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1.
Glycerol, injected into a site between the femoral vessels of the rat, induced neovascularization, both from the preexisting microcirculation and from the side of the femoral vein facing the artery-vein interstitium where the glycerol was administered. The use of glycerol together with a known angiogenic substance (PGE2) did not modify the neocapillary density (NCD) obtained with glycerol alone. In contrast, the lower level of NCD achieved with an acylglycerol (triacetylglycerol) was increased when the latter was associated with PGE2. Values reached were similar to, but never higher than, those for glycerol alone, or combined with PGE2. The results suggest that glycerol and some substances containing glycerol, amongst which 1-butyrylglycerol has been previously considered1, may stimulate angiogenesis by a direct or indirect mechanism of action.  相似文献   

2.
Summary The stimulatory effect of PGE1 on different functions of isolated guinea-pig hearts (Langendorff method, Tyrode solution) was coupled with an increase in the rate of45Ca uptake from the perfusion medium. The total myocardial Ca content and the amount of exchangeable cellular Ca were not affected. This action of PGE1 on the myocardial Ca metabolism seems to be related to the positive inotropic action of PGE1 and can most probably be explained by an increase in the membrane permeability to Ca ions (similar to the action of epinephrine).  相似文献   

3.
Summary In the longitudinal smooth muscle of guinea-pig stomach, verapamil (10–5 M) which showed marked suppression of high K-induced contractures, did not suppress the contractile response to PGE1 (1.5×10–9 to 10–6 M) markedly. These results suggest that the contractile mechanism of PGE1 in guinea-pig stomach may mainly depend on a release of bound Ca in the cell and partly depend on a Ca influx from the extracellular origin.  相似文献   

4.
Identifying the small molecules that permit precise regulation of embryonic stem (ES) cell proliferation should further support our understanding of the underlying molecular mechanisms of self renewal. In the present study, we showed that PGE2 increased [3H]-thymidine incorporation in a time and dose dependent manner. In addition, PGE2 increased the expression of cell cycle regulatory proteins, the percentage of cells in S phase and the total number of cells. PGE2 obviously increased E-type prostaglandin (EP) receptor 1 mRNA expression level compare to 2, 3, 4 subtypes. EP1 antagonist also blocked PGE2-induced cell cycle regulatory protein expression and thymidine incorporation. PGE2 caused phosphorylation of protine kinase C, Src, epidermal growth factor (EGF) receptor, phosphatidylinositol 3-kinase (PI3K)/Akt phosphorylation, and p44/42 mitogen-activated protein kinase (MAPK), which were blocked by each inhibitors. In conclusion, PGE2-stimulated proliferation is mediated by MAPK via EP1 receptor-dependent PKC and EGF receptor-dependent PI3K/Akt signaling pathways in mouse ES cells. Received 30 January 2009; received after revision 03 March 2009; accepted 10 March 2009  相似文献   

5.
Summary PGE2 (10–7 M) caused increased cAMP accumulation in 5 pheochromocytomas, while in 3 human adrenal medullae PGE2 caused a significant decrease of cAMP level on incubating slices in vitro. This finding is discussed in relation to the opposite effect of PGE2 on catecholamine release from human medulla and pheochromocytoma slices in vitro.Acknowledgment. This paper is part of a Ph. D. thesis of Punya Boonyaviroj.Established Investigator of the Chief Scientist's Bureau, Israeli Ministry of Health.  相似文献   

6.
Accumulation of eosinophils in tissue is a hallmark of allergic inflammation. Here we observed that a selective agonist of the PGE2 receptor EP4, ONO AE1-329, potently attenuated the chemotaxis of human peripheral blood eosinophils, upregulation of the adhesion molecule CD11b and the production of reactive oxygen species. These effects were accompanied by the inhibition of cytoskeletal rearrangement and Ca2+ mobilization. The involvement of the EP4 receptor was substantiated by a selective EP4 antagonist, which reversed the inhibitory effects of PGE2 and the EP4 agonist. Selective kinase inhibitors revealed that the inhibitory effect of EP4 stimulation on eosinophil migration depended upon activation of PI 3-kinase and PKC, but not cAMP. Finally, we found that EP4 receptors are expressed by human eosinophils, and are also present on infiltrating leukocytes in inflamed human nasal mucosa. These data indicate that EP4 agonists might be a novel therapeutic option in eosinophilic diseases.  相似文献   

7.
Summary Prostaglandin-(PG) 1,15-lactones and, in smaller amounts, free acids, were isolated from both the mantle and the dorso-lateral appendices of the opisthobranch molluscTethys fimbria. In vivo conversion of PGs into the corresponding lactones and accumulation of PGE2- and PGE3-1,15-lactones in the appendages were shown. The detachment of these appendages from the molested mollusc caused the in vivo conversion of PGE2- and PGE3-lactones back to PGE2 and PGE3 respectively, thus providing the first example of a mechanism by which prostaglandins can be stored and, when needed, released.  相似文献   

8.
Zusammenfassung Die Prostaglandine E1 (PGE1) und E2 (PGE2) haben keinen Einfluss auf die Gerinnung von Rattenblut. Im Gegensatz zu früheren Postulationen können die Ca-Ionen im Plasma nicht von PGE1 ersetzt werden. PGE1 beeinflusst die maximale Amplitude des Thrombelastogramms in vitro nach Zugabe von 0.3–6 g/ml, während PGE2 diesen Effekt nicht aufweist.  相似文献   

9.
Zusammenfassung Die Wirkung des Dinatrium-EDTA auf die Kreislaufreaktionen des Prostaglandin E1 (PGE1) wurde an narkotisierten Hunden untersucht. Das Ausmass der positiv chronotropen und inotropen Einflüsse des PGE1 war während der Infusion von EDTA bedeutend geringer als das des PGE1 vor der EDTA-Gabe. Die Gegenwart oder das Einströmen von Kalziumionen scheint in der pharmakologischen Wirkung des PGE1 eine Rolle zu spielen.  相似文献   

10.
Summary Human polymorphonuclear leukocytes were found to be able to synthetize and release substantial amounts of PGE2, when stimulated by a phagocytic stimulus such as zymosan particles coated with complement. Hydrocortisone, at a concentration of 10–5 M, which proved to be effective in other biological systems, failed to inhibit phagocytosis and PG release.  相似文献   

11.
Summary PGE1 potentiated, while diclofenac, a prostaglandin synthesis inhibitor, antagonized hexobarbitone hypnosis in rats. PGE1-induced potentiation of hexobarbitone sleep was inhibited by a 5HT synthesis inhibitor and by a 5HT receptor blocker, suggesting that this potentiation is 5HT mediated.Acknowledgment. The gift of the following drugs are gratefully acknowledged: PGE1 (Dr.J. E. Pike, Upjohn), diclofenac (Ciba-Geigy), methysergide (Sandoz) and hexobarbitone (Bayer).  相似文献   

12.
Summary PGE1 increases cholesterolemia without lipemia modifications. In bile there are not modifications in cholesterol levels and total lipids appear diminished. PGE2 raise the lipemia and have no effect in cholesterolemia, moreover bile cholesterol and total lipids exhibit no changes. Both PGE1 and PGE2 decreased the bile volume.Acknowledgment. The authors wish to express their thanks to the Upjohn Laboratory for kindly furnishing the prostaglandins employed, with the relevant bibliography, and to Mr.F. A. Mori for the English translation.  相似文献   

13.
Résumé Les effets de la PGE1 ont été étudiés sur les bandelettes ventriculaires isoleés de la grenouille. La PGE1 augmente la force de contraction de ces préparations. Le propranolol antagonise significantivement les effets de la noradrenaline sans altérer les réponses à la PGE1. Un bloqueur des récepteurs -adrenergiques, la phénoxybenzamine n'inhibe pas les effets induits par la PGE1 ou les catécholamines. L'inhibition de la pompe à sodium par l'ouabaine ne modifie pas la réponse du tissu à la PGE1.

We should like to thank Prof.D. A. van Dorp (Unilever Research Vlaardingen) for supplying PGE1.  相似文献   

14.
Summary The erythropoietic effects in exhypoxic polycythemic mice of two endoperoxide analogs were assessed and compared with PGE2. The 9a, 11a epoxymethano analog (U-44069) was found to be a much more potent erythropoietic stimulus than the 11a,9a analog (U-46619) or PGE2.This work was supported by a Senior Research Grant-in-Aid from the American Heart Association-Louisiana (DMG) and USPHS Grant No. AM 13211 (JWF).  相似文献   

15.
Summary PGE1 but not PGF2 at 500–1000 g/kg induced a slow and sparse flow from the parotid and no flow at all from submaxillary glands. Composition of PGE1-induced parotid saliva was quite different from that evoked by any autonomic agonists. The present study suggests that PGE1 might act directly on parotid acinar cells.Acknowledgment. This work was supported by NIDR grant DE05633. The authors wish to thank Ms Sonya Wynn for her technical assistance.  相似文献   

16.
Summary The PGE2-induced cyclic AMP accumulation in the rat anterior pituitary in vitro is inhibited by [desamino1]-, [desamino1] [descarboxy14] and [d-Lys4]-somatostatin similarly to somatostatin, while the [descarboxy14]-somatostatin exhibits reduced activity; [d-Lys9]-somatostatin is ineffective at a higher concentration.The authors acknowledge the technical assistance ofG. Alexander. F. Bellini, D. Mangerel andJ. Rochon and thank Dr.G. Schilling and his associates for the analytical data.  相似文献   

17.
Human lymphocyte melatonin, through membrane and nuclear receptors binding, acts as an activator in IL-2 production. Antagonism of membrane melatonin receptors using luzindole exacerbates the drop of the IL-2 production induced by PGE2 in peripheral blood mononuclear and Jurkat cells. This paper studies the melatonin membrane and nuclear receptors interplay in PGE2-diminished IL-2 production. The decrease in IL-2 production after PGE2 and/or luzindole administration correlated with downregulation in the nuclear receptor RORα. We also highlighted a role of cAMP in the pathway, because forskolin mimicked the effects of luzindole and/or PGE2 in the RORα expression. Finally, a significant RORα downregulation was observed in T cells permanently transfected with inducible MT1 antisense. In conclusion, we show a novel connection between melatonin membrane receptor signalling and RORα expression, opening a new way to understand melatonin regulation in lymphocyte physiology. Received 23 September 2008; received after revision 19 November 2008; accepted 21 November 2008  相似文献   

18.
Zusammenfassung «Narcotic analgesics» und einzelne «narcotic antagonists» hemmen am isolierten Meerschweinchen-Jejunum durch PGE1 ausgelöste Kontraktionen. Die PGE1-antagonistische Wirkung der «narcotic analgesics» kann durch echte «narcotic antagonists» aufgehoben werden.  相似文献   

19.
Summary We investigated whether hypothalamic prostaglandin E2 (PGE2) and corticotropin releasing factor (CRF) are responsible for the development of the adrenocorticotropic hormone (ACTH) response induced by interleukin-1 (IL-1). The present results show that ACTH responses induced by intravenous injection of IL-1 were suppressed by systemic pretreatment with indomethacin and that intrahypothalamic injection of PGE2 stimulates the secretion of ACTH. Furthermore, systemic pretreatment with anti-CRF antibody significantly suppressed the ACTH response induced by intrahypothalamic injection of PGE2. These data suggest that the ACTH response induced by IL-1 is mediated by CRF secretion stimulated by hypothalamic PGE2.  相似文献   

20.
Summary In medium supplemented with serum, PGE1 and PGE2 were equally potent in inducing cells with a fenestrated appearance, whereas PGF2 was comparatively ineffective. In BSA without serum the effects were more persistent and characterized by a high proportion of astrocyte-like cells. The effects were reversed upon removal of the prostaglandins.This work was supported by the National Health and Medical Research Council of Australia.  相似文献   

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