Base de dados : MEDLINE
Pesquisa : D12.644.400.575.281.381.500 [Categoria DeCS]
Referências encontradas : 293 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 30 ir para página                         

  1 / 293 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
[PMID]:22100847
[Au] Autor:Krazinski BE; Koziorowski M; Brzuzan P; Okrasa S
[Ad] Endereço:Department of Animal Physiology, University of Warmia and Mazury in Olsztyn, Olsztyn-Kortowo, Poland.
[Ti] Título:The expression of genes encoding opioid precursors and the influence of opioid receptor agonists on steroidogenesis in porcine adrenocortical cells in vitro.
[So] Source:J Physiol Pharmacol;62(4):461-8, 2011 Aug.
[Is] ISSN:1899-1505
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:Endogenous opioid peptides are involved in the regulation of the HPA-axis function and stress response mechanism. However, there is a scarcity of data on opioid involvement in the regulation of the adrenocortical endocrine function. This study was performed to: 1) establish the expression of proenkephalin, POMC and prodynorphin genes in the porcine adrenal cortex and test in vitro the influence of ACTH, angiotensin II, CRH and epinephrine on this expression, and 2) determine the effects of opioid receptor agonists on basal and ACTH- or angiotensin II-affected secretion of cortisol, aldosterone and progesterone by the cultured adrenocortical cells. Our experiment has demonstrated the presence of mRNAs for opioid precursors in cells isolated from the adrenal cortex and the significant effects of ACTH and angiotensin II, but not CRH or epinephrine, on adrenocortical transcription of the analyzed genes. Angiotensin II reduced the expression of the POMC gene but stimulated that of prodynorphin. In turn, ACTH decreased the transcription of prodynorphin. The study has also demonstrated the effects of selective opioid receptor agonists - DPLPE (delta), FK33-824 (mu) and U50,488 (kappa) - on adrenal steroidogenesis in pigs. Basal secretion of cortisol was enhanced after the activation of mu or kappa receptors, whereas ACTH-stimulated cortisol output was increased only by the mu receptor agonist. Angiotensin II-treated cells significantly decreased aldosterone secretion in the presence of the kappa receptor agonist. The present results suggest that opioid peptides are synthesized in the porcine adrenal cortex, indicating their involvement in the regulation of adrenal steroidogenesis through autocrine and/or paracrine interactions.
[Mh] Termos MeSH primário: Córtex Suprarrenal/efeitos dos fármacos
Expressão Gênica
Peptídeos Opioides/genética
Receptores Opioides/agonistas
Esteroides/biossíntese
[Mh] Termos MeSH secundário: (trans)-Isômero de 3,4-Dicloro-N-metil-N-(2-(1-pirrolidinil)-ciclo-hexil)-benzenoacetamida/farmacologia
Córtex Suprarrenal/citologia
Córtex Suprarrenal/metabolismo
Aldosterona/biossíntese
Aldosterona/secreção
Animais
Técnicas de Cultura de Células
Células Cultivadas
D-Ala(2),MePhe(4),Met(0)-ol-encefalina/farmacologia
D-Penicilina (2,5)-Encefalina/farmacologia
Expressão Gênica/efeitos dos fármacos
Hidrocortisona/biossíntese
Hidrocortisona/secreção
Sistema Hipotálamo-Hipofisário/efeitos dos fármacos
Sistema Hipotálamo-Hipofisário/metabolismo
Sistema Hipófise-Suprarrenal/efeitos dos fármacos
Sistema Hipófise-Suprarrenal/metabolismo
Progesterona/biossíntese
Progesterona/secreção
Reação em Cadeia da Polimerase em Tempo Real
Suínos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Opioid Peptides); 0 (Receptors, Opioid); 0 (Steroids); 4964P6T9RB (Aldosterone); 4G7DS2Q64Y (Progesterone); 64854-64-4 (D-Ala(2),MePhe(4),Met(0)-ol-enkephalin); 67198-13-4 (3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer); 88373-73-3 (Enkephalin, D-Penicillamine (2,5)-); WI4X0X7BPJ (Hydrocortisone)
[Em] Mês de entrada:1205
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:111122
[St] Status:MEDLINE


  2 / 293 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:16310101
[Au] Autor:Kaminski T
[Ad] Endereço:Department of Animal Physiology, Faculty of Biology, University of Warmia and Mazury in Olsztyn, Oczapowski Street 1A, Olsztyn-Kortowo 10-719, Poland. tkam@uwm.edu.pl
[Ti] Título:The involvement of protein kinases in signalling of opioid agonist FK 33-824 in porcine granulosa cells.
[So] Source:Anim Reprod Sci;91(1-2):107-22, 2006 Jan.
[Is] ISSN:0378-4320
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:It is known that acute action of mu opioid receptor agonist, FK 33-824, results in an inhibition of oestradiol (E2) secretion by porcine granulosa cells from large follicles, but the opioid mode of action is unknown. In the present study, the involvement of two signal transduction pathways, phospholipase C/protein kinase C and adenylyl cyclase/protein kinase A, in mechanism of the opioid action was investigated. Treatment of pig granulosa cells with FK 33-824 at the dose 1 nM suppressed E2 secretion. Protein kinase C (PKC) inhibitors - staurosporine (1-100 nM), d-sphingosine (10-500 nM) and PKCi (100-2000 nM) - both alone and in combination with FK 33-824 reduced E2 release from the cells in relation to the control group. The inhibitory effect of the opioid on E2 output was also observed in PKC-deficient granulosa cells. PKC activator, PMA (10 and 100 nM) significantly attenuated the inhibitory effect of the opioid agonist. FK 33-824 also inhibited 3[H]phorbol 12,13 dibutyrate (3[H]PDBu) specific binding by granulosa cells. Adenylyl cyclase (AC) engagement in opioid signal transduction was assayed after 2-h and 4-h incubations of granulosa cells. During 2-h incubation, FK 33-824 at the dose 1 nM decreased cAMP secretion. Prolongation of the incubation up to 4 h caused disappearance of the opioid action. The addition of protein kinase A (PKC) inhibitor, PKAi (100-2000 nM), alone or together with FK 33-824, was followed by an inhibition of E2 secretion. FK 33-824 with the highest dose of PKAi (2000 nM) significantly inhibited E2 secretion by the cells in comparison to these agents tested separately. The opioid added in combination with PKA activator, 8BrcAMP (1000 microM), caused attenuation of stimulatory effect of 8BrcAMP. Collectively, these results suggest that acute action of mu opioid agonist on porcine granulosa cells leads to decrease of enzymatic activity of PKC and AC/PKA. It is not ruled out that other signal transduction pathways - not considered in this study - may also be engaged in the opioid mechanism of action in these cells.
[Mh] Termos MeSH primário: D-Ala(2),MePhe(4),Met(0)-ol-encefalina/farmacologia
Estradiol/secreção
Células da Granulosa/metabolismo
Proteínas Quinases/metabolismo
Receptores Opioides mu/agonistas
Transdução de Sinais
[Mh] Termos MeSH secundário: Adenilil Ciclases/metabolismo
Animais
Proteínas Quinases Dependentes de AMP Cíclico/antagonistas & inibidores
Proteínas Quinases Dependentes de AMP Cíclico/metabolismo
Relação Dose-Resposta a Droga
Sinergismo Farmacológico
Feminino
Células da Granulosa/efeitos dos fármacos
Células da Granulosa/enzimologia
Proteína Quinase C/antagonistas & inibidores
Proteína Quinase C/metabolismo
Inibidores de Proteínas Quinases/farmacologia
Suínos
Fosfolipases Tipo C/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Protein Kinase Inhibitors); 0 (Receptors, Opioid, mu); 4TI98Z838E (Estradiol); 64854-64-4 (D-Ala(2),MePhe(4),Met(0)-ol-enkephalin); EC 2.7.- (Protein Kinases); EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases); EC 2.7.11.13 (Protein Kinase C); EC 3.1.4.- (Type C Phospholipases); EC 4.6.1.1 (Adenylyl Cyclases)
[Em] Mês de entrada:0606
[Cu] Atualização por classe:151119
[Lr] Data última revisão:
151119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:051129
[St] Status:MEDLINE


  3 / 293 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:15519041
[Au] Autor:Kaminski T
[Ad] Endereço:Department of Animal Physiology, University of Warmia and Mazury in Olsztyn, 10-719 Olsztyn-Kortowo 1A, Poland. tkam@uwm.edu.pl
[Ti] Título:The response of phospholipase C/protein kinase C and adenylyl cyclase/protein kinase A pathways in porcine theca interna cells to opioid agonist FK 33-824.
[So] Source:Domest Anim Endocrinol;27(4):379-96, 2004 Nov.
[Is] ISSN:0739-7240
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Opioids were found as factors affecting porcine ovarian steroidogenesis. The mechanism of opioid action, however, on porcine theca interna cells is completely unknown. Therefore, the present study was designed to investigate the possible involvement of two intracellular pathways, phospholipase C/protein kinase C and adenylyl cyclase/protein kinase A, in opioid signal transduction in porcine theca cells treated with mu opioid receptor agonist, FK 33-824. Incubation of the cells for 4 h with FK 33-824 at the dose 1 nM resulted in decreases in inositol phosphate accumulation as well as androstenedione (A(4)), testosterone (T), and estradiol (E(2)) secretions. Protein kinase C (PKC) inhibitors, staurosporine (1-100 nM), D-sphingosine (10-500 nM), and PKCi (100-2000 nM), both added alone and together with the opioid agonist, depressed release of the steroid hormones. PKC activator, phorbol ester (PMA, 1-100 nM), used alone was without effect on theca cell steroidogenesis, but added in combination with FK 33-824 abolished inhibitory influence of the opioid on A(4), T, and E(2) output. The steroid hormone secretion by PKC-deficient theca cells was inhibited by the opioid agonist. FK 33-824 also suppressed PKC activity reducing [(3)H]PDBu specific binding to theca cells, whereas ionomycin (a positive control) increased labeled phorbol ester binding to the cells. In the next experiment, cAMP release from theca cells during 2 and 4 h incubations with FK 33-824 (1-100 nM), naloxone (10 microM; opioid receptor antagonist), and LH (100 ng/mL; a positive control) was examined. FK 33-824 at the dose 1 nM inhibited cAMP secretion during 2 h incubation, but had no effect during longer incubation. LH in a manner independent on incubation time multiplied cAMP release. Protein kinase A inhibitor, PKAi (100-2000 nM), alone and in combination with FK 33-824 (1 nM), inhibited A(4), T, and E(2) secretions by theca cells. PKA activator, 8BrcAMP (10-1000 microM), stimulated the steroid hormone release, but this stimulatory effect was diminished in the presence of FK 33-824. The results allow to suggest that opioid peptides affect porcine theca cell steroidogenesis and their acute action on the cells is connected with the inhibition of phospholipase C/protein kinase C and adenylyl cyclase/protein kinase A signal transduction systems.
[Mh] Termos MeSH primário: D-Ala(2),MePhe(4),Met(0)-ol-encefalina/farmacologia
Enzimas/efeitos dos fármacos
Hormônios Esteroides Gonadais/secreção
Receptores Opioides mu/agonistas
Transdução de Sinais/efeitos dos fármacos
Células Tecais/enzimologia
[Mh] Termos MeSH secundário: Adenilil Ciclases/efeitos dos fármacos
Adenilil Ciclases/metabolismo
Análise de Variância
Androstenodiona/secreção
Animais
Proteínas Quinases Dependentes de AMP Cíclico/efeitos dos fármacos
Proteínas Quinases Dependentes de AMP Cíclico/metabolismo
Inibidores Enzimáticos/farmacologia
Enzimas/metabolismo
Estradiol/secreção
Feminino
Hormônio Luteinizante/fisiologia
Naloxona/farmacologia
Antagonistas de Entorpecentes/farmacologia
Proteína Quinase C/efeitos dos fármacos
Proteína Quinase C/metabolismo
Suínos
Testosterona/secreção
Células Tecais/citologia
Células Tecais/efeitos dos fármacos
Células Tecais/secreção
Fosfolipases Tipo C/efeitos dos fármacos
Fosfolipases Tipo C/metabolismo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Enzyme Inhibitors); 0 (Enzymes); 0 (Gonadal Steroid Hormones); 0 (Narcotic Antagonists); 0 (Receptors, Opioid, mu); 36B82AMQ7N (Naloxone); 3XMK78S47O (Testosterone); 409J2J96VR (Androstenedione); 4TI98Z838E (Estradiol); 64854-64-4 (D-Ala(2),MePhe(4),Met(0)-ol-enkephalin); 9002-67-9 (Luteinizing Hormone); EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases); EC 2.7.11.13 (Protein Kinase C); EC 3.1.4.- (Type C Phospholipases); EC 4.6.1.1 (Adenylyl Cyclases)
[Em] Mês de entrada:0501
[Cu] Atualização por classe:151119
[Lr] Data última revisão:
151119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:041103
[St] Status:MEDLINE


  4 / 293 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:15129917
[Au] Autor:Kaminski T; Siawrys C; Bogacka I; Okrasa S; Przala J
[Ad] Endereço:Department of Animal Physiology, Faculty of Biology, University of Warmia and Mazury in Olsztyn, Olsztyn-Kortowo, Poland. tkam@uwm.edu.pl
[Ti] Título:The influence of opioid peptides on steroidogenesis in porcine granulosa cells.
[So] Source:Reprod Domest Anim;39(1):25-32, 2004 Feb.
[Is] ISSN:0936-6768
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:The present studies were undertaken to examine the influence of mu (beta-endorphin, DAMGO, FK 33-824), delta (met-enkephalin, leu-enkephalin, DPLPE) and kappa opioid receptor agonists (dynorphin A, dynorphin B, U 50488) used at different doses (1-1000 nM) alone and in combination with LH (100 ng/ml) on steroidogenesis in porcine granulosa cells derived from large follicles. The effects of mu, delta and kappa receptor agonists on both basal and LH-induced progesterone (P4) secretion were negligible. Agonists of mu opioid receptors reduced basal androstenedione (A4), testosterone (T) and oestradiol (E2) release. Co-treatment with LH entirely abolished the inhibitory effect of these agonists on A4 and E2 secretion and resulted in an increase in T release. The addition of delta receptor agonists was followed by a decrease in basal A4, T and E2 secretion. The cells incubated in the presence of LH increased the androgen production and abrogated the inhibitory effect of delta agonists on E2 output. Basal A4, T and E2 release was also suppressed by kappa receptor agonists. The presence of LH in culture media extended the inhibitory effect of these opioids on E2 output and caused either abolition of the inhibitory influence of kappa agonists or even augmentation of both androgen release in response to the opioids. In conclusion, these data support the involvement of three major types of opioid receptors in the regulation of porcine granulosa cell steroidogenesis.
[Mh] Termos MeSH primário: Peptídeos Opioides/farmacologia
Folículo Ovariano/efeitos dos fármacos
[Mh] Termos MeSH secundário: (trans)-Isômero de 3,4-Dicloro-N-metil-N-(2-(1-pirrolidinil)-ciclo-hexil)-benzenoacetamida/farmacologia
Animais
D-Ala(2),MePhe(4),Met(0)-ol-encefalina/farmacologia
Relação Dose-Resposta a Droga
Dinorfinas/farmacologia
Endorfinas/farmacologia
Ala(2)-MePhe(4)-Gly(5)-Encefalina/farmacologia
D-Penicilina (2,5)-Encefalina/farmacologia
Encefalinas/farmacologia
Feminino
Células da Granulosa/efeitos dos fármacos
Hormônio Luteinizante/farmacologia
Peptídeos Opioides/administração & dosagem
Folículo Ovariano/citologia
Suínos
beta-Endorfina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Endorphins); 0 (Enkephalins); 0 (Opioid Peptides); 100929-53-1 (Enkephalin, Ala(2)-MePhe(4)-Gly(5)-); 60617-12-1 (beta-Endorphin); 64854-64-4 (D-Ala(2),MePhe(4),Met(0)-ol-enkephalin); 67198-13-4 (3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer); 74913-18-1 (Dynorphins); 83335-41-5 (rimorphin); 88373-73-3 (Enkephalin, D-Penicillamine (2,5)-); 9002-67-9 (Luteinizing Hormone)
[Em] Mês de entrada:0405
[Cu] Atualização por classe:061115
[Lr] Data última revisão:
061115
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:040508
[St] Status:MEDLINE


  5 / 293 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:15121763
[Au] Autor:Chen F; Lawrence AJ
[Ad] Endereço:Howard Florey Institute, The University of Melbourne, Parkville, Victoria 3010, Australia. f.chen@hfi.unimelb.edu.au
[Ti] Título:Chronic antidepressant treatment causes a selective reduction of mu-opioid receptor binding and functional coupling to G Proteins in the amygdala of fawn-hooded rats.
[So] Source:J Pharmacol Exp Ther;310(3):1020-6, 2004 Sep.
[Is] ISSN:0022-3565
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We have previously documented that chronic alcohol consumption or alcohol withdrawal affects mu-opioid receptor density and receptor-mediated G protein coupling in Fawn-Hooded (FH) rat brain, especially in mesolimbic regions. FH rats demonstrate comorbid depression and high voluntary alcohol consumption; treatment with standard antidepressants improves both facets of this phenotype. Accordingly, we sought to examine whether mu-opioid receptor binding and the receptor-mediated functional coupling to G protein is affected by this drug treatment. Using quantitative autoradiography, binding of mu-opioid receptors labeled by [125I]FK33,824 (D-Ala2,N-Me-Phe4,Met(O)5-ol enkephalin) and the coupling between receptors and G proteins determined by agonist-stimulated guanosine 5'-O -(3-[35S]thio)triphosphate ([35S]GTPgammaS) binding was mapped throughout brain sections of FH rats after 10-day treatment with vehicle, desipramine, or sertraline. Both desipramine and sertraline produced significant decreases of [125I]FK33,824 binding in many brain regions; 13 of 20 measured regions for desipramine and 16 of 20 measured regions for sertraline. The coupling efficiency of mu-opioid receptors to G proteins was determined by an increase of [35S]GTPgammaS binding induced by stimulation with the mu-opioid receptor agonist [D-Ala2,N-Me-Phe4,Gly5-ol]-enkephalin (10 microM). In contrast to the receptor binding profile, functional coupling of receptors to G proteins was only significantly reduced in the amygdala, whereas it remained unchanged in other regions compared with control. The present findings suggest that antidepressants regulate opioid systems; however, this occurs differentially, and region-specific alteration of functional coupling of mu-opioid receptors to G proteins in the amygdala suggests that opioid function within the amygdala may be modulated by antidepressants.
[Mh] Termos MeSH primário: Tonsila do Cerebelo/efeitos dos fármacos
Antidepressivos/farmacologia
Proteínas de Ligação ao GTP/metabolismo
Receptores Opioides mu/metabolismo
[Mh] Termos MeSH secundário: Tonsila do Cerebelo/metabolismo
Animais
D-Ala(2),MePhe(4),Met(0)-ol-encefalina/farmacologia
Desipramina/farmacologia
Interações Medicamentosas
Ala(2)-MePhe(4)-Gly(5)-Encefalina/farmacologia
Guanosina 5'-O-(3-Tiotrifosfato)/metabolismo
Masculino
Ratos
Sertralina/farmacologia
Radioisótopos de Enxofre
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antidepressive Agents); 0 (Receptors, Opioid, mu); 0 (Sulfur Radioisotopes); 100929-53-1 (Enkephalin, Ala(2)-MePhe(4)-Gly(5)-); 37589-80-3 (Guanosine 5'-O-(3-Thiotriphosphate)); 64854-64-4 (D-Ala(2),MePhe(4),Met(0)-ol-enkephalin); EC 3.6.1.- (GTP-Binding Proteins); QUC7NX6WMB (Sertraline); TG537D343B (Desipramine)
[Em] Mês de entrada:0411
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:040504
[St] Status:MEDLINE


  6 / 293 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:12753784
[Au] Autor:Kaminski T; Siawrys G; Bogacka I; Okrasa S; Przala J
[Ad] Endereço:Department of Animal Physiology, University of Warmia and Mazury in Olsztyn, 10-718 Olsztyn-Kortowo 5, Poland.
[Ti] Título:The regulation of steroidogenesis by opioid peptides in porcine theca cells.
[So] Source:Anim Reprod Sci;78(1-2):71-84, 2003 Sep 15.
[Is] ISSN:0378-4320
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The present study was designed to investigate basal and LH-induced steroidogenesis in porcine theca cells from large follicles in response to various concentrations (1-1000 nM) of mu opioid receptor agonists (beta-endorphin, DAMGO, FK 33-824), delta receptor agonists (met-enkephalin, leu-enkephalin, DPLPE) and kappa receptor agonists (dynorphin A, dynorphin B, U 50488). Agonists of mu opioid receptors suppressed basal androstenedione (A4), testosterone (T) and oestradiol-17beta (E2) secretion and enhanced LH-induced A4 and T release by theca cells. The inhibitory effect of the agonists on E2 secretion was abolished in the presence of LH. All delta receptor agonists depressed basal progesterone (P4) output. However, the influence of these agents on LH-treated cells was negligible. Among delta receptor agonist used only leu-enkephalin and DPLPE at the lowest concentrations inhibited basal A4 release. The presence of LH in culture media changed the influence of these opioids from inhibitory to stimulatory. Similarly, DPLPE reduced T secretion by non-stimulated theca cells and enhanced T secretion of stimulated cells. All of delta agonists inhibited basal E2 secretion and unaffected its release from LH-treated theca cells. Agonists of kappa receptors inhibited basal, non-stimulated, P4 secretion and two of them (dynorphin B, U 50488) potentiated LH-induced P4 output. Basal A4 and T release remained unaffected by kappa agonist treatment, but the cells cultured in the presence of LH generally increased both androgen production in response to these opioids. Basal secretion of E2 was also suppressed by kappa agonists. This inhibitory effect was not observed when the cells were additionally treated with LH. In view of these findings we suggest that opioid peptides derived from three major opioid precursors may directly participate in the regulation of porcine theca cell steroidogenesis.
[Mh] Termos MeSH primário: Peptídeos Opioides/farmacologia
Esteroides/biossíntese
Suínos/metabolismo
Células Tecais/efeitos dos fármacos
Células Tecais/metabolismo
[Mh] Termos MeSH secundário: (trans)-Isômero de 3,4-Dicloro-N-metil-N-(2-(1-pirrolidinil)-ciclo-hexil)-benzenoacetamida/farmacologia
Animais
Células Cultivadas
D-Ala(2),MePhe(4),Met(0)-ol-encefalina/farmacologia
Dinorfinas/farmacologia
Endorfinas/farmacologia
Ala(2)-MePhe(4)-Gly(5)-Encefalina/farmacologia
D-Penicilina (2,5)-Encefalina/farmacologia
Encefalina Leucina/farmacologia
Encefalina Metionina/farmacologia
Estradiol/biossíntese
Estradiol/secreção
Feminino
Progesterona/biossíntese
Progesterona/secreção
Receptores Opioides delta/agonistas
Receptores Opioides delta/efeitos dos fármacos
Receptores Opioides kappa/agonistas
Receptores Opioides kappa/efeitos dos fármacos
Receptores Opioides mu/agonistas
Receptores Opioides mu/efeitos dos fármacos
Testosterona/biossíntese
Testosterona/secreção
beta-Endorfina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Endorphins); 0 (Opioid Peptides); 0 (Receptors, Opioid, delta); 0 (Receptors, Opioid, kappa); 0 (Receptors, Opioid, mu); 0 (Steroids); 100929-53-1 (Enkephalin, Ala(2)-MePhe(4)-Gly(5)-); 3XMK78S47O (Testosterone); 4G7DS2Q64Y (Progesterone); 4TI98Z838E (Estradiol); 58569-55-4 (Enkephalin, Methionine); 58822-25-6 (Enkephalin, Leucine); 60617-12-1 (beta-Endorphin); 64854-64-4 (D-Ala(2),MePhe(4),Met(0)-ol-enkephalin); 67198-13-4 (3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer); 74913-18-1 (Dynorphins); 83335-41-5 (rimorphin); 88373-73-3 (Enkephalin, D-Penicillamine (2,5)-)
[Em] Mês de entrada:0310
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:030520
[St] Status:MEDLINE


  7 / 293 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:11702344
[Au] Autor:Kaminski T; Okrasa S; Bogacka I; Siawrys G; Przala J
[Ad] Endereço:Department of Animal Physiology, University of Warmia and Mazury in Olsztyn, 10-718 Olsztyn-Kortowo 5, Poland.
[Ti] Título:Porcine theca cells produce immunoreactive beta-endorphin and change steroidogenesis in response to opioid agonist.
[So] Source:Acta Vet Hung;49(3):319-29, 2001.
[Is] ISSN:0236-6290
[Cp] País de publicação:Hungary
[La] Idioma:eng
[Ab] Resumo:In earlier in vitro experiments opioids affected steroidogenesis in porcine luteal and granulosa cells. The present studies were undertaken to examine the effects of FK 33-824 (opioid agonist) alone or in combination with LH, PRL or naloxone (NAL, opioid antagonist) on steroidogenesis in cultured porcine theca cells. Moreover, we have tested beta-endorphin-like immunoreactivity (beta-END-LI) concentrations in culture media under control conditions and following treatments of theca cells with LH, PRL, progesterone (P4), oestradiol (E2) or testosterone (T). FK 33-824 and NAL significantly increased P4 release by theca cells and inhibited stimulatory effect of LH on this steroid output. PRL-induced P4 secretion from the cells was blunted only by FK 33-824. Secretion of androstenedione (A4) and T was essentially elevated in the presence of FK 33-824 and this potentiation of both androgen release was completely abolished by PRL. NAL blocked stimulatory effect of the opioid agonist only in case of T. Secretion of oestradiol and oestrone was completely free from the influence of both the opioid agonist and antagonist. Pig theca cells were able to produce beta-END-LI but none of tested hormones (LH, PRL, P4, E2 and T alone or in combination) significantly affected this production. In conclusion, these data indicate that porcine theca cells may produce beta-END-LI and change their steroidogenesis in response to opioid peptides.
[Mh] Termos MeSH primário: D-Ala(2),MePhe(4),Met(0)-ol-encefalina/farmacologia
Entorpecentes/agonistas
Suínos/fisiologia
Células Tecais/metabolismo
beta-Endorfina/biossíntese
[Mh] Termos MeSH secundário: Animais
D-Ala(2),MePhe(4),Met(0)-ol-encefalina/antagonistas & inibidores
Feminino
Hormônios Esteroides Gonadais/farmacologia
Hormônios Esteroides Gonadais/secreção
Gonadotropinas Hipofisárias/farmacologia
Naloxona/farmacologia
Antagonistas de Entorpecentes/farmacologia
Células Tecais/efeitos dos fármacos
beta-Endorfina/secreção
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Gonadal Steroid Hormones); 0 (Gonadotropins, Pituitary); 0 (Narcotic Antagonists); 0 (Narcotics); 36B82AMQ7N (Naloxone); 60617-12-1 (beta-Endorphin); 64854-64-4 (D-Ala(2),MePhe(4),Met(0)-ol-enkephalin)
[Em] Mês de entrada:0203
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:011113
[St] Status:MEDLINE


  8 / 293 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:11531100
[Au] Autor:Reddy PS; Basha MR
[Ad] Endereço:Department of Biotechnology, S.V. University, Tirupati, India. psreddy@vsnl.com
[Ti] Título:On the mode of action of methionine enkephalin, FK 33-824 and naloxone in regulating the hemolymph glucose level in the fresh water field crab Oziotelphusa senex senex.
[So] Source:Z Naturforsch C;56(7-8):629-32, 2001 Jul-Aug.
[Is] ISSN:0939-5075
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:The possible involvement of opioid system in the regulation of hemolymph glucose level in the fresh water crab Oziotelphusa senex senex Fabricius, was investigated. Opioid agonist and antagonist was also used in addition to methionine-enkephalin itself. Injection of the opioid, methionine-enkephalin and FK 33-824 significantly elevated hemolymph glucose level. In contrast, injection of naloxone in to crab resulted in decrease in hemolymph glucose level. Injection of naloxone prior to injection of methionine-enkephalin blocked the hyperglycemic action of methionine-enkephalin. Injection of methionine-enkephalin, FK 33824 and naloxone produced no significant effect on hemolymph glucose level in eyestalk-less crab. The alterations in the intact crab hemolymph glucose level hypothesised to be due to stimulation of release of hyperglycemic hormone during methionine-enkephalin and FK 33824 treatment and blocking of release of hyperglycemic hormone during naloxone treatment from the eyestalks of crab Oziotelphusa senex senex.
[Mh] Termos MeSH primário: Braquiúros/fisiologia
D-Ala(2),MePhe(4),Met(0)-ol-encefalina/farmacologia
Encefalina Metionina/farmacologia
Glucose/metabolismo
Hemolinfa/fisiologia
Naloxona/farmacologia
[Mh] Termos MeSH secundário: Animais
Água Doce
Hemolinfa/efeitos dos fármacos
Homeostase
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
36B82AMQ7N (Naloxone); 58569-55-4 (Enkephalin, Methionine); 64854-64-4 (D-Ala(2),MePhe(4),Met(0)-ol-enkephalin); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:0110
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:010904
[St] Status:MEDLINE


  9 / 293 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:11500514
[Au] Autor:Liu JG; Ruckle MB; Prather PL
[Ad] Endereço:Department of Pharmacology and Toxicology, College of Medicine, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA.
[Ti] Título:Constitutively active mu-opioid receptors inhibit adenylyl cyclase activity in intact cells and activate G-proteins differently than the agonist [D-Ala2,N-MePhe4,Gly-ol5]enkephalin.
[So] Source:J Biol Chem;276(41):37779-86, 2001 Oct 12.
[Is] ISSN:0021-9258
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The most convincing evidence demonstrating constitutive activation of mu-opioid receptors is the observation that putative inverse agonists decrease basal G-protein activity in membrane preparations. However, it is not clear whether constitutively active receptors in isolated membranes have any physiological relevance in intact cells. GH3 cells expressing mu-opioid receptors (GH3MOR) exhibit higher basal G-protein activity and lower basal cAMP levels than wild-type GH3 cells, indicative of constitutively active receptors. This study determined whether alkylation of mu-opioid receptors by the irreversible antagonist beta-funaltrexamine would decrease spontaneous receptor activity in intact cells, revealing constitutive activity. GH3MOR cells were pretreated with increasing concentrations of beta-funaltrexamine followed by functional testing after removal of unbound drug. beta-Funaltrexamine pretreatment produced a concentration-dependent decrease in mu-opioid receptor binding with an IC50 of 0.98 nm and an Emax of 77%. Similar concentrations of beta-funaltrexamine pretreatment produced a half-maximal reduction in basal [35S]GTPgammaS binding, a decrease in basal photolabeling of G-proteins with azidoanilido-[alpha-32P]GTP, and an increase in basal adenylyl cyclase activity in intact cells. Therefore, mu-opioid receptors are constitutively active in intact cells, producing stimulation of G-proteins and inhibition of adenylyl cyclase. Importantly, photolabeling of Galpha-subunits with azidoanilido-[alpha-32P]GTP demonstrated that constitutively active mu-opioid receptors activate individual G-proteins differently than the agonist [d-Ala2,N-MePhe4,Gly-ol5]enkephalin.
[Mh] Termos MeSH primário: Inibidores de Adenilil Ciclase
D-Ala(2),MePhe(4),Met(0)-ol-encefalina/farmacologia
Proteínas de Ligação ao GTP/metabolismo
Naltrexona/análogos & derivados
Receptores Opioides mu/fisiologia
[Mh] Termos MeSH secundário: Toxina Adenilato Ciclase
Linhagem Celular
Ala(2)-MePhe(4)-Gly(5)-Encefalina/farmacologia
Naltrexona/farmacologia
Cloreto de Potássio/farmacologia
Ligação Proteica
Receptores Opioides mu/agonistas
Receptores Opioides mu/metabolismo
Fatores de Virulência de Bordetella/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, U.S. GOV'T, P.H.S.
[Nm] Nome de substância:
0 (Adenylate Cyclase Toxin); 0 (Adenylyl Cyclase Inhibitors); 0 (Receptors, Opioid, mu); 0 (Virulence Factors, Bordetella); 100929-53-1 (Enkephalin, Ala(2)-MePhe(4)-Gly(5)-); 5S6W795CQM (Naltrexone); 64854-64-4 (D-Ala(2),MePhe(4),Met(0)-ol-enkephalin); 660YQ98I10 (Potassium Chloride); 72782-05-9 (beta-funaltrexamine); EC 3.6.1.- (GTP-Binding Proteins)
[Em] Mês de entrada:0112
[Cu] Atualização por classe:151119
[Lr] Data última revisão:
151119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:010814
[St] Status:MEDLINE


  10 / 293 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
[PMID]:10898106
[Au] Autor:Kaminski T; Gawronska B; Derecka K; Okrasa S; Przala J
[Ad] Endereço:Department of Animal Physiology, University of Warmia and Mazury in Olsztyn, Poland.
[Ti] Título:Gene expression and peptide localization for LH/hCG receptor in porcine small and large luteal cells: possible regulation by opioid peptides.
[So] Source:J Physiol Pharmacol;51(2):359-68, 2000 Jun.
[Is] ISSN:0867-5910
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:The aim of the present studies was to investigate (1) the presence of LH receptor (LHR) in porcine separated small (SLCs) and large (LLCs) luteal cells taken from mid-luteal corpora lutea and (2) the influence of opioid agonist, FK 33-824 (FK) on LHR gene expression in these cells. Immunocytochemistry revealed intense staining for LHR in both SLCs and LLCs. Reverse transcription-polymerase chain reaction (RT-PCR) and Southern hybridization were used to check the effect of FK and hCG on LHR gene expression. The LHR gene expression was observed in non-stimulated LLCs and in both types of cells after treatment with FK or hCG. FK stimulated LHR gene expression in SLCs and inhibited the gene expression in LLCs. Moreover, FK inhibited and potentiated stimulatory influence of hCG on the gene expression in LLCs and SLCs, respectively. These results suggest that LHR gene expression in porcine luteal cells can be regulated by opioid peptides.
[Mh] Termos MeSH primário: Corpo Lúteo/metabolismo
Endorfinas/fisiologia
Expressão Gênica
Receptores do LH/genética
Receptores do LH/metabolismo
[Mh] Termos MeSH secundário: Animais
Tamanho Celular
Células Cultivadas
Gonadotropina Coriônica/farmacologia
Corpo Lúteo/citologia
Corpo Lúteo/efeitos dos fármacos
D-Ala(2),MePhe(4),Met(0)-ol-encefalina/farmacologia
Endorfinas/antagonistas & inibidores
Feminino
Expressão Gênica/efeitos dos fármacos
Suínos
Distribuição Tecidual
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, U.S. GOV'T, P.H.S.
[Nm] Nome de substância:
0 (Chorionic Gonadotropin); 0 (Endorphins); 0 (Receptors, LH); 64854-64-4 (D-Ala(2),MePhe(4),Met(0)-ol-enkephalin)
[Em] Mês de entrada:0010
[Cu] Atualização por classe:071114
[Lr] Data última revisão:
071114
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:000718
[St] Status:MEDLINE



página 1 de 30 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde