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International Journal of Fertility 1979Prostaglandins E and F (PGE and PGF) levels and the biosynthetic ability of rat uterine tissue have been estimated in the various phases of oestrous cycle by...
Prostaglandins E and F (PGE and PGF) levels and the biosynthetic ability of rat uterine tissue have been estimated in the various phases of oestrous cycle by radioimmunoassay technique. Significantly high PGF concentration was found during metaoestrous phase. In comparison, PGE levels did not show as high elevation. The metaoestrous phase also showed significantly higher biosynthesis of prostaglandins E and F. Our experimental findings support the role of prstaglandins in ovulation and luteolysis of the corpus luteum.
Topics: Animals; Estrus; Female; Pregnancy; Prostaglandins E; Prostaglandins F; Rats; Uterus
PubMed: 40907
DOI: No ID Found -
The Journal of Biological Chemistry Jun 1976The biosynthesis of prostaglandins E2 and F2alpha as well as the catabolism of [9beta- 3H1]prostaglandin F2alpha by homogenates of whole brain from fetal and neonatal...
The biosynthesis of prostaglandins E2 and F2alpha as well as the catabolism of [9beta- 3H1]prostaglandin F2alpha by homogenates of whole brain from fetal and neonatal lambs was investigated. The biosynthetic measurements utilized the mass spectrometric deuterium isotope dilution-dual ion monitoring technique (Samulsson, B., Hamberg, M., and Sweeley, C.C. (1970) Anal. Biochem. 38, 301-304; Wolfe, L.S., and Pace-Asciak, C. (1972) in Prostaglandins in Fertility Control (Bergström, S., Green, K., and Samuelsson, B., eds) Vol. 2. pp. 201-207, WHO, Karolinska Institutet, Stockholm), whereas the activity of the catabolizing system was measured by the radiolabel dilution-thin layer chromatographic technique reported previously (Pace-Asciak, C. (1975) J. Biol. Chem. 250, 2795-2800). The structures of all products were confirmed by mass spectrometry. Early fetal brain (gestational age 30 to 32 days) contained the highest activity of NAD-dependent prostaglandin 15-hydroxy dehydrogenase which varied inversely with age of the fetus, dropping to almost undetectable levels by neonatal Day 4. Both prostaglandins E2 and F2alpha, were formed by brain from all ages tested and the total prostaglandins formed rose gradually with age. Thus, the period of maximal prostaglandin catabolism which we term the "critical prostaglandin period" appears in the fetal lamb brain around 30 days gestational age or earlier. These findins together with others previously reported by us in other tissues, support the concept that prostaglandin catabolism might play an important role in protecting the developing organ from possible adverse effects of locally formed or circulating prostaglandins. These adverse effects on the developing brain might relate to the known vasoconstrictor properties of the prostaglandins, as well as to their known effects on the induction of cell differentiation.
Topics: Aging; Animals; Animals, Newborn; Brain; Female; Fetus; Gas Chromatography-Mass Spectrometry; Gestational Age; Hydroxyprostaglandin Dehydrogenases; Pregnancy; Prostaglandins E; Prostaglandins F; Sheep
PubMed: 931990
DOI: No ID Found -
The Journal of Physiology Mar 19881. The effects of microinjection of prostaglandin D2, E2 and F2 alpha and of endogenous pyrogen on the rectal temperature of rabbits were extensively examined in...
1. The effects of microinjection of prostaglandin D2, E2 and F2 alpha and of endogenous pyrogen on the rectal temperature of rabbits were extensively examined in sixty-eight brain regions and in the third cerebral ventricle. 2. Intracerebroventricular injection of both prostaglandins E2 and F2 alpha produced dose-dependent fever over a range of 100-1000 ng. The selective brain regions, the nucleus broca ventralis, preoptic area, anterior hypothalamus and the ventromedial hypothalamus, responded to microinjections of a small dose (less than 200 ng) of prostaglandins E2 and F2 alpha by producing fever. Furthermore, the lateral hypothalamus, ventral thalamus, substantia nigra and the trigeminal nucleus were also sensitive to high concentrations of prostaglandins E2 and F2 alpha, fever being produced. It is likely that prostaglandin D2 is not involved in fever induction. 3. The ventricular injection of endogenous pyrogen also produced fever. However, brain regions sensitive to microinjection of endogenous pyrogen were exclusively localized to regions near the organum vasculosum laminae terminalis (OVLT), such as the nucleus broca ventralis and the preoptic area. In contrast to the monophasic fever induced by prostaglandins E2 and F2 alpha, about 30 min after ventricular or cerebral injection of endogenous pyrogen the rectal temperature gradually started to rise and the fever was prolonged over 4 h. 4. We investigated the effect of an inhibitor of prostaglandin synthesis, sodium salicylate, on biphasic fever induced by intravenous injection of bacterial endotoxin. The microinjections of sodium salicylate into the bilateral regions near the OVLT suppressed the second peak but had no effect on the first peak. 5. The present study clarifies that there exist two separate mechanisms of induction of biphasic fever. Correlating with the first peak of biphasic fever, prostaglandins synthesized outside the blood-brain barrier act on multiple sites in the central nervous system to induce fever. Correlating with the second peak, endogenous pyrogen acts on regions near the OVLT to synthesize and release pyrogenic prostaglandins.
Topics: Animals; Body Temperature; Brain; Cerebral Ventricles; Dinoprost; Dinoprostone; Dose-Response Relationship, Drug; Fever; Injections, Intraventricular; Interleukin-1; Male; Prostaglandin D2; Prostaglandins; Prostaglandins D; Prostaglandins E; Prostaglandins F; Rabbits; Time Factors
PubMed: 3261794
DOI: 10.1113/jphysiol.1988.sp017000 -
Animal : An International Journal of... Jan 2021The roles of fibroblast growth factor 2 (FGF2) in the corpus luteum (CL) function and its modulatory effect on prostaglandin (PG) F during the bovine estrous cycle were...
The roles of fibroblast growth factor 2 (FGF2) in the corpus luteum (CL) function and its modulatory effect on prostaglandin (PG) F during the bovine estrous cycle were studied using the following design of in vivo and in vitro experiments: (1) effects of FGF2 and FGF receptor 1 inhibitor (PD173074) on bovine CL function in the early (PGF-resistant) and mid (PGF-responsive) luteal stage in vivo, (2) the modulatory effect of FGF2 on PGF action during the luteal phase in vivo and (3) effects of FGF2 and PD173074 on bovine CL secretory function in vitro. Cows were treated by injection into the CL with: (1) saline (control), (2) FGF2, (3) PD173074, (4) FGF2 followed by intramuscular (i.m.) PGF, (5) PD173074 followed by i.m. PGF and (6) i.m. PGF as a positive control. For in vitro experiments, CL explants were treated with the aforementioned factors. Progesterone (P) concentrations of blood samples or culture media were determined by radioimmunoassay. Relative mRNA expressions of the genes involved in angiogenesis and steroidogenesis were determined by quantitative real-time PCR. Although FGF2 treatment on day 4 of the estrous cycle did not change the cycle length, FGF2 with PGF decreased the P concentrations observed during the estrous cycle compared to the control group (P < 0.001). Moreover, FGF2 treatment on day 10 prolonged CL function as indicated by a significantly greater concentration of P on day 21 compared to the control group. In the in vitro study, FGF2 decreased cytochrome P450 family 11 subfamily A member 1 (CYP11A1) and hydroxy-delta-5-steroid dehydrogenase (HSD3B1) mRNA expression (P < 0.01) and decreased P production in the early-stage CL (P < 0.001). However, FGF2 + PGF or PGF alone resulted in an elevation of steroidogenic acute regulatory protein and CYP11A1 mRNA expression and P secretion in the early-stage CL (P < 0.01). In the mid-luteal phase, FGF2 upregulated CYP11A1 and HSD3B1 mRNA expression (P < 0.01), while FGF2 + PGF increased only HSD3B1 mRNA expression (P < 0.001). In conclusion, FGF2 seems to play a modulatory role in CL development or luteolysis, differentially regulating steroidogenesis and angiogenic factors as well as PGF actions.
Topics: Animals; Cattle; Corpus Luteum; Dinoprost; Estrous Cycle; Female; Fibroblast Growth Factor 2; Luteolysis; Progesterone; Prostaglandins F
PubMed: 33516003
DOI: 10.1016/j.animal.2020.100048 -
Journal of Andrology 1987Three cyclooxygenase (prostaglandin synthetase) inhibitors, indomethacin, phenylbutazone, and oxyphenbutazone, decreased fertilization in vitro when mixed with...
Three cyclooxygenase (prostaglandin synthetase) inhibitors, indomethacin, phenylbutazone, and oxyphenbutazone, decreased fertilization in vitro when mixed with capacitated mouse spermatozoa before addition of the treated gametes to oocytes. Fertilization was inhibited whether the oocytes were intact, follicle cell-free, or both follicle cell-free and zona-free. At various concentrations of inhibitor, no effect was observed on the motility or forward progression of the spermatozoa. These cyclooxygenase inhibitors also decreased the guinea pig acrosome reaction. Inhibition of the acrosome reaction did not occur when a mixture of the prostaglandins (PGE2 or PGF2 alpha) and one of the inhibitors was added to the spermatozoa. Alone, these prostaglandins tended to enhance the rate at which the acrosome reaction took place. Lowered calcium levels reduced the occurrence of the acrosome reaction, an effect that could be reversed at least partially by the addition of PGE2. Even in the nominal absence of calcium, some acrosome reaction took place when PGE2 was present in the medium. These results support an essential role for cyclooxygenase and arachidonic acid metabolites, including prostaglandins, in the events leading to the acrosome reaction and fertilization.
Topics: Acrosome; Animals; Cyclooxygenase Inhibitors; Dinoprost; Dinoprostone; Female; Fertilization; Guinea Pigs; Indomethacin; Male; Mice; Oocytes; Oxyphenbutazone; Phenylbutazone; Prostaglandin-Endoperoxide Synthases; Prostaglandins; Prostaglandins E; Prostaglandins F; Spermatozoa
PubMed: 3108222
DOI: 10.1002/j.1939-4640.1987.tb00953.x -
British Medical Journal Jun 1980
Topics: Epoprostenol; Female; Humans; Platelet Aggregation; Pregnancy; Prostaglandins; Prostaglandins F
PubMed: 7000245
DOI: 10.1136/bmj.280.6231.1581 -
Infection and Immunity Jan 1980Mechanisms whereby prostaglandins and other cyclic adenosine 3',5'-monophosphate (cAMP) modulators might enhance the growth of herpes simplex virus (HSV) in human skin...
Mechanisms whereby prostaglandins and other cyclic adenosine 3',5'-monophosphate (cAMP) modulators might enhance the growth of herpes simplex virus (HSV) in human skin fibroblasts were explored. Prostaglandins A1, B1, E1, E2, and F2 alpha, as well as isoproterenol, imidazole, carbamylcholine, and dibutyryl cAMP had no effect on HSV growth. On the other hand, the phosphodiesterase inhibitors 1-methyl-3-isobutylxanthine and theophylline delayed the growth, suppressed the cell-to-cell spread, but inhibited neither the adsorption nor the penetration of the virus. Although none of the cAMP-elevating reagents directly enhanced HSV growth, they were found to inhibit dose dependently the antiviral action of both type I and HSV antigen-induced human interferon preparations. Furthermore, these reagents suppressed the production of HSV antigen-induced interferon by immune human mononuclear leukocytes. These data support the hypothesis that prostaglandin elaboration in vivo could contribute to exacerbations of HSV infections by compromising the host's interferon defense system.
Topics: Cyclic AMP; Humans; Interferon Inducers; Interferons; Prostaglandins; Prostaglandins A; Prostaglandins B; Prostaglandins E; Prostaglandins F; Simplexvirus
PubMed: 6244226
DOI: 10.1128/iai.27.1.158-167.1980 -
The Journal of Clinical Investigation Sep 1977The effects of several prostaglandins on lipoprotein lipase activity of mammary gland and adipose tissue and serum triacylglycerol were studied during late pregnancy in...
The effects of several prostaglandins on lipoprotein lipase activity of mammary gland and adipose tissue and serum triacylglycerol were studied during late pregnancy in rats. Prostaglandins were injected twice daily for 2 days before and once on the day of analysis. In rats pregnant 20 days, prostaglandin F(2alpha) (PGF(2alpha)) increased the activity of lipoprotein lipase in mammary gland fourfold, reduced the activity in adipose tissue about 60%, and decreased serum concentration of triacylglycerol 50%. PGF(2alpha) also reduced serum concentration of progesterone 90% and increased that of prolactin fivefold, but had no effect on serum concentrations of either immuno-reactive insulin or 17beta-estradiol. Injections of 13,14-dihydro-15-keto PGF(2alpha), a metabolite of PGF(2alpha), had similar effects in rats pregnant 20 days, whereas prostaglandins E(1) and E(2) did not. In rats pregnant 16 days, PGF(2alpha) did not affect lipoprotein lipase activity in the tissues or the concentration of triacylglycerol and prolactin in serum, although it decreased serum progesterone 80%.2-Br-alpha-ergocryptine prevented the increase in serum prolactin in response to PGF(2alpha), but did not alter the effect of PGF(2alpha) on lipoprotein lipase activity or serum triacylglycerol. Progesterone completely blocked the effects of PGF(2alpha) on lipoprotein lipase activity and serum triacylglycerol and prolactin concentrations. These findings indicate that the changes in lipoprotein lipase activity and serum triacylglycerol in PGF(2alpha)-treated rats are probably related to the inhibitory action of PGF(2alpha) on progesterone secretion. They also suggest that endogenous F prostaglandins may play a role in the regulation of lipoprotein lipase activity in mammary gland and adipose tissue near parturition.
Topics: Adipose Tissue; Animals; Bromocriptine; Female; Glycerol; Lipoprotein Lipase; Mammary Glands, Animal; Pregnancy; Pregnancy, Animal; Progesterone; Prolactin; Prostaglandins; Prostaglandins E; Prostaglandins F; Rats
PubMed: 893673
DOI: 10.1172/JCI108822 -
The Journal of Investigative Dermatology Oct 1983The inside skin of the forearm of healthy volunteers was irradiated with an infrared (IR) lamp for 1 hr, resulting in the rapid appearance of an erythema and an...
The inside skin of the forearm of healthy volunteers was irradiated with an infrared (IR) lamp for 1 hr, resulting in the rapid appearance of an erythema and an elevation of skin surface temperature from 30 +/- 1 degree C to 38 +/- 2 degrees C within 5 min. The erythema and elevated skin surface temperature decayed within 10-30 min when the IR irradiation was stopped. Suction blisters were raised on nonirradiated skin and on irradiated skin both during irradiation and at various times after irradiation stopped. Elevated levels of free arachidonic acid, PGE2, PGD2, PGF2 alpha and 6-oxo-PGF1 alpha were found up to 24 h after irradiation. By 48 h the prostaglandin levels had returned to control values whereas the free arachidonic acid levels were still elevated at 72 h. The peak level of 6-oxo-PGF1 alpha appears between 0-6 h whereas for PGE2, D2, and F2 alpha it is between 6-16 h, suggesting a different cellular source for this prostaglandin.
Topics: 6-Ketoprostaglandin F1 alpha; Adolescent; Adult; Aged; Arachidonic Acids; Dinoprost; Dinoprostone; Erythema; Female; Forearm; Humans; Male; Middle Aged; Prostaglandin D2; Prostaglandins; Prostaglandins D; Prostaglandins E; Prostaglandins F; Skin; Skin Temperature; Ultraviolet Rays
PubMed: 6578272
DOI: 10.1111/1523-1747.ep12519261 -
BMJ Open Apr 2019Bimatoprost-timolol (bimatoprost 0.03%-timolol 0.5% fixed-dose combination [FDC]) and tafluprost-timolol (tafluprost 0.0015%-timolol 0.5% FDC) eye drops are currently...
OBJECTIVES
Bimatoprost-timolol (bimatoprost 0.03%-timolol 0.5% fixed-dose combination [FDC]) and tafluprost-timolol (tafluprost 0.0015%-timolol 0.5% FDC) eye drops are currently the only topical intraocular pressure (IOP)-reducing therapies available as preservative-free (PF) prostaglandin and timolol FDC. The aim of this study was to investigate changes to ocular signs and symptoms when patients with ocular hypertension (OH) or open-angle glaucoma (OAG) switched from PF or benzalkonium chloride (BAK)-preserved bimatoprost-timolol to PF tafluprost-timolol eye drops.
DESIGN
This was a 12-week, open-label, phase IV study.
SETTING
Sixteen centres in Finland, Germany, Italy and the UK.
PARTICIPANTS
Patients with OH or OAG (IOP on medication ≤21 mm Hg), treated with PF or BAK-preserved bimatoprost-timolol for ≥4 weeks before screening, and presenting with conjunctival hyperaemia and ≥1 ocular symptom.
INTERVENTIONS
Patients were switched to PF tafluprost-timolol once daily in the treated eye(s).
PRIMARY AND SECONDARY OUTCOME MEASURES
The primary endpoints were change from screening to week 12 in conjunctival hyperaemia and worst ocular symptom. The secondary outcome measures were changes from screening in ocular signs (other than conjunctival hyperaemia) and symptoms at week 12.
RESULTS
Of 123 enrolled patients, 121 were included in the intention-to-treat dataset, of which all were Caucasian and 54.5% were female; 76 patients used BAK-preserved bimatoprost-timolol and 45 used PF drops. Conjunctival hyperaemia and severity of worst ocular symptom following switch to PF tafluprost-timolol significantly reduced from screening to week 12 in all patients (p<0.001). The percentage of patients with ocular signs and symptoms was significantly reduced at week 12 compared with screening (p<0.001). IOP was not affected by the change of treatment.
CONCLUSIONS
Switching from BAK-preserved or PF bimatoprost-timolol to tafluprost-timolol reduced both signs and symptoms of ocular surface disease with no clinically relevant effect on IOP.
TRIAL REGISTRATION NUMBER
EudraCT2014-005273-37; Results.
Topics: Adult; Aged; Aged, 80 and over; Antihypertensive Agents; Bimatoprost; Drug Administration Schedule; Drug Combinations; Female; Glaucoma, Open-Angle; Humans; Intention to Treat Analysis; Intraocular Pressure; Male; Middle Aged; Ocular Hypertension; Ophthalmic Solutions; Preservatives, Pharmaceutical; Prostaglandins F; Quality of Life; Timolol
PubMed: 30944129
DOI: 10.1136/bmjopen-2018-024129