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1.
The effects of oestradiol, oxytocin, progesterone and hydrocortisone
on prostaglandin (PG) output from guinea-pig endomerium, removed on days 7 and 15 of the oestrous cycle and maintained in tissue culture for 3 days, have been investigated. Oetradiol (3.7 to 3700nM) and oxytocin ( 2 to 200pM) did not stimulate endometrial PGF2α output, thus not confirming the findings of a previous report (Leaver & Seawright, 1928), nor did they stimulate the outputs of PGE2 and 6-keto-PGF1α. In fact, oestradiol (3700nM) inhibited the outputs of PGF2α, PGE2 and, to a lesser extent, 6-keto-PGF1α. Progesterone (3.2 to 3200nM) inhibited the outputsof PGF2α and PGE2; hydrocortisone (2.8 to 2800nM) had no effect on endometrial PG output. These findings indicate that the inhibitory effect of progesterone on endometrial PG synthesis and release in the guinea-pig is not due to progesterone having a glucocorticoid-like action. Furthermore, progesterone had no effect on 6-keto-PGF1α output, suggesting that the mechanisms controlling endometrial PGI2 synthesis (as reflected by measuring 6-keto-PGF1α) are different from those controlling endometrial PGF2α and PGE2 synthesis. 相似文献
2.
Dilatation of the cervix with prostaglandin analogues prior to vaginal termination of pregnancy was attempted in 125 nulliparous women in the first trimester of pregnancy. The patients were divided into five groups (25 in each group) and given a single extra-amniotic dose of one of the following prostaglandin analogues 14–16 hours prior to the evacuation of the uterus by vacuum aspiration. (Group A) 15 (S) 15 methyl PGE2 (free acid); (Group B) 15 (S) 15 methyl PGE2 methyl ester; (Group C) 15 (S) 15 methyl PGF2α (free acid); (Group D) 15 (S) 15 methyl PGF2α methyl ester and(Group E) a mixture of 15 (S) 15 methyl PGE2 methyl ester and 15 (S) 15 methyl PGF2α methyl ester. Evacuation of the uterus without mechanical dilatation of the cervix was possible in 111 (90%) of the patients. In an additional 10 patients (8%) there was some degree of cervical dilatation and further mechanical dilatation could be performed easily. With the combination of 15 (S) 15 methyl PGE2 methyl ester and 15 (S) 15 methyl PGF2α methyl ester the incidence of gastrointestinal side effects and pyrexia were considerably reduced. 相似文献
3.
A.L. Gimeno M. Chaud A. Bonacossa A.M. Franchi M.F. Gimeno 《Prostaglandins & other lipid mediators》1983,26(4):663-676
Dose-response curves for several prostaglandins (PGI2; PGD2; PGF2 and PGE2); BaCl2 or prostaglandin metabolites (15-keto-PGF2α; 13, 14-diOH-15-keto-PGF2α; 6-keto-PGF1α and 6-keto-PGE1 in quiescent (indomethacin-treated) uterine strips from ovariectomized rats, were constructed. All PGs tested as well as BaCl2, triggered at different concentrations, evident phasic contractions. Within the range of concentrations tested the portion of the curves for the metabolites of PGF2α was shifted to the right of that for PGF2α itself; the curve for 6-keto-PGF1α was displaced to the right of the curve for PGI2 and that for 6-keto-PGE1 to the left.It was also demonstrated that the uterine motility elicited by 10−5 M PGF2α and its metabolites was long lasting (more than 3 hours) and so it was the activity evoked by PGI2; 6-keto-PGF1α and BaCl2, but not the contractions following 6-keto-PGE1, which disappeared much earlier. The contractile tension after PGF2α; 15-keto-PGF2α; 13, 14-diOH-15-keto-PGF2α and PGI2, increased as time progressed whilst that evoked by 6-keto-PGF2α or BaCl2 fluctuated during the same period around more constant levels.The surprising sustained and gradually increasing contractile activity after a single dose of an unstable prostaglandin such as PGI2, on the isolated rat uterus rendered quiescent by indomethacin, is discussed in terms of an effect associated to its transformation into more stable metabolites (6-keto-PGF1α, or another not tested) or as a consequence of a factor which might protects prostacyclin from inactivation. 相似文献
4.
Anna-Riitta Fuchs Klaus Goeschen Anne B. Rasmussen Jaana V. Rehnstrm 《Prostaglandins & other lipid mediators》1984,28(2):217-227
Two modes of cervical application of a gel containing PGE2 have been compared in a total of 30 patients with indication for induction of labor and unripe cervix. Fifteen patients had gel injected endocervically; in 10 patients the gel contained 400μg PGE2, in 5 controls the gel was inactive. Fifteen subjects had a 15 ml Foley catheter passed through the cervix and placed extra-amniotically; in 10 of them 3 ml gel with 400 or 800μg PGE2 was injected, while 5 controls received inactive gel. Plasma levels of 13,14-dihydro-15-keto-PGF2α (PGFM) were measured in blood samples drawn before and
, 1, 2, 4, 6, and 8 hours after gel application. Neither the Foley catheter nor the application of inactive gel caused significant changes in the cervical scores or the PGFM levels. PGE2 in the endocervix increased cervical scores without altering plasma PGFM levels. Extra-amniotic PGE2 caused a more rapid increase of the cervical scores and a progressive rise in PGFM levels. The plasma (PGFM) levels were found to be related to the degree and to the rate of cervical dilatation. The correlation with cervical dilatation was highly significant. Labor began spontaneously or after artificial rupture of the membranes in 80% of the extra-amniotic, and 50% of the endocervical PGE2-group, but in none of the controls. These data indicate that the increased uterine PGF2α production is not necessary for the early stages of cervical ripening, whereas dilatation beyond 4 cm does not proceed without such increase. 相似文献
5.
The biosynthesis of prostaglandins by isolated epithelial glandular and stromal cells was studied after collagenase digestion of endometrium collected from women at various stages of the menstrual cycle. Homogenates of the separate cell types were incubated for 60 minutes with 2.08 μg 114C arachidonic acid and the products separated by thin layer chromatography. Both glandular and stromal homogenates synthesised PGF2α. More PGF2α was synthesised by glandular epithelium separated from both proliferative and secretory endometrium than by stroma. The ratio of PGF2α/PGE2 was greater in glands and stroma isolated from secretory than proliferative endometrium. Small but significant amounts of 6-keto-PGF1α were produced by all cell types. These results suggest that the increased synthesis of PGF2α from secretory endometrium is due, at least in part, to increased activity of cyclo-oxygenase enzyme in the glandular epithelium. 相似文献
6.
Anders
lund Hans Kindahl Ernst Oliw ke Lindgren Jan Bertil Larsson 《Prostaglandins & other lipid mediators》1980,19(5):791-803
Abortion or delivery were induced by extra-amniotic instillation of Rivanol during the second trimester in twelve patients and during the third trimester in two patients with fetal death and one patient with fetal acrania. Serial sampling of amniotic fluid was performed through a transabdominal catheter and the levels of free arachidonic acid (AA), prostaglandin F2α (PGF2α), prostaglandin E2 (PGE2), 6-keto-prostaglandin F1α (6-keto-PGF1α) and thromboxane B2 (TXB2) were determined. The levels of AA, PGF2α, PGE2, 6-keto-PGF1α and TXB2 in amniotic fluid increased significantly during induction with the exception of AA in fetal death which was high and remained constant during induction. Furthermore, PGF2α, 6-keto-PGF1α and TXB2 were all significantly correlated to AA.These observations suggested that free AA is released during Rivanol-induction of abortion and labour giving an increased synthesis of PGF2α, PGE2 prostacyclin and thromboxane A2 in the fetal membranes and the decidua but not in the fetus. This increase might be relevant for the initiation and progress of abortion and labour in these patients. 相似文献
7.
We cultured phagocytic cells derived from the thymic reticulum in order to study the regulation of prostaglandin (PG) production by antiinflammatory or immunostimulating agents. The kinetics of PGE2, 6-keto-PGF1α and PGF2α production were measured by specific radioimmunoassays of the supernatants harvested from cells treated with dexamethasone, a steroidal antiinflammatory drug and by two non steroidal inhibitors (indomethacin and sulindac) or by various immunostimulating agents, one of them, RU 41740 is currently being used in humans. Our results revealed that ech of these drugs exerts a differential effect on the PG production, with a striking action on PGE2 synthesis, a lesser effect on 6-keto-PGF1α production and almost no effect on PGF2α synthesis. The possible mechanisms responsible for this complex regulation of PG production are discussed. 相似文献
8.
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
9.
Prostanoids play an important role throughout all of pregnancy and during the initiation and progress of labor. The human placenta at term produces large quantities of prostanoids, yet little is known of the factors that regulate their biosynthesis. Herein, we report the effect of estradiol or estradiol and progesterone on the basal release of placental prostanoids from fresh human term placental explants using a perifusion system.The basal release of prostaglandin E2 (PGE2, prostaglandin F2α (PGF2α), thromboxane (TxB2) and 6-keto-prostaglandin F1α (6-keto-PGF1α) increased about 50% from the fifth to the ninth hour in culture, while the release of 13, 14-dihydro-15-keto-PGF (PGFM) remained constant and hCG release decreased. The dose-related effect of estradiol (20–2,000 ng/ml) in the perifusing medium starting at the fifth hour of perifusiOn (i.e., the zero treatment time) effected no change in the release of TxB2, PGF2α, PGFM or hCG. A biphasic action on the release of 6-keto-PGF,. was observed, i.e. it was significantly decreased when incubated with 20 ng/ml of estradiol, but effected an increase after exposure to 200 ng/ml. The concomitant addition of progesterone (2,000 ng/ml) with estradiol (200 ng/ml) significantly inhibited the stimulatory action of estradiol at this dose. The release of PGE2 was inhibited in a dose-related fashion with increasing dose of estradiol. The addition of progesterone with estradiol (2,000 and 200 ng/ml, respectively) reversed the inhibition of PGE2 by estradiol alone.These data demonstrate that physiologic levels of estradiol affect 6-keto-PGFα and PGE2 release from the human term placenta, but do not significantly alter production of TxB2, PGFM or hCG under these conditions. 相似文献
10.
A. Jawerbaum A.M. Franchi E.T. Gonzalez V. Novaro M.A.F. de Gimeno 《Prostaglandins & other lipid mediators》1995,50(1)
The relationship between high glucose concentrations and arachidonic acid metabolism in uterine tissue from control and diabetic ovariectomized rats was evaluated. Uterine tissue from diabetic rats produced amounts of PGE2 and PGF2α similar to controls, while a lower production of 6-keto-PGF1α (indicating the production of prostacyclin) and a higher production of TXB2 (indicating the generation of TXA2) was found in the diabetic group. A group of diabetic rats was treated with phlorizin to diminish plasma glucose levels. Phlorizin treatment did not alter production of PGE2, PGF2α, and 6-keto-PGF1α in the diabetic group. A diminished production of TXB2 was found in the treated diabetic uteri when compared to the non-treated diabetic group. Moreover, a positive correlation between plasma glucose levels and uterine TXB2 generation was observed. When control uterine tissue was exposed in vitro to high concentrations of glucose (22 mM) and compared to control tissue incubated in the presence of glucose 11 mM alterations in the generation of PGE2, PGF2α, and 6-keto-PGF1α were not found, but a higher production of TXB2 was observed and values were similar to those obtained in the diabetic tissue. Alteration in the production of the prostanoids evaluated were not observed when diabetic tissue was incubated in the presence of high concentrations of glucose. These results provide evidence of a direct relationship between plasma glucose levels and uterine production of TXA2. 相似文献
11.
Michael L. Booker B.S. Wayne W. LaMorte M.D. 《Prostaglandins & other lipid mediators》1983,25(2):143-153
In order to study prostaglandin in release from guinea pig gallbladder, full thickness tissue sections were incubated for one hour in Kreb's solution. Extraction and two dimensional chromatography of incubation media obtained in the presence of radio-labelled arachidonic acid demonstrated the presence of PGE2, PGF2α, 6-keto-PGF1α and thromboxane B2. These results were supported by radioimmunoassay of incubations conducted in the absence of exogenous arachidonate and in the presence of varying concentrations of unlabelled exogenous arachidonate. The previously reported predominance of PGE2 was only seen at high concentrations of exogenous arachidonate. 相似文献
12.
Patricia A. Craven Frederick R. DeRubertis 《Prostaglandins & other lipid mediators》1983,26(4):583-604
Prostaglandin (PG) synthesis and degradation were examined in different regions (epithelial versus non-epithelial structures) of the rat distal colon by both HPLC analysis of [14C] arachidonate (AA) metabolites and by specific radioimmunoassays. Intact isolated colonic epithelial cells synthesized mainly PGF2α and TXA2, as monitored from the formation of its stable degradation product TXB2 (PGF2α > TXB2 > 6-keto-PGF1α, the stable degradation product of PGI2=PGD2=PGE2=13,14-dihydro-15-keto-PGF2α). The profile of PG products of isolated surface epithelial cells was identical to that of proliferative epithelial cells. However, generation of PGs by surface epithelium was 2 to 3-fold higher than by proliferative cells both basally and in the presence of a maximal stimulating concentration (0.1 mM) of AA. The latter implied a greater synthetic capacity of surface epithelium, rather than differences due to endogenous AA availability. The major sites of PG synthesis in colon clearly resided in submucosal structures; the residual colon devoid of epithelial cells accounted for at least 99% of the total PGs produced by intact distal colon. The profile of AA metabolites formed by submucosal structures also differed markedly from that of the epithelium. The dominant submucosal product was PGE2. PGE2 and its degradation product 13,14-dihydro-15-keto-PGE2 accounted for 63% of the PG products formed by submucosal structures (PGE2 PGD2 > 13,14-dihydro-15-keto-PGE2 > PGF2α=TXB2=6-keto-PGF1α > 13,14-dihydro- 15-keto-PGF2α). By contrast, epithelial cells, and particularly surface epithelium, contributed disproportionately to the PG degradative capacity of colon, as assessed from the metabolism of either PGE2 or PGF2α. When expressed as a percentage, epithelial cells accounted for 71% of total colonic PGE2 degradative capacity but only 23% of total colonic protein. Approximately 15% of [3H] PGE2 added to the serosal side of everted colonic loops crossed to the mucosal side intact. Thus, at least a portion of the PGE2 formed in the submucosa reaches, and thereby can potentially influence functions of the epithelium. 相似文献
13.
R.D. Nolan G.J. Dusting J. Jakubowski T.J. Martin 《Prostaglandins & other lipid mediators》1982,24(6):887-902
Cyclo-oxygenase products of arachidonic acid metabolism formed by the pericardium and epicardial surface of dog heart were identified and quantitated by radioimmunoassay after separation by high-pressure liquid chromatography. Pieces of pariental pericardium, of dog, ox and rat, when incubated
produced mainly 6-keto-PGF1α, with lesser amounts of PGE2, PGF2α and thromboxane B2. Biosynthesis of all prostanoids increased during incubation of the pariental pericardium of each species with arachidonic acid, but 6-keto-PGF1α was still the major metabolite. When slices of dog heart were incubated with arachidonic acid (1 μg/ml) the rates of 6-keto-PGF1α formation by the pariental pericardium was much greater than that of the myocardium and endocardium. Epicardial slices appeared to be intermediate in 6-keto-PGF1α formation. The hearts of anesthetized dogs were also irrigated
with Krebs' solution, and during the first 5 min of epicardial irrigation the pericardial fluid leaving the heart again contained high levels of 6-keto-PGF1α, with lesser amounts of the other prostanoids. Addition of arachidonic acid (3 μg/ml) to the irrigating fluid caused an increase in all measured prostanoid levels, although 6-keto-PGF1α remained the predominant metabolite. In contrast, intravenous infusion of isoproterenol selectively increased the release of 6-keto-PGF1α from the irrigated heart. It is concluded that the pericardium and epicardium continuously release prostacyclin into the pericardial fluid, and that the increased release of this substance observed when cardiac workload increases derives mainly from these membranous sources. This raises the interesting possibility that pericardial prostacyclin might influence coronary vascular tone and chemoreflexes which arise from the epicardium during myocardial ischemia. 相似文献
14.
Hydrocortisone (10 μg/ml) had no effect on the basal outputs and A23187-stimulated outputs of PGF2α, PGE2 and 6-keto-PGF1α from the Day 15 guinea-pig uterus superfused
. These findings indicate that the high output of PGF2α from the guinea-pig uterus during the last one-third of the oestrous cycle is not modulated by the adrenal glucocorticoid hormones. Progesterone (10 gmg/ml) had no effect on the A23187-induced increases in PG output from the Day 15 guinea-pig uterus. However, oestradiol (10 gmg/ml but not 1 μg/ml) significantly reduced the increases in outputs of PGF2α, PGE2 and 6-keto-PGF1α induced by A23187 from the Day 15 guinea-pig uterus, without affecting basal PG outputs. The increase in uterine tone induced by A23187 in the Day 15 guinea-pig uterus was reduced by 20–50% by oestradiol (10 μg/ml). The addition of oestradiol (10 μg/ml) and progesterone together (10 gmg/ml) produced the same effects on the Day 15 guinea-pig uterus as oestradiol alone. Oestradiol (10 μg/ml) also reduced the A23187-induced increases in PG output from the Day 7 guinea-pig uterus, but did not reduce the increase in uterine tone. Oestradiol (10 gmg/ml) reduced the increases in outputs of PGF2α, PGE2 and 6-keto-PGF1α induced by exogenous arachidonic acid from the Day 7 and Day 15 guinea-pig uterus. Previous studies have shown that oestradiol is not a cyclo-oxygenase inhibitor. The present findings suggest that oestradiol, at a relatively high concentration, may interfere with the access of arachidonic acid to the cyclo-oxygenase enzyme. This action of oestradiol may explain its anti-luteolytic action when administered to guinea-pigs in large doses after Day 9 of the cycle. 相似文献
15.
Wolfgang Jelkmann Armin Kurtz Ulrich Frstermann Josef Pfeilschifter Christian Bauer 《Prostaglandins & other lipid mediators》1985,30(1):109-118
In view of recent findings which suggest that renal prostaglandins mediate the effect of hypoxia on erythropoietin production, we have studied whether hypoxia is a stimulus for in vitro prostaglandin synthesis. Studies were carried out in rat renal mesangial cell cultures which produce erythropoietin in an oxygen-dependent manner. Production rates of PGE2 and in specified samples also of 6-keto-PGF1α, as a measure of PGI2, and PGF2α were determined by radioimmunoassay after incubation at either 20% O2 (normoxic) or 2% O2 (hypoxic) in gas permeable dishes for 24 hrs. Considerable variation in PGE2 production was noted among independent cell lines. PGE2 production appeared to be inversely correlated to the cellular density of the cultures. In addition, PGE2 production was enhanced in hypoxic cell cultures. The mean increase was 50 to 60%. PGF2α and 6-keto-PGF1α increased by about the same rate. These results indicate that hypoxia is a stimulus for in vitro prostaglandin production. 相似文献
16.
Burkhard Scherer Sven Fischer Wolfgang Siess Peter C. Weber 《Prostaglandins & other lipid mediators》1982,23(1):41-52
A radioimmunoassay (RIA) for the estimation of 6-keto-PGF1α in human urine is described in detail. The RIA method was validated by direct comparison to gas chromatography-mass spectrometry. In adults and in one year old children basal excretion of 6-keto-PGF1α was found to be lower than that reported for PGE2 or PGF2α. However, during the first week of life, significantly more 6-keto-PGF1α was excreted. The very high levels of 6-keto-PGF1α in urine seen on the third day of life seemed already to decrease during the first week of life. It is concluded that prostacyclin may have a major role for kidney function in the newborn, possibly by protecting the immature kidney from high levels of angiotensin II. 相似文献
17.
Background
Eicosapentaenoic acid-derived prostaglandin (PG) E3, PGF3α, and thromboxane (TX) B3 are bioactive lipid mediators which have anti-cancer and anti-inflammatory effects. To exert their effects, PGE3, PGF3α, and TXB3 must be released to the extracellular space from cells, but the release mechanism has been unclear. We therefore investigated the contribution of ATP-binding cassette transporter C4 (ABCC4), which has been known as a prostanoids efflux transporter, to the release of PGE3, PGF3α, and TXB3.Materials and Methods
ATP-dependent transport of PGE3, PGF3α, and TXB3 via ABCC4 was investigated by using inside-out membrane vesicles prepared from ABCC4-overexpressing HEK293 cells. To evaluate the contribution of ABCC4 to the release of PGE3, PGF3α, and TXB3, we measured the extracellular and intracellular levels of PGE3, PGF3α, and TXB3 in A549 cells when we used ABCC4 inhibitors (dipyridamole, MK571, and probenecid) or ABCC4 siRNAs. The quantification of PGE3, PGF3α, and TXB3 was performed by using liquid chromatography-tandem mass spectrometry.Results
The apparent Km values for ABCC4-mediated transport were 2.9±0.1 µM for PGE3, 12.1±1.3 µM for PGF3α, and 11.9±1.4 µM for TXB3 and the ATP-dependent accumulation of PGE3, PGF3α, and TXB3 into vesicles was decreased by using typical substrates and inhibitors of ABCC4. ABCC4 inhibitors and ABCC4 knockdown showed the reduction of extracellular/intracellular ratio of PGE3 (40–60% of control) and PGF3α (60–80% of control) in A549 cells.Conclusions
Our results suggest that PGE3, PGF3α, and TXB3 are substrates of ABCC4 and ABCC4 partially contributes to the release of PGE3 and PGF3α. 相似文献18.
Wu Ruifang Wang Zhenhai Lu Lichang Zhang Fenger Ge Xinglin 《Prostaglandins & other lipid mediators》1996,51(2):161-167
Pelvic congestion may cause chronic pelvic pain in women. The aim of the study is to elucidate a possible role in this condition for prostaglandin. Prostaglandin levels in peritoneal fluid were measured in 18 women with pelvic pain caused by pelvic congestion following sterilization, 10 women without pain following sterilization, and 10 normal healthy women. Peritoneal fluid was aspirated by a silastic catheter from the cul-de-sac under laparoscopic direct vision. Concentration of 6-keto-PGF1α, TXB2, PGF2α and PGE2 were measured with the standard radioimmunoassay method in all samples. Results showed that 6-keto-PGF,. levels in peritoneal fluid from patients with pelvic congestion were markedly higher than those from two control women (P < 0.05); 6-keto-PGF1α/TXB2 in pelvic congestion and control groups were markedly different (P < 0.05); the total amounts of peritoneal fluid was higher in pelvic congestion than that in two control groups (P < 0.001). These data suggested that 6-ketoPGF1α is increased in peritoneal fluid of women with pelvic congestion and the change might play an important role in attack of this disease. 相似文献
19.
A.M. Franchi M. Chaud E.T. Gonzalez M.A.F. Gimeno A.L. Gimeno 《Prostaglandins & other lipid mediators》1988,35(2)
Spontaneous changes in isometric developed tension (IDT) as a function of time after isolation (contractile constancy) in uteri from control-castrated and castrated chronic streptozotocin-diabetic rats, were explored. The effects of injecting 17-beta estradiol (E0) were also studied. No differences in the minor changes of contractile constancy, between control and diabetic preparations, during a period of 60 min, were detected, whereas uteri from non-diabetic EO injected animals (0.5+1.0 ug, prior to sacrifice), exhibited a profound reduction of IDT, significantly greater than in tissues obtained from E0 injected-diabetic rats. Moreover, basal generation and outputs into the suspending solution of prostaglandins (PGs) E1, E2 and F2α, were explored in the same groups, at 60 min following tissue isolation. The basal outputs of these three PGs were similar in castrated control rats, but preparations from castrated-diabetics released significantly more PGE1. The administration of E0 to castrated-diabetics, failed to alter the releases of the three PGs explored. In addition, the metabolism of labelled arachidonic acid (AA) into different prostanoids (6-keto-PGF1, PGF2, PGE2 and thromboxane B2-TXB2), was also investigated. The non-diabetic spayed rat uterus converted AA into these four prostanoids, the transformation into 6-keto-PGF1α (as an index of PGI2 formation) being the most prominent. In preparations from diabetic rats the formation) being the most prominent. In preparations from diabetic rats the formation of 6-keto-PGF1α, PGF2α and PGE2, was significantly smaller than in controls, whereas a greater % of TXB2 formation (as an index of TXA2), was detected. On the other hand uterine preparations from non-diabetic spayed rats injected with E0 formed less 6-
amounts of PGF2α or of TXB2 from AA, than E0 injected controls, whereas uteri from castrated diabetic animals injected with E0, formed a similar % of 6-keto-PGF1α, PGF2α and PGE2 from AA, than tissue preparations from non-estrogenized controls. However, the enhanced transformation of the labelled fatty acid precursor (AA) into TXB2 in the diabetic group, was significantly reduced by the steroid. The role of the augmented generation and release of PGE1 in uteri from diabetic rats is discussed in terms of precedents indicating the relevance of PGs type E supporting rat uterine motility. In addition the influence of E0 is attractive, because its reducing effect on TX production, in diabetes, a disease known to be accompanied by enhanced synthesis of vasoconstrictor and platelet aggregation TXA2, and by frequent obstructive circulatory problems. 相似文献
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20.
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