共查询到20条相似文献,搜索用时 437 毫秒
1.
C.H. Spilman D.C. Beuving A.D. Forbes F.A. Kimball 《Prostaglandins & other lipid mediators》1977,14(3):477-488
The effects of prostaglandin (PG)F2α and PGF2α, 1–15 lactone were compared in luteal phase, non-pregnant and in early pregnant rhesus monkeys. Animals treated with either PG after pretreatment with human chorionic gonadotropin (hCG) had peripheral plasma progesterone concentrations that were not statistically different from those in animals treated with hCG and vehicle. However, menstrual cycle lengths in monkeys treated with PGF2α, 1–15 lactone were significantly (P <0.02) shorter than those in vehicle treated animals. In the absence of hCG pretreatment, plasma progesterone concentrations were significantly (P <0.008) lower by the second day after the initial treatment with either PGF2α or PGF2α, 1–15 lactone than in vehicle treated monkeys. Menstrual cycle lengths in monkeys treated with either PG were significantly (P <0.04) shorter than those in animals treated with vehicle. There were no changes in plasma progesterone concentrations in early pregnant monkeys treated with PGF2α, and pregnancy was not interrupted. In contrast, plasma progesterone declined and pregnancy was terminated in 5 of 6 early pregnant monkeys treated with PGF2α, 1–15 lactone. These data indicate that PGF2α, 1–15 lactone decreases menstrual cycle lengths in non-pregnant rhesus monkeys. More importantly, PGF2α, 1–15 lactone terminates early pregnancy in the monkey at a dose which is less than an ineffective dose of PGF2α. 相似文献
2.
T.A. Fitz E.J. Mock M.H. Mayan G.D. Niswender 《Prostaglandins & other lipid mediators》1984,28(1):127-138
Purified preparations of ovine large luteal cells were utilized in a series of experiments to test the effects of prostaglandins (PG) E2 abd F2α on cell morphology, viability and secretion of progesterone. Luteal cells were allowed to attach to culture dishes overnight before experiments. In the first series of experiments incubation of large steroidogenic cells with PGF2α for 6 hr resulted in morphological changes including a retraction of the cell cytoplasm and apparent extrusion of cytoplasmic components which became more pronounced after 12 hr. In a second series of experiments, PGF2α decreased and PGE2 increased progesterone accumulation in media after 6 hr when media were not replaced during the incubation period, while progesterone accumulation was not different than that observed in control dishes when both prostaglandins were present. Hourly replacement of the media negated the inhibitory effects of PGF2α but had no effect on the stimulated secretion of progesterone induced by PGE2. Finally, in incubations without media replacement, PGF2α induced a dose-dependent decrease in progesterone accumulation while PGE2 elicited a biphasic response with progesterone secretion increasing from 0.1 ng/ml to maximal levels at 10 ng/ml followed by a dose-dependent decrease at 100 and 1000 ng/ml. These data are compatible with the hypotheses that: 1) luteolysis is initiated, at least in part, by an action of PGF2α on large luteal cells; and 2) the embryonic signal from the pregnant uterus which rescues the ovine corpus luteum may be PGE2. 相似文献
3.
PGI2 and 6-keto-PGF1α were converted to 6-methoxime-PGF1α (6-MeON-PGF1α) by treatment with methoxyamine HCl in acetate buffer. The formed 6-MeON-PGF1α was measured by radioimmunoassay. Antisera were raised in rabbits after immunization against 6-MeON-PGF1α-BSA conjugate. Diluted 1:20.000 to bind 50% of the tracer (3H-6-MeON-PGF1α, 100 Ci/mmol), the antiserum cross reacted 0.8% with PGE2, 1% with PGF2α and less than 0.2% with PGD2, PGF1α, PGF2β and TXB2. The radioimmunoassay was used to estimate release of PGI2 and 6-keto-PGF1α from chopped rabbit renal medulla and cortex incubated in Krebs-Ringer bicarbonate buffer (37°C, 30 min). The 6-keto-PGf1α radioimmunoassay was validated in biological samples by mass fragmentography. The chopped medulla (n=5) released 38±9 ng/g/min and the cortex (n=5) 4.7±2.0 ng/g/min, while the release of immunoreactive PGE2 (iPGE2) and iPGF2α was 171±26 and 74±13 ng/g/min from the medulla and 4.3±1.3 and 2.7±0.3 ng/g/min from the cortex, respectively. The results confirm previous findings, which indicate that in the renal medulla prostaglandin endoperoxides are mainly transformed to prostaglandins, while in the cortex transformation to PGI2 seems to be of greater
importance. 相似文献
4.
Pregnant hamsters were administered (SC) prostaglandin or vehicle on the morning of the 4th day of pregnancy. Serum progesterone was significantly depressed (p<.01) at 0.5, 2, and 6 hours after treatment with 100 μg PGF2α. Serum progesterone levels were unchanged 2 hours and 6 hours after treatment with 100 μg PGF2β and 2 hours after treatment with 1 mg PGF2β. Progesterone levels were depressed to less than 1 ng/ml 6 hours after treatment with 1 mg PGF2β. The specific uptake of 3H-PGF2α in whole hamster corpora lutea was significantly depressed 2 hours and 6 hours following 100 μg PGF2α treatment. A 15% depression in specific uptake occurred 0.5 hour post-treatment. Treatment with 100 μg PGF2β resulted in no change. Administration of 1 mg PGF2β resulted in depressed 3H-PGF2α uptake at both 2 and 6 hours post-treatment.Prostacyclin (PGI2) treatment resulted in no change in either 3H-PGF2α specific uptake or serum progesterone 2 hours after 100 μg treatment SC. These parameters were both reduced approximately 30% 6 hours post-treatment. Treatment with 6-keto-PGF1α resulted in a complete lack of measurable 3H-PGF2α uptake and serum progesterone levels less than 1 ng/ml at both 2 and 6 hours after treatment with 1 mg SC. 相似文献
5.
Claudia Weber Michael Hller Johan Beetens Fred De Clerck Frank Tegtmeier 《Journal of chromatography. B, Analytical technologies in the biomedical and life sciences》1991,562(1-2)
A method for quantification of 6-keto-PGF1α, 2,3-dinor-6-keto-PGF1α, TXB2, 2,3-dinor TXB2, PGE2, PGD2 and PGF2α in human urine samples, using gas chromatography—negative ion chemical ionization mass spectrometry, is described. Deuterated analogues were used as internal standards. Methoximation was carried out in urine samples which were subsequently applied to phenylboronic acid cartridges, reversed-phase cartridges and thin-layer chromatography. The eluents were further derivatized to pentafluorobenzyl ester trimethylsilyl ethers for final quantification by gas chromatography—mass spectrometry. The overall recovery was 77% for tritiated 6-keto-PGF1α and 55% for tritiated TXB2. Urinary levels of prostanoids were determined in a group of six volunteers before and after intake of the thromboxane synthase inhibitor Ridogrel, and related to creatinine clearance. 相似文献
6.
J. N. Stellflug T. M. Louis H. D. Hafs B. E. Seguin 《Prostaglandins & other lipid mediators》1975,9(4):609-615
During diestrus in three consecutive estrous cycles, each of six heifers was given (im) 30 mg, 15 mg (twice at 6-hr intervals) and 60 mg prostaglandin F2α (PGF2α) tham salt. Neither the decline in blood progesterone, the increase in blood estradiol, the duration or the peak of the LH surge, the interval to onset of estrus, nor the interval to ovulation was affected significantly by dose of PGF2α. Thus, relative to that after 30 mg PGF2α im, two injections of 15 mg at 6-hr intervals or 60 mg PGF2α did not hasten luteolysis. Thirty mg was an ample im dose of PGF2α to cause luteolysis. Regardless of im dose of PGF2α, blood PGF peaked at about 6.0 ng/ml within 10 minutes and returned to basal values (<1.0 ng/ml) within 90 minutes. In another trial, after a single iv injection of 5 mg PGF2α, blood PGF peaked (25 ng/ml) within 5 minutes and returned to basal values within 15 minutes. During a 30-minute infusion (0.5 mg/minute) of PGF2α, blood PGF plateaued at 29.5 ng/ml with a metabolic clearance rate of 17.0 liters per minute. 相似文献
7.
The present study has been performed to investigate how PGs would participate the hatching process. Effects of indomethacin, an antagonist to PGs biosynthesis, on the hatching of mouse blastocysts were examined in vitro. Furthermore, it was studied that prostaglandin E2 (PGE2), prostaglandin F2α (PGF2α) or 6-keto-prostaglandin F1α (6-keto-PGF1α) were added to the culture media with indomethacin. (1) The hatching was inhibited by indomethacin yet the inhibition was reversible. (2) In the groups with indomethacin and PGE2, no improvement was seen in the inhibition of hatching and the inhibition was irreversible. (3) In the groups with indomethacin and PGF2α, inhibition of hatching was improved in comparison with the group with indomethacin. (4) In the groups with indomethacin and 6-keto-PGF1α, no improvement was seen. The above results indicated that PGF2α possibly had an accelerating effect on hatching and a high concentration of PGE2 would exert cytotoxic effect on blastocysts. 相似文献
8.
Hideya Hayashi Seiji Ito Teruo Tanaka Manabu Negishi Hideo Kawabe Yokohama Hiromitsu Kikuko Watanabe Osamu Hayaishi 《Prostaglandins & other lipid mediators》1987,33(4)
In view of the recent finding that prostaglandin D2 is stereospecifically converted to 9α,11β-prostaglandin F2, an isomer of prostaglandin F2α, a highly specific and sensitive radioimmunoassay for 9α,11β-prostaglandin F2 was developed and applied to determine the content of this prostaglandin in various rat tissues. Antisera against 9α-11β-prostaglandin F2 were raised in rabbits immunized with the bovine serum albumin conjugate, and [3H]9α,11β-prostaglandin F2 was enzymatically prepared from [3H]prostaglandin D2. The assay detected 9α,11β-prostaglandin F2 over the range of 20 pg to 1 ng, and the antiserum showed less than 0.04% cross-section with prostaglandin F2α, prostaglandin F2β and 9β,11β-prostaglandin F2. To avoid postmortem changes, tissues were frozen in liquid nitrogen immediately after removal. The basal level of 9α,11β-prostaglandin F2 was hardly detectable in various tissues of the rat examined, including spleen, lung, liver and brain; although it was found to be 0.31 ± 0.06 ng/g wet weight in the small intestine. During convulsion induced by pentylenetetrazole, enormous amounts of prostaglandin D2 (ca. 180 ng/g wet weight) and prostaglandin F2α (ca. 70 ng/g) were produced in the brain; however, 9α,11β-prostaglandin F2 was detected neither there nor in the blood. This result demonstrates that the conversion to 9α,11β-prostaglandin F2 is a minor pathway, if one at all, of prostaglandin D2 metabolism in the rat brain. 相似文献
9.
Marc E. Goldyne Jan ke Lindgren Hans-Erik Claesson Sven Hammarstrm 《Prostaglandins & other lipid mediators》1980,19(1):155-163
Prostaglandins (PG)E1, E2 and I2 were produced by polyoma virus transformed (py) 3T3 fibroblasts. The levels of PGE1, PGE2 and 6-keto-PGF1α (degradation product of PGI2) were 22.7, 225 and 33.2 ng/ml medium, respectively, 72 h after medium change. The stimulatory potencies of exogenous PGE1, PGE2 and PGI2 on adenosine 3′:5′-monophosphate (cyclic AMP) formation were similar. Therefore, the prostaglandin mediated increase in cyclic AMP levels observed during growth of these cells (Claesson, H.-E., Lindgren, J.Å. and Hammarström, S. (1977) Eur. J. Biochem.
, 13) is largely (>80%) mediated by PGE2 and to lesser extents by PGE1 and PGI2. 相似文献
10.
Prostaglandin F2α (PGF2α) was measured by immunoassay in plasma and milk of four cows (six experiments). After 30 mg PGF2α im, plasma PGF2α peaked at 15 minutes (2.4 ± 0.7 ng/ml) and declined toward basal values by 3 hours; maximum milk PGF2α (0.91 ± 0.12 ng/ml) occurred at 1 hour. The average excretion rate in milk was 2.9 μg/day 0.9 μg (0.003%) of which was due to the 30 mg PGF2α injected. In six non-pregnant control cows, daily changes of milk PGF2α and progesterone were not consistently related. 相似文献
11.
Ray V. Haning Jr. Leslie Choi Amber J. Kiggens Donna L. Kuzma John W. Summerville 《Prostaglandins & other lipid mediators》1982,23(1):29-40
Explants from term human placentas were maintained in culture with daily changes of medium. Daily output of PGF2α and PGFM1 decreased during the course of the incubation. Addition of 4 μg/ml DHEAS or 67 μg/ml LDL cholesterol had no effect on output of PGF2α or PGFM. Addition of 1.6, 3.2, or 6.4 μg/ml of LHRH to the culture plates had no effect on output of PGFM or PGF2α, but LHRH increased hCG output. Dibutyryl cAMP (1mM, 2mM, and 4mM) increased output of PGF2α, PGFM, and hCG. Aromatase inhibitor decreased hCG output, but it was without effect on output of PGF2α, or PGFM. Significant correlations were demonstrated between progesterone, PGFM, PGF2α, and hCG, suggesting that PGF2α originates in the syncytiotrophoblast cell. The ability of LHRH to stimulate output of hCG but not PGF2α while dbcAMP stimulated both suggests that either PGF2α and hCG arise in different cells or that LHRH does not act through cAMP. 相似文献
12.
T. Obata T. Nagakura M. Kammuri T. Masaki K. Maekawa K. Yamashita 《Journal of chromatography. B, Analytical technologies in the biomedical and life sciences》1994,655(2)
Sensitive and specific assay methods for 9α,11β-prostaglandin F2 (9α,11β-PGF2) by gas chromatography—mass spectrometry with electron impact ionization are described. The mass spectrometric assay for 9α,11β-PGF2 was based on the use of the methyl ester—dimethylisopropylsilyl ether derivative, and pentadeuterated PGF2α as a convenient internal standard. The calibration graph for 9α,11β-PGF2 was linear from 5 pg to 100 ng for both the standard and spiked biological samples. The limit of detection was 50 pg/ml for urine and 25 pg/ml for plasma (signal-to-noise RATIO = 2.3). The method was applied to the determination of 9α,11β-PGF2 in urine and plasma samples from patients with bronchial asthma. 相似文献
13.
David M. Olson K arolina Skinner John R.G. Challis 《Prostaglandins & other lipid mediators》1983,25(5):639-651
Prostaglandin (PGE, 6-keto PGF1α) output by cells dispersed from human amnion and decidua in the presence of increasing levels (0–5000 ng/ml) of estradiol-17β (E2) or 2-hydroxyestradiol-17β (2-OH E2) was studied in relation to parturition. Tissues were obtained from women at term either before (CS) or after (SL) spontaneous labor and vaginal delivery. In the absence of estrogens, the output of both PGs from amnion increased significantly with labor. No significant increase in decidua PG output occurred with labor. Neither estrogen influenced CS amnion PG output. However, both E2 and 2-OH E2 stimulated SL amnion PGE output (2-OH E2>E2) while having no affect on 6-keto PGF1α output. Only the highest dose of 2-OH E2 stimulated PGE output in CS decidua, but both estrogens significantly inhibited 6-keto PGF1α output in this tissue. In SL decidua only 2-OH E2 significantly stimulated PGE, and neither estrogen affected 6-keto PGF1α output. These results might suggest that estrogens modulate PG biosynthesis at the level of endoperoxide to primary PG conversion. 相似文献
14.
Our reported data on the cortical inhibitory actions of prostaglandin F2α (PGF2α) and the diversity of data in the literature on cerebral PG actions are examined here in the light of intracellular recording which provides the requisite membrane data for the first time. Thus, 1) intracellular recording from the cat cerebral cortex is obtained for the actions of PGF2α and for norepinephrine (NE) and serotonin (5HT). 2) The parallel changes in firing and polarization and the simultaneous transmembrane conductance changes are qualitatively identical for PGF2α, NE and 5HT. 3) The reduction in firing accompanied by hyperpolarization indicates that PGF2α, NE and 5HT all inhibit these cells. 4) The ionic species responsible for this inhibition is such that it increased the transmembrane resistance, and this was true for all three. 5) The changes in membrane parameters, identical in direction for PGF2α and NE, but stronger for the latter, constitute conditions that can lead to competitive inhibition and therefore conote, presumably, actions at the same or related receptors. Such competition with evoked cortical field potentials is shown in the preceding paper. 相似文献
15.
Potential interactions between PGD2 and PGF2α in the mesenteric and renal vascular beds were investigated in the anesthetized dog. Regional blood flows were measured with electromagnetic flow probes. PGD2, PGF2α and Norepinephrine (NE) were injected as a bolus directly into the appropriate artery, and responses to these agents were obtained before, during and after infusion of either PGD2 or PGF2α into the left ventricle. In each case, the infused prostaglandin caused vascular effects of its own. Left ventricular infusion of PGD2 reduced responses to local injections of PGD2 in the intestine, and a similar effect was observed for PGF2α, suggesting significant receptor or receptor-like interactions for each of the prostanoids. However, systemic infusion of prostaglandin F2α (20–100 ng/kg/min) had no effect on renal or mesenteric vascular responses to local injection of prostaglandin D2. Similarly, PGD2 administration (100 ng/kg/min) did not affect responses to PGF2α in the intestine. The present results therefore suggest that these prostaglandins, i.e., D2 and F2α, act through separate receptors in the mesenteric and renal vascular beds. In addition, increased prostaglandin F2α levels produced by infusion of F2α reduced mesenteric but not renal blood flow, suggesting that redistribution of cardiac output might participate in side effects often observed with clinical use of this prostaglandin, such as nausea and abdominal pain. 相似文献
16.
C. N. Hensby 《Prostaglandins & other lipid mediators》1974,8(5):369-375
Prostaglandins E2 and D2 were both converted to prostaglandin F2α (9α, 11α) by an enzyme present in sheep blood. Neither the 9β, 11α epimer nor the 9α, 11β epimer was produced from PGE2 or PGD2 respectively. The rate of reduction was measured using isotope dilution (D4 PGF2α) and multiple-ion detection gas chromatography-mass spectrometry. 相似文献
17.
John F. Gerkens John G. Gerber David G. Shand Robert A. Branch 《Prostaglandins & other lipid mediators》1978,16(5):815-823
Prostaglandins (PG)I2, PGE2 and 6-keto PGF1α were infused directly into the gastric arterial supply at 10−9, 10−8 and 10−7 g/kg/min during an intra-gastric artery pentagastrin infusion in anesthetized dogs. 6-keto PGF1α was also infused at 10−6 g/kg/min. Gastric arterial blood flow was measured continuously with a non-cannulating electromagnetic flow probe and gastric acid collected directly from the stomach. PGI2 and PGE2 produced similar dose-dependent increases in blood flow with an increase of more than four-fold at the highest dose. Both PGs inhibited acid output over this dose range with PGE2 having 10 times the potency of PGI2. 6-keto PGF1α was at least 1000 times less active than PGI2 or PGE2 at increasing blood flow and failed to inhibit acid output even at 10−6 g/kg/min. 相似文献
18.
Earlier work had shown that the lactogen, LTH and HPL, foster testosterone binding by the prostate. This study was undertaken to see if prostaglandin F2α would oppose the effect of the lactogen on the prostate as it does the luteotrophic action of the hormone on the corpus luteum. When it was found instead that the PGF increases steroid binding and that its interaction with lactogen was neither antagonistic nor additive, attention was directed to further characterization of the prostaglandin's effect. A dosage/response study of F2α alone showed that concentrations of 4 ng/ml and 40 ng/ml increased binding but that 400 ng/ml did not. Glands with stromal hyperplasia and/or inflammation were more responsive than those with epithelial hyperplasia. Assays of water extracts of the tissue revealed concentrations of about 340 ng of F2α per gram fresh weight and that the concentration varied inversely as the β-glucuronidase activity. If the enzyme level is considered an index of the epithelial cell density within the specimen, the inverse relationship suggests a non-epithelial (stromal) site of prostaglandin concentration. 相似文献
19.
Sylvie Ben Slama Christine Bnistant Fabienne Achard Evelyne Vricel Michel Lagarde 《Prostaglandins & other lipid mediators》1995,50(2)
The cross-reactivity of the PGI3 metabolite, Δ17-6-keto-PGF1α, with antibodies against 6-keto-PGF1α for radioimmunoassays (RIA) has been investigated. Δ17-6-keto-PGF1α was obtained either from commercial sources or after its purification from endothelial cells. In the latter case, primary cultured bovine aortic endothelial cells were incubated for 20 min at 37°C with 10 μM eicosapentaenoic acid (EPA) in the presence of 2 μM 13-hydroperoxy-octadecadienoic acid, an activator of the EPA cyclooxygenation, and the 6-keto-PGF1α and Δ17-6keto-PGF1α produced were separated by RP-HPLC. Then, cross-reactivities of the commercial and purified Δ17-6-keto-PGF1α with 6-keto-PGF1α antibodies were determined and found not to exceed 10%. In addition, the amounts of prostacyclin-related compounds detected by direct measurements in media of cells loaded with EPA were compared with those obtained after purification of 6-keto-PGF1α. In accordance with the cross-reactivity data, we found that RIA in media mainly measured 6-keto-PGF1α, the Δ17-6-keto-PGF1α formed being undetected at 90%. It is concluded that 6-keto-PGF1α antibodies generally used for RIA of 6-keto-PGF1α are highly specific since they can discriminate a metabolite bearing an additional double bond such as the PGI3 metabolite Δ17-6-keto-PGF1α. 相似文献
20.
Enhanced expression of transforming growth factor-β1(TGF-β1) demonstrated in human colonic mucosa of patients with ulcerative colitis (UC), indicates its possible significance in the pathogenesis of this disease. The aim of this study was to evaluate plasma TGF-β1concentration in patients with different degrees of colonic mucosal injury, as a possible indicator of ulcerative colitis activity. TGF-β1concentration was measured with an enzyme immunoassay (EIA) in plasma of 45 patients with endoscopically confirmed UC. Values observed in UC patients (40.5±15.9 ng/ml) were significantly higher than in healthy people (18.3±11.6 ng/ml) and higher than in patients with irritable colon syndrome (ICS), (20.5±13.6 ng/ml). The highest plasma TGF-β1(58.6±112.1 ng/ml) was in patients with the severe UC course. TGF-β1level analysed in all UC patients revealed significant positive correlation with scored degree of mucosal injury (r=0.396;P<0.01). Among other possible laboratory markers of the disease activity, only C-reactive protein concentration demonstrated significant correlation. Enhanced production of TGF-β1can be related to inflammation activity. Measurement of plasma TGF-β1may be considered as a biomarker of the disease activity. 相似文献