL. Hasil uji statistik Chi-Square hubungan prostaglandin terhadap kejadian premenstrual syndrome pada remaja putri pada taraf kepercayaan 0,05 menunjukkan bahwa p Value = 0,047, jadi p Value ≤ α sehingga Ha diterima dan H0 ditolak.Simpulan: Terdapat hubungan prostaglandin terhadap kejadian premenstrual syndrome di Akademi Kebidanan Pelamonia Makassar Tahun 2020.
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Zorzano, A., T. W. Balon, J. A. Jakubowski, M. N. Goodman, D. Deykin, and N. B. Ruderman. "Effects of insulin and prior exercise on prostaglandin release from perfused rat muscle Evidence that prostaglandins do not mediate changes in glucose uptake." Biochemical Journal 240, no. 2 (December 1, 1986): 437–43. http://dx.doi.org/10.1042/bj2400437.
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Prostaglandin generation and its inter-relation to the metabolic effects of insulin and prior exercise were examined in perfused muscle of fed rats. During a 60 min perfusion of the rat hindquarter, a substantial release of the prostaglandins PGF2 alpha, PGE2 and 6-oxoPGF1 alpha was observed. Blood cells present in the perfusate released these substances in negligible amounts indicating the prostaglandins were produced by the hindquarter. Addition of insulin to the perfusate increased both glucose uptake and the generation of PGE2 and 6-oxoPGF1 alpha. At 30 min after intense treadmill exercise, glucose and alpha-aminoisobutyric acid (AIB) uptake by the hindquarter were increased in the absence of added insulin, but prostaglandin release was not increased. Insulin further increased glucose and AIB uptake; however, in contrast with its effects in non-exercised rats, insulin no longer stimulated prostaglandin generation. Indomethacin (10 microM) added to the perfusate inhibited the release of PGF2 alpha and PGE2 by 90% and the release of 6-oxoPGF1 alpha by 54%. It had no effect on the stimulation of glucose uptake by either insulin or prior exercise. The data indicate that insulin increases prostaglandin synthesis by perfused rat muscle, and that prior exercise blocks this effect. They suggest that under the conditions studied prostaglandins do not mediate the effects of insulin or prior exercise on glucose uptake.
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Braun, Marina, and K. Schrör. "Pharmakologische Grundlagen der Prostaglandin-Therapie." Hämostaseologie 13, no. 02 (March 1993): 53–57. http://dx.doi.org/10.1055/s-0038-1655212.
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ZusammenfassungVasodilatierende Prostaglandine werden zur Therapie fortgeschrittener Stadien der peripheren arteriellen Verschlußkrankheit und der Thrombangiitis obliterans eingesetzt. Der klinische Nutzen liegt vor allem in der therapeutischen Anwendung in Fällen, wo chirurgische Maßnahmen nicht angezeigt bzw. erfolglos geblieben sind. Eine Reihe von klinischen Studien belegt die klinische Wirksamkeit der systemischen Anwendung von Prostaglandin E1 und lloprost. Die pharmakologischen Wirkungen dieser Substanzen betreffen nicht nur den Vasotonus, sondern auch Zellen des strömenden Blutes sowie das Fibrinolyseund Gerinnungssystem. Neuere experimentelle Befunde weisen auf eine antiatherosklerotische Wirkung der Prostaglandine hin.
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Ortega-Moreno, J. "Influence of prostaglandins E2 and F2α on passage pressure across the uterotubal junction and isthmus in the rat." Laboratory Animals 29, no. 3 (July 1, 1995): 327–34. http://dx.doi.org/10.1258/002367795781088333.
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The influence of prostaglandins E2 and F2α on passage pressure across the uterotubal junction (UTJ) and isthmus were studied in rats that were either in the pro-oestrus, oestrus, metoestrus or dioestrus phases. Effects of these prostaglandins were also investigated in rats that had been either ovariectomized and treated with oestradiol or medroxiprogesterone acetate, or only ovariectomized. In each rat, the left UTJ was surgically resected and the isthmus anastomosed to the uterine horn, whereas the right UTJ was left untouched. The passage pressures across the left isthmus and the right UTJ were measured before and after prostaglandin treatment. The pressures obtained in the UTJ in the oestrus phase and oestrogen-treated ovariectomized animals were lower than those registered in the remaining groups. Prostaglandin E2 decreased the pressures when compared with pre-treatment measures in all groups. Significantly higher pressures were registered across the UTJ in prostaglandin F2α than in E2 treatment, with these higher pressures being similar to pre-treatment pressures. Both hormonal changes throughout the oestrous cycle and prostaglandin E2 treatment had a similar influence on the passage pressure across the isthmus, as that described for UTT, but with lower values. The results indicate that prostaglandin E2 decreases the passage pressure across both UTJ and isthmus and can have an influence on the regulation of transport across these 2 areas.
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Deenarn, Pacharawan, Punsa Tobwor, Vanicha Vichai, Suwanchai Phomklad, Panomkorn Chaitongsakul, Rungnapa Leelatanawit, and Wananit Wimuttisuk. "Polychaete consumption increased prostaglandin biosynthesis in female Penaeus monodon." Reproduction 160, no. 6 (December 2020): 873–85. http://dx.doi.org/10.1530/rep-20-0217.
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The polychaete Perinereis nuntia is preferred over commercial feed pellets for boosting ovarian maturation of the female black tiger shrimp Penaeus monodon. High levels of prostaglandins in polychaetes are believed to enhance shrimp ovarian development. However, the impact of polychaete feeding on shrimp prostaglandin biosynthesis and fatty acid regulatory pathways have yet to be investigated. As polychaetes contain higher levels of arachidonic acid (ARA), eicosapentaenoic acid (EPA), prostaglandin E2 (PGE2) and prostaglandin F2α (PGF2α) than feed pellets, we examined the effects of polychaete feeding alone and in combination with eyestalk ablation on shrimp hepatopancreases and ovaries. Shrimp fed with polychaetes contained higher levels of EPA, PGE2 and PGF2α in hepatopancreases than those of pellet-fed shrimp. Similarly, higher levels of ARA and higher transcription levels of cyclooxygenase (COX) and prostaglandin F synthase (PGFS) were detected in ovaries of polychaete-fed shrimp compared to those of pellet-fed shrimp. The combination of polychaete-feeding and eyestalk ablation, commonly practiced to induce ovarian development, increased levels of ARA and EPA and transcription levels of COX in hepatopancreases and ovaries of polychaete-fed shrimp compared to those of pellet-fed shrimp. In ovaries, prostaglandin biosynthesis gene transcripts were induced by polychaete feeding while transcriptional levels of fatty acid regulatory genes were regulated by shrimp feed and eyestalk ablation. Our findings not only elucidate the effects of polychaete consumption on shrimp prostaglandin biosynthesis and fatty acid regulatory pathways during larvae production, but also suggests that high levels of dietary ARA, EPA and prostaglandins are essential during P. monodon ovarian development.
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Curtis, Glenn H., D. Grant Gall, John L. Wallace, and Wallace K. MacNaughton. "Intraluminal pH modulates gastric prostaglandin synthesis." Canadian Journal of Physiology and Pharmacology 73, no. 1 (January 1, 1995): 130–34. http://dx.doi.org/10.1139/y95-018.
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Prostaglandins play an important role in modulating gastric mucosal integrity and in regulating gastric acid secretion, but little is known regarding regulation of prostaglandin synthesis by the stomach. We have therefore examined the effects of changes in gastric intraluminal pH on the capacity of gastric tissue to synthesize prostaglandin E2. Oral administration of solutions with a pH of 8.3 or 10 markedly reduced the capacity of the gastric tissue to synthesize prostaglandin E2, but did not affect synthesis of leukotriene B4. This phenomenon was observed in three strains of rats. Administration of the same solutions subcutaneously did not affect gastric prostaglandin synthesis. On the other hand, oral administration of a solution of pH 1 significantly increased prostaglandin synthetic capacity, while a solution with a pH of 3 had no effect. The effects observed were not attributable to differences in the osmolarity of the test solutions. These studies suggest that changes in gastric intraluminal pH result in changes in gastric prostaglandin synthesis. It is possible that this represents a physiological response aimed at maintaining gastric mucosal integrity when intraluminal pH is low, while also providing a feedback inhibition of gastric acid secretion.Key words: prostaglandin, stomach, acid, gastrin, cytoprotection.
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Laurent, Fabrice, Martin F. Kagnoff, Tor C. Savidge, Muriel Naciri, and Lars Eckmann. "Human Intestinal Epithelial Cells Respond toCryptosporidium parvum Infection with Increased Prostaglandin H Synthase 2 Expression and Prostaglandin E2and F2α Production." Infection and Immunity 66, no. 4 (April 1, 1998): 1787–90. http://dx.doi.org/10.1128/iai.66.4.1787-1790.1998.
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ABSTRACT Cryptosporidium parvum is an important cause of diarrhea in humans and several animal species. Prostaglandins play a central role in regulating intestinal fluid secretion in animal models of cryptosporidiosis, but their cellular sources and mechanisms of induction are unclear. Here, we show that C. parvuminfection directly activates prostaglandin H synthase 2 expression and prostaglandin E2 and F2α production in human intestinal epithelial cells.
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Rayhel, E. J., D. A. Prentice, P. S. Tabor, W. H. Flurkey, R. W. Geib, R. F. Laherty, S. B. Schnitzer, R. Chen, and J. P. Hughes. "Inhibition of Nb2 T-lymphoma cell growth by transforming growth factor-β." Biochemical Journal 253, no. 1 (July 1, 1988): 295–98. http://dx.doi.org/10.1042/bj2530295.
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Transforming growth factor-beta (TGF-beta) inhibits proliferation of Nb2 cells, a rat T lymphoma, in response to lactogens and interleukin-2. Prostaglandins may play an important role in the pathway through which TGF-beta exerts its inhibitory actions, because prostaglandin E2 also inhibits proliferation of Nb2 cells, and indomethacin, an inhibitor of prostaglandin synthesis, reverses the inhibitory effects of TGF-beta on Nb2 cell proliferation.
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Tanase, Constantin I., Lucia Pintilie, and Elena Mihai. "A Molecular Docking of New 9β-Halogenated Prostaglandin Analogues." Proceedings 41, no. 1 (November 14, 2019): 21. http://dx.doi.org/10.3390/ecsoc-23-06504.
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Prostaglandins (PGs) with cytoprotective activity were studied for a long time, and a few PGE1 and PGE2 stable analogues were promoted as drugs: arbaprostil, enprostil, misoprostol, and rioptostol. Similarly, nocloprost, a 9β-chlorine prostaglandin analogue, and many 9β- and 11β-substituted prostaglandins were synthesized and studied for their biological activity. We previously synthesized new 9β-halogenated prostaglandins with an ester group at the carbon atom 6 (PGs numbering) by the reaction of a δ-lactone intermediate with diols in acid catalysis. These compounds were used in the current molecular docking study to determine their potential cytoprotective (anti-ulcer) activity. The current study was done with the CLC Drug Discovery Workbench 2.4. software and an oxidoreductase enzyme receptor, chosen from the Protein Data Bank, ID: 4KEW (www.rcsb.org). We used two recognized drugs, omeprazole (co-crystallized with the enzyme) and nocloprost, as the standard. The 9β-halogenated prostaglandin analogs were docked. Nocloprost and all 9β-halogenated compounds had docking scores greater than that of omeprazole. The majority of the 9β-halogenated analogs had docking scores even greater than that of nocloprost, indicating that these compounds could have potential cytoprotective (anti-ulcer) activity. A few correlations between docking score and substituents on the prostaglandin skeleton were found.
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Kunapuli, S. P., G. Fen Mao, M. Bastepe, L. Y. Liu-Chen, S. Li, P. P. Cheung, J. K. DeRiel, and B. Ashby. "Cloning and expression of a prostaglandin E receptor EP3 subtype from human erythroleukaemia cells." Biochemical Journal 298, no. 2 (March 1, 1994): 263–67. http://dx.doi.org/10.1042/bj2980263.
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Prostaglandins inhibit platelet activation by stimulating intracellular cyclic AMP formation. We have postulated that intracellular cyclic AMP levels in platelets are buffered by a distinct prostaglandin receptor that mediates inhibition of cyclic AMP formation. In order to provide evidence for the model, we have cloned the cDNA coding for a prostaglandin receptor EP3 subtype, which is coupled to inhibition of adenylate cyclase, from the megakaryocytic cell line human erythroleukaemia (HEL) cells. A PCR-generated hybridization probe, produced using primers based on the sequence of the mouse prostaglandin EP3 receptor published by Sugimoto, Namba, Honda, Hayashi, Negishi, Ichikawa and Narumiya [(1992) J. Biol. Chem. 267, 6463-6466], was used to screen a lambda gt11 HEL cell cDNA library. The composite full-length cDNA clone HEP3, generated from the two partial clones pHEP3-7 and pHEP3-5, is 1.6 kb long with an open reading frame coding for 390 amino acids. This clone is 83% identical to the alpha subtype of the mouse EP3 receptor. The full-length construct was transfected into COS-1 cells. The cloned receptor exhibited the properties of a prostaglandin EP3 subtype, inhibiting forskolin-stimulated cyclic AMP formation in response to prostaglandin E2 (PGE2) and binding PGE2 with high specificity and a Kd of 3.2 nM. Radiolabelled PGE2 could be displaced by prostaglandins in the order PGE2 = PGE1 > iloprost = PGD2. Northern blot analysis revealed that the receptor is also present in human kidney.
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Antonova, M. "Prostaglandins and prostaglandin receptor antagonism in migraine." Journal of Headache and Pain 1, Suppl 1 (2013): P114. http://dx.doi.org/10.1186/1129-2377-1-s1-p114.
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Bosisio, E. "Prostaglandins and prostaglandin-like compounds in plants." Pharmacological Research Communications 20 (December 1988): 99–103. http://dx.doi.org/10.1016/s0031-6989(88)80851-8.
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Isay, S. V., T. V. Kafanova, and N. U. Kim. "An example of oscillatory (cyclic) reaction for prostaglandin chemistry." Biomeditsinskaya Khimiya 59, no. 1 (January 2013): 104–6. http://dx.doi.org/10.18097/pbmc20135901104.
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Cui, Jian, Patrick McQuillan, Afsana Momen, Cheryl Blaha, Raman Moradkhan, Vernon Mascarenhas, Cynthia Hogeman, Anandi Krishnan, and Lawrence I. Sinoway. "The role of the cyclooxygenase products in evoking sympathetic activation in exercise." American Journal of Physiology-Heart and Circulatory Physiology 293, no. 3 (September 2007): H1861—H1868. http://dx.doi.org/10.1152/ajpheart.00258.2007.
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Animal studies suggest that prostaglandins in skeletal muscles stimulate afferents and contribute to the exercise pressor reflex. However, human data regarding a role for prostaglandins in this reflex are varied, in part because of systemic effects of pharmacological agents used to block prostaglandin synthesis. We hypothesized that local blockade of prostaglandin synthesis in exercising muscles could attenuate muscle sympathetic nerve activity (MSNA) responses to fatiguing exercise. Blood pressure (Finapres), heart rate, and MSNA (microneurography) were assessed in 12 young healthy subjects during static handgrip and postexercise muscle ischemia (PEMI) before and after local infusion of 6 mg of ketorolac tromethamine in saline via Bier block (regional intravenous anesthesia). In the second experiment ( n = 10), the same amount of saline was infused via the Bier block. Ketorolac Bier block decreased the prostaglandins synthesis to ∼33% of the baseline. After ketorolac Bier block, the increases in MSNA from the baseline during the fatiguing handgrip was significantly lower than that before the Bier block (before ketorolac: Δ502 ± 111; post ketorolac: Δ348 ± 62%, P = 0.016). Moreover, the increase in total MSNA during PEMI after ketorolac was significantly lower than that before the Bier block ( P = 0.014). Saline Bier block had no similar effect. The observations indicate that blockade of prostaglandin synthesis attenuates MSNA responses seen during fatiguing handgrip and suggest that prostaglandins contribute to the exercise pressor reflex.
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Iskandar, Patricia, and Nia Ayu Ismaniati. "Peran prostaglandin pada pergerakan gigi ortodontik." Journal of Dentomaxillofacial Science 9, no. 2 (April 30, 2010): 92. http://dx.doi.org/10.15562/jdmfs.v9i2.238.
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Orthodontic tooth movement is a complex process, in which cellular and chemicalchanges occur. When a force is applied onto a tooth, it causes tissue injury,compression of periodontal ligament and bone deformation. These procedures lead tofollowed by certain biochemical reactions at cellular level which results in boneremodeling. Thus a process of signal transduction occurs. In this process, somemessengers are released, including prostaglandin. Prostaglandin is an arachidonicacid metabolite, released when cell membrane is deformed. Prostaglandin,particularly PGE, play a role in bone metabolism and orthodontic tooth movement.Prostaglandin will stimulate the release of second messengers, i.e. cAMP and calciumintracellular. These second messengers will activate osteoclasts. Prostaglandin willalso induce RANKL (receptor activator of nuclear factor κβ ligand) to initiateosteoclasts differentiation. Some researchers proved that application of prostaglandinin orthodontic treatment can accelerate tooth movement.
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Smith, D. M., and P. H. Sugden. "Effects of pressure overload and insulin on protein turnover in the perfused rat heart. Prostaglandins are not involved although their synthesis is stimulated by insulin." Biochemical Journal 243, no. 2 (April 15, 1987): 473–79. http://dx.doi.org/10.1042/bj2430473.
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A modified anterogradely perfused rat heart preparation is described in which all the cardiac output passes through the coronary circulation. Such a preparation develops hypertensive aortic pressures. Hypertensive aortic pressures or insulin stimulate the rate of cardiac protein synthesis and inhibit the rate of protein degradation. Aortic pressure and insulin may be important in the regulation of cardiac nitrogen balance in vivo. By abolishing cardiac prostaglandin synthesis with 4-biphenylacetate, we were able to investigate the possible involvement of prostaglandins in the modulation of protein turnover by pressure overload or insulin. There was no evidence of any involvement. However, insulin stimulated and cycloheximide inhibited cardiac prostaglandin synthesis. These findings are consonant with an enzyme involved in prostaglandin synthesis being short-lived and prostaglandin synthesis being rapidly influenced by activators and inhibitors of protein synthesis and degradation.
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Fuchs, Michaela A. A., Julia Schrankl, Christina Leupold, Charlotte Wagner, Armin Kurtz, and Katharina A. E. Broeker. "Intact prostaglandin signaling through EP2 and EP4 receptors in stromal progenitor cells is required for normal development of the renal cortex in mice." American Journal of Physiology-Renal Physiology 322, no. 3 (March 1, 2022): F295—F307. http://dx.doi.org/10.1152/ajprenal.00414.2021.
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Cyclooxygenase-2 (Cox-2) produces prostaglandins that are essential for normal renal development. It is unclear in which cells Cox-2 and the receptors for prostaglandin E2 (EP receptors) are expressed during late nephrogenesis. This study identified the expression sites for EP subtypes and Cox-2 in neonatal mouse kidneys. Furthermore, it shows that stromal progenitor cells may require intact prostaglandin E2 signaling through EP2 and EP4 receptors for normal renal development.
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Bergelson, L. D. "The interaction of prostaglandins with human serum lipoproteins." Bioscience Reports 9, no. 1 (February 1, 1989): 27–40. http://dx.doi.org/10.1007/bf01117509.
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Using high density and low density lipoproteins (HDL and LDL) labeled with fluorescent analogues of phosphatidylcholine or sphingomyelin it was found that low amounts (10−12 M) of prostaglandins E1 and F2α induced different structural rearrangements of the lipoprotein surface, whereas prostaglandins E2 and F1α had no effect. The effects of prostaglandin E1 on HDL were largely paralled by those of this prostaglandin on synthetic recombinants prepared from pure apolipoprotein A1, phospholipids and cholesterol and were demonstrated to be caused by prostaglandin-apolipoprotein interaction. The interaction resembled that of a ligand with a specific receptor protein because it was specific, reversible, concentration and temperature dependent and saturable. However the retaining capacity of HDL or LDL for prostaglandin E1 as determined by equilibrium dialysis was very low and a single prostaglandin E1 molecule was able to induce structural changes in large numbers of discrete lipoprotein particles. To explain this remarkable fact a non-equilibrium model of ligand-receptor interaction is proposed. According to that model in open systems characterized by weak ligand-receptor binding, high diffusion rate of the ligand and long relaxation times which exceed the interval between two successive receptor occupations, the ligand-induced changes will accumulate, resulting in transformation of the system into a new state which may be far away from equilibrium. It is emphasized that the low mobility of lipids constituting the environment of the receptor protein plays a critcal role in this type of signal amplification. It was further demonstrated that the PGE1-induced changes of the lipoprotein surface resulted in an enhancement of LDL-to-HDL transfer of cholesterol esters and phosphatidylcholine especially in the presence of serum lipid transfer proteins. The acceleration of the interlipoprotein transfer caused by prostaglandin E1 in turn increases the rate of cholesterol esterification in serum. It is suggested that in such a way prostaglandin E1 may influence the homeostasis of cholesterol.