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At least 19 recordsLinked to original sources
PubMed1981

Structural features of PGBX (a prostaglandin polymer) deduced by analogies with dimers derived from 15-keto-prostaglandin B.

The polymeric prostaglandin, PGBX, has a beneficial effect on oxidative phosphorylation of damaged mitochondria in vitro and has manifested interesting effects in vivo. Its chemical structure has been partially elucidated by comparison of its 13C-NMR (nuclear magnetic resonance) spectrum with the spectra of prostaglandin monomers. Reported here is subsequent comparison of PGBX with two prostaglandin dimers derived from 15-keto-PGB1, which provide more complete structural information. The two prostaglandin dimers were synthesized and analyzed by 13C-MNR and by other techniques, with particular attention to positions of linkages between the two monomeric prostaglandin subunits of the dimers. Based on these data, some proposals are presented regarding probable locations of linkages between prostaglandin monomeric subunits in the polymeric PGBX.

Magnetic Resonance Spectroscopy↗
PubMed1989

Cerebral ischemia in gerbils: improvement of survival after postischemic treatment with oligo-prostaglandin B.

Gerbils were subjected to bilateral carotid artery occlusion for either 15 or 20 min. After ischemia the animals were injected i.p. with oligo-prostaglandin B (oligo-PGB; trimer of 16,16'-dimethyl-15-dehydro-prostaglandin B1) dissolved in 4% sodium-bicarbonate, or with the vehicle. The dosing regimen of oligo-PGB was 0.5, 1, 2, 5, 10 mg/kg injected 5 min postischemia, or 1 mg/kg injected 30, 60, 90, 120 min after ischemia, or 10 mg/kg injected 5 min and 24 h postischemia. Behaviour of the animals and their mortality were studied for 14 days after ischemia. Administration of the drug did not affect recovery of the electrical activity in the brain and did not reduce the number of postischemic seizures. Following 15 min ischemia, administration of oligo-PGB resulted in statistically valid improvement of survival (P less than 0.04 or better) in all treatment groups. After 20 min ischemia only the double injection (10 mg/kg at 5 min and 24 h postischemia) resulted in a substantial survival improvement (64%, P less than 0.005). The mechanism of the drug action is unknown but, based on the available data, the authors believe it to be related to the modification of arachidonic acid metabolism in the late postischemic period.

Animals↗
PubMed1981

Distribution of prostaglandins B, E and F series in plasma of cancer patients.

Plasma prostaglandins (PGs) of normal individuals and cancer patients have been examined. With the exception of a breast carcinoma patient, all patients demonstrated significant elevations in PGE levels. Lung cancer patients showed a significant decrease in PGF, while stomach cancer patients showed a marked decrease in PGB. It is suggested that the changes in PGs may play a significant role in host-tumor metabolism.

Humans↗
PubMed2000

Prostaglandin B(2) delivers a co-stimulatory signal leading to T cell activation.

Most of the data accumulated to date on the immunoregulatory effects of prostaglandins (PG) on T cell activation stem from the archetypal inhibitory effect of PGE(2). In this study we provide instead, the first evidence that exogenous PGB(2), a catabolic metabolite of PGE(2), synergizes with signals delivered by T cell receptor (TCR) engagement to induce interleukin-2 (IL-2) production and IL-2 receptor (IL-2R) alpha-expression in Jurkat cells. Accordingly, PGB(2) enhances the proliferation of anti-CD3-activated peripheral blood lymphocytes (PBL). In terms of cellular signaling, we present evidence that PGB(2) activates tyrosine kinase activities and efficiently increases c-fos mRNA expression and nuclear factor-kappa B (NF-kappa B) translocation to the nucleus. Owing to these features, PGB(2) appears as a new lipid mediator capable of delivering an ancillary signal leading to T lymphocyte activation.

Antigens, CD↗
PubMed1977

Utilization of cyclodextrin complexation for separation of E, A, and B prostaglandins by ion-exchange liquid chromatography.

Application of cyclodextrin complexation to the separation of E-, A-, and B-type prostaglandins by ion-exchange liquid chromatography is demonstrated. The addition of alpha-or beta-cyclodextrin into the mobile phase on an anion-exchange support decreased the retention times of the prostaglandins significantly because of soluble complex formation. Chromatographic separation behavior is discussed on the basis of the stability of the inclusion complex. A rapid and sensitive method for the separation and quantification of the prostaglandins, using beta-cyclodextrin in the mobile phase, is described.

Chemical Phenomena↗
PubMed2000

Estrus synchronization and pregnancy rates in beef cattle given CIDR-B, prostaglandin and estradiol, or GnRH.

Two experiments were conducted to determine estrous response and pregnancy rate in beef cattle given a controlled internal drug release (CIDR-B) device plus prostaglandin F2 alpha (PGF) at CIDR-B removal, and estradiol or gonadotropin releasing hormone (GnRH). In Experiment I, crossbred beef heifers received a CIDR-B device and 1 mg estradiol benzoate (EB), plus 100 mg progesterone (E + P group; n = 41), 100 micrograms gonadotropin releasing hormone (GnRH group; n = 42), or no further treatment (Control group; n = 42), on Day 0. On Day 7, CIDR-B devices were removed and heifers were treated with PGF. Heifers in the E + P group were given 1 mg EB, 24 h after PGF, and then inseminated 30 h later. Heifers in the GnRH group were given 100 micrograms GnRH, 54 h after PGF, and concurrently inseminated. Control heifers were inseminated 12 h after onset of estrus. The estrous rate was lower (P < 0.01) in the GnRH group (55%) than in either the E + P (100%) or Control (83%) groups. The mean interval from CIDR-B removal to estrus was shorter (P < 0.01) and less variable (P < 0.01) in the E + P group than in the GnRH or Control groups. Pregnancy rate in the E + P group (76%) was higher (P < 0.01) than in the GnRH (48%) or Control (38%) groups. In Experiment II, 84 cows were treated similarly to the E + P group in Experiment I. Cows received 100 mg progesterone and either 1 mg EB or 5 mg estradiol-17 beta (E-17 beta) on Day 0 and either 1 mg of EB or 1 mg of E-17 beta on Day 8 (24 h after CIDR-B removal), in a 2 x 2 factorial design, and were inseminated 30 h later. There were no differences among groups for estrous rates or conception rates. The mean interval from CIDR-B removal to estrus was 44.2 h, s = 11.2. Conception rates were 67%, 62%, 52%, and 71% in Groups E-17 beta/E-17 beta, E-17 beta/EB, EB/E-17 beta, and EB/EB, respectively. In cattle given a CIDR-B device and estradiol plus progesterone, treatment with either EB or E-17 beta effectively synchronized estrus and resulted in acceptable conception rates to fixed-time artificial insemination.

Animals↗
PubMed1981

Effect of prostaglandins on phosphorylase b.

Prostaglandins at mM concentration are able to induce a small activation to rabbit muscle glycogen phosphorylase b (1,4-alpha-D-glucan: orthophosphate alpha-D-glucosyltransferase, EC 2.4.1.1) in the absence of AMP. The extent of this activation depends on the nature of the molecular structure of prostaglandins. Saturated and unsaturated higher fatty acids were unable to substitute for prostaglandins. The main findings of our studies can be summarized as follows: (1) Prostaglandins inhibit the AMP-induced activation of phosphorylase b. (2) Modification of the AMP binding site with 2,3-butanedione could not inhibit the activity induced by prostaglandins. (3) Enzyme activation by prostaglandins is stimulated by spermine. (4) Phosphorylase b activation by prostaglandins and the observed stimulation of this activation by spermine were found to be temperature dependent. (5) Prostaglandins affect the quaternary structure of phosphorylase b inducing a partial enzyme tetramerization which is enhanced in the presence of spermine. The extent of this tetramerization is temperature dependent.

Adenosine Monophosphate↗
PubMed1984

[A method for determination of prostaglandins in human seminal fluid].

Human seminal fluid has been shown to contain mainly eleven different prostaglandins. Methods for quantitative determination of prostaglandin E and 19-OH prostaglandin E are described. The methods include extraction with acetone and alkali treatment. After alkali treatment prostaglandin E was transformed to prostaglandin B, and 19-OH prostaglandin E to 19-OH prostaglandin B. Prostaglandins were separated by using Lipidex column chromatography and silicic acid column chromatography. Prostaglandin B was quantitated by gas chromatography using C24 fatty acid methyl ester as internal standard. 19-OH prostaglandin B was quantitated by measuring ultraviolet photoabsorbance at 278 nm.

Alprostadil↗
PubMed1988

[Chemical synthesis of tritium-labeled prostaglandins A, B and F].

Formation of prostaglandins A, B and F from prostaglandin E has been studied. Synthesis of tritium-labelled prostaglandins A1, A2, B1, B2, F1 alpha, F2 alpha, F1 beta, F2 beta of high molar radioactivity from highly labelled PGE1 and PGE2 is described.

Chemical Phenomena↗
PubMed1996

Bovine luteal cell production in vitro of prostaglandin E2, oxytocin and progesterone in response to pregnancy-specific protein B and prostaglandin F2 alpha.

A study was conducted to determine the effects of pregnancy-specific protein B (PSPB) and prostaglandin F2 alpha (PGF2 alpha) on bovine luteal cell progesterone, prostaglandin E2 (PGE2) and oxytocin production in vitro. Corpora lutea were enucleated from multiparous cows with normal oestrous cycles during the mid-luteal (days 10-12; n = 5) or late-luteal (days 17-18; n = 5) stage. Mixed large and small cells (1.5 x 10(5) cells per well) were incubated in 500 microliters modified Ham's F-12 medium. Cells were incubated for 18 h before treatments were added. Cells were treated with PSPB (0, 2.5, 5.0 micrograms) and PGF2 alpha (0, 100, 200 ng) in a 3 x 3 factorial arrangement. After treatments were added, media samples were collected at 6 and 12 h. During the 18 h pretreatment incubation, progesterone, PGE2 and oxytocin production was similar between the prospective treatment groups. Progesterone production was greater (P < 0.001) by mid-stage than by late-stage cells. In addition, progesterone decreased (P < 0.001) as incubation time increased. Progesterone production was not affected by PGF2 alpha, but PSPB increased (P < 0.02) progesterone at the 5.0 micrograms dose. Late-stage luteal cells produced more (P < 0.001) PGE2 than did mid-stage cells; PGE2 production decreased (P < 0.001) with increased incubation time. Luteal PGE2 production increased in response to PSPB treatment (P < 0.01) and PGF2 alpha treatment (P < 0.001). Luteal oxytocin production was greater (P < 0.01) by mid-stage compared with late-stage cells. Oxytocin production decreased (P < 0.001) with incubation time in mid-stage cells, but in late-stage cells oxytocin production was similar over time. Neither PSPB nor PGF2 alpha had an effect on oxytocin. These results indicate that PSPB does not affect luteal oxytocin, but does increase progesterone and PGE2 production. In addition, PGF2 alpha increases luteal PGE2, but does not affect progesterone or oxytocin production. These data do not show an interaction between PSPB and PGF2 alpha in regulating bovine luteal cell endocrine function.

Animals↗