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Pesquisa : D12.776.543.750.695.700.720 [Categoria DeCS]
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[PMID]:28468962
[Au] Autor:Gohar EY; Kasztan M; Becker BK; Speed JS; Pollock DM
[Ad] Endereço:Cardio-Renal Physiology & Medicine, Division of Nephrology, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama.
[Ti] Título:Ovariectomy uncovers purinergic receptor activation of endothelin-dependent natriuresis.
[So] Source:Am J Physiol Renal Physiol;313(2):F361-F369, 2017 Aug 01.
[Is] ISSN:1522-1466
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We recently reported that natriuresis produced by renal medullary salt loading is dependent on endothelin (ET)-1 and purinergic (P2) receptors in male rats. Because sex differences in ET-1 and P2 signaling have been reported, we decided to test whether ovarian sex hormones regulate renal medullary ET-1 and P2-dependent natriuresis. The effect of medullary NaCl loading on Na excretion was determined in intact and ovariectomized (OVX) female Sprague-Dawley rats with and without ET-1 or P2 receptor antagonism. Isosmotic saline (284 mosmol/kgH O) was infused in the renal medullary interstitium of anesthetized rats during a baseline urine collection period, followed by isosmotic or hyperosmotic saline (1,800 mosmol/kgH O) infusion. Medullary NaCl loading significantly enhanced Na excretion in intact and OVX female rats. ET or P2 receptor blockade did not attenuate the natriuretic effect of medullary NaCl loading in intact females, whereas ET or P2 receptor blockade attenuated the natriuretic response to NaCl loading in OVX rats. Activation of medullary P2Y and P2Y receptors by UTP infusion had no significant effect in intact females but enhanced Na excretion in OVX rats. Combined ET receptor blockade significantly inhibited the natriuretic response to UTP observed in OVX rats. These data demonstrate that medullary NaCl loading induces ET-1 and P2-independent natriuresis in intact females. In OVX, activation of medullary P2 receptors promotes ET-dependent natriuresis, suggesting that ovarian hormones may regulate the interplay between the renal ET-1 and P2 signaling systems to facilitate Na excretion.
[Mh] Termos MeSH primário: Endotelina-1/metabolismo
Medula Renal/metabolismo
Natriurese
Ovariectomia
Receptores Purinérgicos P2Y2/metabolismo
Receptores Purinérgicos P2/metabolismo
Eliminação Renal
Sódio/urina
[Mh] Termos MeSH secundário: Animais
Antagonistas dos Receptores de Endotelina/farmacologia
Endotelina-1/genética
Feminino
Medula Renal/efeitos dos fármacos
Natriurese/efeitos dos fármacos
Agonistas do Receptor Purinérgico P2/farmacologia
Antagonistas do Receptor Purinérgico P2/farmacologia
Ratos Sprague-Dawley
Receptores Purinérgicos P2/efeitos dos fármacos
Receptores Purinérgicos P2Y2/efeitos dos fármacos
Eliminação Renal/efeitos dos fármacos
Transdução de Sinais
Cloreto de Sódio/administração & dosagem
Cloreto de Sódio/metabolismo
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Endothelin Receptor Antagonists); 0 (Endothelin-1); 0 (P2ry2 protein, rat); 0 (Purinergic P2 Receptor Agonists); 0 (Purinergic P2 Receptor Antagonists); 0 (Receptors, Purinergic P2); 0 (Receptors, Purinergic P2Y2); 0 (purinoceptor P2Y4); 451W47IQ8X (Sodium Chloride); 9NEZ333N27 (Sodium)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180208
[Lr] Data última revisão:
180208
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1152/ajprenal.00098.2017


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[PMID]:29017923
[Au] Autor:Shinjo Y; Makide K; Satoh K; Fukami F; Inoue A; Kano K; Otani Y; Ohwada T; Aoki J
[Ad] Endereço:Graduate School of Pharmaceutical Sciences, Tohoku University, 6-3, Miyagi 980-8578, Japan.
[Ti] Título:Lysophosphatidylserine suppresses IL-2 production in CD4 T cells through LPS /GPR174.
[So] Source:Biochem Biophys Res Commun;494(1-2):332-338, 2017 Dec 09.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Lysophosphatidylserine (LysoPS) has been shown to have lipid mediator-like actions to induce mast cell degranulation and suppress T lymphocyte proliferation. Recently, three G protein-coupled receptors (GPCRs), LPS /GPR34, LPS /P2Y10, and LPS /GPR174, were found to react specifically with LysoPS, raising the possibility that LysoPS exerts its roles through these receptors. In this study, we show that LPS is expressed in various T cell subtypes and is involved in suppression of Interleukin-2 (IL-2) production in CD4 T cells. We found that LysoPS suppressed the IL-2 production from activated T cells at the mRNA and protein levels. In addition, LysoPS did not have such an effect on the splenocytes and CD4 T cells isolated from LPS -deficient mice. In LPS -deficient splenocytes and CD4 T cells, anti-CD3/anti-CD28-triggered IL-2 production is somewhat increased. Interestingly, LysoPS with various fatty acids was up-regulated upon T cell activation. The present study raised the possibility that LysoPS exerts its immunosuppressive roles by down-regulating IL-2 production through a LysoPS-LPS axis in T cells.
[Mh] Termos MeSH primário: Linfócitos T CD4-Positivos/efeitos dos fármacos
Interleucina-2/genética
Lisofosfolipídeos/farmacologia
Receptores Acoplados a Proteínas-G/genética
Receptores de Lisofosfolipídeos/genética
Receptores Purinérgicos P2/genética
[Mh] Termos MeSH secundário: Animais
Anticorpos/farmacologia
Antígenos CD28/antagonistas & inibidores
Antígenos CD28/genética
Antígenos CD28/imunologia
Complexo CD3/genética
Complexo CD3/imunologia
Linfócitos T CD4-Positivos/citologia
Linfócitos T CD4-Positivos/imunologia
Separação Celular
Regulação da Expressão Gênica
Interleucina-2/imunologia
Lisofosfolipídeos/imunologia
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C57BL
Cultura Primária de Células
Receptores Acoplados a Proteínas-G/imunologia
Receptores de Lisofosfolipídeos/imunologia
Receptores Purinérgicos P2/imunologia
Transdução de Sinais
Baço/citologia
Baço/efeitos dos fármacos
Baço/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies); 0 (CD28 Antigens); 0 (CD3 Complex); 0 (G-protein-coupled receptor 34); 0 (GPR174 protein, mouse); 0 (Interleukin-2); 0 (Lysophospholipids); 0 (Receptors, G-Protein-Coupled); 0 (Receptors, Lysophospholipid); 0 (Receptors, Purinergic P2); 0 (lysophosphatidylserine)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171012
[St] Status:MEDLINE


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[PMID]:29017492
[Au] Autor:Huang J; You X; Liu W; Song C; Lin X; Zhang X; Tao J; Chen L
[Ad] Endereço:College of Rehabilitation Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian, 350122, China.
[Ti] Título:Electroacupuncture ameliorating post-stroke cognitive impairments via inhibition of peri-infarct astroglial and microglial/macrophage P2 purinoceptors-mediated neuroinflammation and hyperplasia.
[So] Source:BMC Complement Altern Med;17(1):480, 2017 Oct 10.
[Is] ISSN:1472-6882
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: During ischemic stroke (IS), adenosine 5'-triphosphate (ATP) is released from damaged nerve cells of the infract core region to the extracellular space, invoking peri-infarct glial cellular P2 purinoceptors singling, and causing pro-inflammatory cytokine secretion, which is likely to initiate or aggravate motor and cognitive impairment. It has been proved that electroacupuncture (EA) is an effective and safe strategy used in anti-inflammation. However, EA for the role of purine receptors in the central nervous system has not yet been reported. METHODS: Ischemia-reperfusion injured rat model was induced by middle cerebral artery occlusion and reperfusion (MCAO/R). EA treatment at the DU 20 and DU 24 acupoints treatment were conducted to rats from the 12 h after MCAO/R injury for consecutive 7 days. The neurological outcomes, infarction volumes and the level of astroglial and microglial/macrophage hyperplasia, inflammatory cytokine and P2X7R and P2Y1R expression in the peri-infarct hippocampal CA1and sensorimotor cortex were investigated after IS to evaluate the MCAO/R model and therapeutic mechanism of EA treatment. RESULTS: EA effectively reduced the level of pro-inflammatory cytokine interleukin-1ß (IL-1ß) as evidenced by reduction in astroglial and microglial/macrophage hyperplasia and the levels of P2X7R and ED1, P2X7R and GFAP, P2Y1R and ED1, P2Y1R and GFAP co-expression in peri-infarct hippocampal CA1 and sensorimotor cortex compared with that of MCAO/R model and Non-EA treatment, accompanied by the improved neurological deficit and the motor and memory impairment outcomes. Therefore, our data support the hypothesis that EA could exert its anti-inflammatory effect via inhibiting the astroglial and microglial/macrophage P2 purinoceptors (P2X7R and P2Y1R)-mediated neuroinflammation after MCAO/R injury. CONCLUSION: Astroglial and microglial/macrophage P2 purinoceptors-mediated neuroinflammation and hyperplasia in peri-infarct hippocampal CA1 and sensorimotor cortex were attenuated by EA treatment after ischemic stroke accompanied by the improved motor and memory behavior performance.
[Mh] Termos MeSH primário: Eletroacupuntura
Hiperplasia/metabolismo
Infarto da Artéria Cerebral Média/terapia
Inflamação/metabolismo
Receptores Purinérgicos P2/metabolismo
[Mh] Termos MeSH secundário: Pontos de Acupuntura
Animais
Encéfalo/diagnóstico por imagem
Encéfalo/patologia
Região CA1 Hipocampal/metabolismo
Infarto da Artéria Cerebral Média/diagnóstico por imagem
Infarto da Artéria Cerebral Média/metabolismo
Infarto da Artéria Cerebral Média/patologia
Interleucina-1beta/metabolismo
Imagem por Ressonância Magnética
Masculino
Ratos
Ratos Sprague-Dawley
Traumatismo por Reperfusão
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukin-1beta); 0 (Receptors, Purinergic P2)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171027
[Lr] Data última revisão:
171027
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171012
[St] Status:MEDLINE
[do] DOI:10.1186/s12906-017-1974-y


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[PMID]:28800362
[Au] Autor:Jiang P; Xing F; Guo B; Yang J; Li Z; Wei W; Hu F; Lee I; Zhang X; Pan L; Xu J
[Ad] Endereço:The Key Laboratory of Weak-Light Nonlinear Photonics, Ministry of Education, TEDA Institute of Applied Physics and School of Physics, Nankai University, Tianjin, China.
[Ti] Título:Nucleotide transmitters ATP and ADP mediate intercellular calcium wave communication via P2Y12/13 receptors among BV-2 microglia.
[So] Source:PLoS One;12(8):e0183114, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Nerve injury is accompanied by a liberation of diverse nucleotides, some of which act as 'find/eat-me' signals in mediating neuron-glial interplay. Intercellular Ca2+ wave (ICW) communication is the main approach by which glial cells interact and coordinate with each other to execute immune defense. However, the detailed mechanisms on how these nucleotides participate in ICW communication remain largely unclear. In the present work, we employed a mechanical stimulus to an individual BV-2 microglia to simulate localized injury. Remarkable ICW propagation was observed no matter whether calcium was in the environment or not. Apyrase (ATP/ADP-hydrolyzing enzyme), suramin (broad-spectrum P2 receptor antagonist), 2-APB (IP3 receptor blocker) and thapsigargin (endoplasmic reticulum calcium pump inhibitor) potently inhibited these ICWs, respectively, indicating the dependence of nucleotide signals and P2Y receptors. Then, we detected the involvement of five naturally occurring nucleotides (ATP, ADP, UTP, UDP and UDP-glucose) by desensitizing receptors. Results showed that desensitization with ATP and ADP could block ICW propagation in a dose-dependent manner, whereas other nucleotides had little effect. Meanwhile, the expression of P2Y receptors in BV-2 microglia was identified and their contributions were analyzed, from which we suggested P2Y12/13 receptors activation mostly contributed to ICWs. Besides, we estimated that extracellular ATP and ADP concentration sensed by BV-2 microglia was about 0.3 µM during ICWs by analyzing calcium dynamic characteristics. Taken together, these results demonstrated that the nucleotides ATP and ADP were predominant signal transmitters in mechanical stimulation-induced ICW communication through acting on P2Y12/13 receptors in BV-2 microglia.
[Mh] Termos MeSH primário: Difosfato de Adenosina/metabolismo
Trifosfato de Adenosina/metabolismo
Cálcio/metabolismo
Microglia/metabolismo
Receptores Purinérgicos P2Y12/metabolismo
Receptores Purinérgicos P2/metabolismo
[Mh] Termos MeSH secundário: Animais
Apirase/farmacologia
Fenômenos Biomecânicos
Compostos de Boro/farmacologia
Sinalização do Cálcio/efeitos dos fármacos
Comunicação Celular/efeitos dos fármacos
Linhagem Celular Transformada
Expressão Gênica
Fosfatos de Inositol/farmacologia
Mecanotransdução Celular/efeitos dos fármacos
Camundongos
Microglia/citologia
Microglia/efeitos dos fármacos
Imagem Molecular
Receptores Purinérgicos P2/genética
Receptores Purinérgicos P2Y12/genética
Suramina/farmacologia
Tapsigargina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (2-aminoethyl diphenylborinate); 0 (Boron Compounds); 0 (Inositol Phosphates); 0 (P2ry12 protein, mouse); 0 (P2ry13 protein, mouse); 0 (Receptors, Purinergic P2); 0 (Receptors, Purinergic P2Y12); 2831-74-5 (inositol 3-phosphate); 6032D45BEM (Suramin); 61D2G4IYVH (Adenosine Diphosphate); 67526-95-8 (Thapsigargin); 8L70Q75FXE (Adenosine Triphosphate); EC 3.6.1.5 (Apyrase); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171006
[Lr] Data última revisão:
171006
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170812
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0183114


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[PMID]:28669743
[Au] Autor:Caglayan B; Caglayan AB; Beker MC; Yalcin E; Beker M; Kelestemur T; Sertel E; Ozturk G; Kilic U; Sahin F; Kilic E
[Ad] Endereço:Istanbul Medipol University, Regenerative and Restorative Medical Research Center, Istanbul, Turkey; Istanbul Medipol University, Dept. of Physiology, Istanbul, Turkey; Yeditepe University, Dept. of Genetics and Bioengineering, Istanbul, Turkey.
[Ti] Título:Evidence that activation of P2X7R does not exacerbate neuronal death after optic nerve transection and focal cerebral ischemia in mice.
[So] Source:Exp Neurol;296:23-31, 2017 Oct.
[Is] ISSN:1090-2430
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Conflicting data in the literature about the function of P2X7R in survival following ischemia necessitates the conductance of in-depth studies. To investigate the impacts of activation vs inhibition of the receptor on neuronal survival as well as the downstream signaling cascades, in addition to optic nerve transection (ONT), 30min and 90min of middle cerebral artery occlusion (MCAo) models were performed in mice. Intracellular calcium levels were assessed in primary cortical neuron cultures. Here, we show that P2X7R antagonist Brilliant Blue G (BBG) decreased DNA fragmentation, infarct volume, brain swelling, neurological deficit scores and activation of microglial cells after focal cerebral ischemia. BBG also significantly increased the number of surviving retinal ganglion cells (RGCs) after ONT and the number of surviving neurons following MCAo. Importantly, receptor agonist BzATP resulted in increased activation of microglial cells and induced phosphorylation of ERK, AKT and JNK. These results indicated that inhibition of P2X7R with BBG promoted neuronal survival, not through the activation of survival kinase pathways, but possibly by improved intracellular Ca overload and decreased the levels of Caspase 1, IL-1ß and Bax proteins. On the other hand, BzATP-mediated increased number of activated microglia and increased survival kinase levels in addition to increased caspase-1 and IL-1ß levels indicate the complex nature of the P2X7 receptor-mediated signaling in neuronal injury.
[Mh] Termos MeSH primário: Isquemia Encefálica/metabolismo
Isquemia Encefálica/patologia
Neurônios/patologia
Traumatismos do Nervo Óptico/metabolismo
Traumatismos do Nervo Óptico/patologia
Receptores Purinérgicos P2/metabolismo
[Mh] Termos MeSH secundário: Trifosfato de Adenosina/análogos & derivados
Trifosfato de Adenosina/farmacologia
Trifosfato de Adenosina/uso terapêutico
Animais
Animais Recém-Nascidos
Encéfalo/irrigação sanguínea
Encéfalo/efeitos dos fármacos
Edema Encefálico/etiologia
Isquemia Encefálica/tratamento farmacológico
Proteínas de Ligação ao Cálcio/metabolismo
Células Cultivadas
Córtex Cerebral/citologia
Citocinas/metabolismo
Fragmentação do DNA/efeitos dos fármacos
Modelos Animais de Doenças
Infusões Intraventriculares
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Proteínas dos Microfilamentos/metabolismo
Neurônios/efeitos dos fármacos
Traumatismos do Nervo Óptico/tratamento farmacológico
Inibidores da Agregação de Plaquetas/farmacologia
Inibidores da Agregação de Plaquetas/uso terapêutico
Corantes de Rosanilina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aif1 protein, mouse); 0 (Calcium-Binding Proteins); 0 (Cytokines); 0 (Microfilament Proteins); 0 (Platelet Aggregation Inhibitors); 0 (Receptors, Purinergic P2); 0 (Rosaniline Dyes); 0 (purinergic P2X8 receptor); 4P5DXU1F8Q (3'-O-(4-benzoyl)benzoyladenosine 5'-triphosphate); 8L70Q75FXE (Adenosine Triphosphate); M1ZRX790SI (coomassie Brilliant Blue)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170822
[Lr] Data última revisão:
170822
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170704
[St] Status:MEDLINE


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[PMID]:28668846
[Au] Autor:Lertsuwan J; Ruchirawat M
[Ad] Endereço:Laboratory of Chemical Carcinogenesis, Chulabhorn Research Institute, Bangkok, Thailand jomnarong@cri.or.th.
[Ti] Título:Inhibitory Effects of ATP and Adenosine on Cholangiocarcinoma Cell Proliferation and Motility.
[So] Source:Anticancer Res;37(7):3553-3561, 2017 07.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIM: Inhibitory effects of extracellular nucleotides have been investigated in many types of cancers. Herein, we aimed to determine the effects of ATP and adenosine and their receptor profile on cholangiocarcinoma (CCA) cells. MATERIALS AND METHODS: Two CCA and one immortalized cholangiocyte cell line were used. The effects of ATP and adenosine on cell proliferation and motility were examined by MTT and wound-healing/trans-well invasion assays, respectively. Purinergic receptor profiling was carried out by reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: ATP and adenosine induced proliferation-inhibitory and motility-inhibitory effects in all cell lines tested. However, immortalized cholangiocytes showed resistance in proliferation inhibition. Several P2 receptors were commonly expressed in all cells, whereas no adenosine receptor was expressed. Furthermore, no synergistic effects of ATP and adenosine were observed in CCA cells. CONCLUSION: ATP and adenosine had anti-proliferative and anti-motility effects in CCA cells, while there was a smaller effect on normal cholangiocytes. These data indicate the potential use of ATP and odenosine as a novel therapy for CCA.
[Mh] Termos MeSH primário: Trifosfato de Adenosina/farmacologia
Adenosina/farmacologia
Neoplasias dos Ductos Biliares/tratamento farmacológico
Movimento Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Colangiocarcinoma/tratamento farmacológico
Colangiocarcinoma/metabolismo
[Mh] Termos MeSH secundário: Neoplasias dos Ductos Biliares/metabolismo
Linhagem Celular Tumoral
Seres Humanos
Receptores Purinérgicos P2/metabolismo
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Purinergic P2); 8L70Q75FXE (Adenosine Triphosphate); K72T3FS567 (Adenosine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170703
[St] Status:MEDLINE


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[PMID]:28631703
[Au] Autor:Muslimova EF; Afanasiev SA; Rebrova TY; Sergienko TN; Repin AN
[Ad] Endereço:Cardiology Research Institute, Tomsk National Research Medical Center, Russian Academy of Sciences, Tomsk, Russia.
[Ti] Título:[Association of ITGB3, P2RY12, and CYP2C19 gene polymorphisms with platelet functional activity in patients with coronary heart disease during dual antiplatelet therapy].
[Ti] Título:Assotsiatsiia polimorfizmov genov ITGB3, P2RY12, CYP2C19 s funktsional'noi aktivnost'iu trombotsitov u patsientov s ishemicheskoi bolezn'iu serdtsa na fone dvukhkomponentnoi antiagregantnoi terapii..
[So] Source:Ter Arkh;89(5):74-78, 2017.
[Is] ISSN:0040-3660
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:AIM: To assess the association of CYP2C19 G681A, P2RY12 H1/H2, and ITGB3 T1565C polymorphisms with the extent of platelet aggregation in patients with coronary heart disease (CHD) during antiplatelet therapy. SUBJECTS AND METHODS: 166 male patients with CHD, living in the Western Siberian Region, were examined. All the patients underwent a test for platelet aggregation induced by ADP (2.5 and 5.0 µm) and epinephrine (0.2 µm). Genotyping was performed using an allele-specific polymerase chain reaction technique. RESULTS: The polymorphic variants of the P2RY12 and ITGB3 genes were ascertained to have no impact on the extent of platelet aggregation in patients receiving clopidogrel and acetylsalicylic acid. An association was found between CYP2C19 681A allele carriage and the increased extent of platelet aggregation induced by ADP. CONCLUSION: The carriage of the cytochrome P450 CYP2C19 681A allele rather than platelet receptor gene polymorphisms determines a risk for clopidogrel resistance in patients with CHD.
[Mh] Termos MeSH primário: Aspirina
Doença da Artéria Coronariana
Citocromo P-450 CYP2C19/genética
Agregação Plaquetária/efeitos dos fármacos
Ticlopidina/análogos & derivados
[Mh] Termos MeSH secundário: Alelos
Aspirina/administração & dosagem
Aspirina/efeitos adversos
Plaquetas/efeitos dos fármacos
Doença da Artéria Coronariana/tratamento farmacológico
Doença da Artéria Coronariana/epidemiologia
Doença da Artéria Coronariana/genética
Resistência a Medicamentos/genética
Seres Humanos
Integrina beta3/genética
Masculino
Meia-Idade
Farmacogenética
Inibidores da Agregação de Plaquetas/administração & dosagem
Inibidores da Agregação de Plaquetas/efeitos adversos
Testes de Função Plaquetária/métodos
Polimorfismo Genético
Receptores Purinérgicos P2/genética
Sibéria/epidemiologia
Ticlopidina/administração & dosagem
Ticlopidina/efeitos adversos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ITGB3 protein, human); 0 (Integrin beta3); 0 (P2RY13 protein, human); 0 (Platelet Aggregation Inhibitors); 0 (Receptors, Purinergic P2); A74586SNO7 (clopidogrel); EC 1.14.14.1 (CYP2C19 protein, human); EC 1.14.14.1 (Cytochrome P-450 CYP2C19); OM90ZUW7M1 (Ticlopidine); R16CO5Y76E (Aspirin)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170831
[Lr] Data última revisão:
170831
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170621
[St] Status:MEDLINE
[do] DOI:10.17116/terarkh201789574-78


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[PMID]:28527783
[Au] Autor:Ito M; Egashira SI; Yoshida K; Mineno T; Kumagai K; Kojima H; Okabe T; Nagano T; Ui M; Matsuoka I
[Ad] Endereço:Laboratory of Pharmacology, Faculty of Pharmacy, Takasaki University of Health and Welfare, Takasaki-shi, Gunma 370-0033, Japan. Electronic address: mito@takasaki-u.ac.jp.
[Ti] Título:Identification of novel selective P2Y receptor antagonists by high-throughput screening assay.
[So] Source:Life Sci;180:137-142, 2017 Jul 01.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: The P2Y nucleotide receptor is widely involved in inflammatory responses, and is a promising molecular target for the treatment of inflammatory diseases. Although several P2Y receptor antagonists have been developed and evaluated thus far, none has successfully been developed into a therapeutic drug. In this study, we explored new promising compounds that inhibit the human P2Y receptor. MAIN METHODS: High-throughput screening (HTS) was used to study the effects of various compounds on human P2Y receptors expressed in 1321N1 human astrocytoma cells by monitoring intracellular Ca concentration ([Ca ]i) levels using an FDSS7000 real-time fluorescence detector. IL-8 concentration was measured by enzyme-linked immunosorbent assay. KEY FINDINGS: Among structurally diverse chemical libraries totalling 141,700 compounds, 43 compounds with an inhibitory activity against the P2Y receptor were identified. Further studies using a dose-response assay, receptor selectivity assay, and chemokine measurement assay revealed the selective P2Y receptor inhibitor TIM-38, which inhibited UDP-induced [Ca ]i elevation in a dose-dependent manner. TIM-38 had an IC value of 4.3µM and inhibited P2Y without affecting the response induced by four other human P2Y or muscarinic receptors. In addition, TIM-38 inhibited UDP-induced interleukin-8 release in a dose-dependent manner without affecting releases caused by other stimulus such as interleukin-1ß or tumour necrosis factor-α. Analyses of TIM-38 derivatives revealed that the nitro moiety is vital to P2Y receptor inhibition. SIGNIFICANCE: TIM-38 acts as a novel structural antagonist of P2Y receptor and may be a good lead compound for developing a P2Y receptor-targeted anti-inflammatory drug.
[Mh] Termos MeSH primário: Anti-Inflamatórios/farmacologia
Desenho de Drogas
Ensaios de Triagem em Larga Escala/métodos
Antagonistas do Receptor Purinérgico P2Y/farmacologia
Receptores Purinérgicos P2/efeitos dos fármacos
[Mh] Termos MeSH secundário: Anti-Inflamatórios/administração & dosagem
Anti-Inflamatórios/química
Astrocitoma/metabolismo
Cálcio/metabolismo
Linhagem Celular Tumoral
Relação Dose-Resposta a Droga
Ensaio de Imunoadsorção Enzimática
Seres Humanos
Concentração Inibidora 50
Interleucina-1beta/metabolismo
Interleucina-8/metabolismo
Antagonistas do Receptor Purinérgico P2Y/administração & dosagem
Antagonistas do Receptor Purinérgico P2Y/química
Receptores Purinérgicos P2/metabolismo
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Interleukin-1beta); 0 (Interleukin-8); 0 (Purinergic P2Y Receptor Antagonists); 0 (Receptors, Purinergic P2); 0 (Tumor Necrosis Factor-alpha); 0 (purinoceptor P2Y6); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170629
[Lr] Data última revisão:
170629
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170522
[St] Status:MEDLINE


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[PMID]:28494003
[Au] Autor:Huipao N; Borwornpinyo S; Wiboon-Ut S; Campbell CR; Lee IH; Hiranyachattada S; Sukasem C; Thitithanyanont A; Pholpramool C; Cook DI; Dinudom A
[Ad] Endereço:Department of Physiology, Faculty of Science, Prince of Songkla University, Songkhla, Thailand.
[Ti] Título:P2Y6 receptors are involved in mediating the effect of inactivated avian influenza virus H5N1 on IL-6 & CXCL8 mRNA expression in respiratory epithelium.
[So] Source:PLoS One;12(5):e0176974, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:One of the key pathophysiologies of H5N1 infection is excessive proinflammatory cytokine response (cytokine storm) characterized by increases in IFN-ß, TNF-α, IL-6, CXCL10, CCL4, CCL2 and CCL5 in the respiratory tract. H5N1-induced cytokine release can occur via an infection-independent mechanism, however, detail of the cellular signaling involved is poorly understood. To elucidate this mechanism, the effect of inactivated (ß-propiolactone-treated) H5N1 on the cytokine and chemokine mRNA expression in 16HBE14o- human respiratory epithelial cells was investigated. We found that the inactivated-H5N1 increased mRNA for IL-6 and CXCL8 but not TNF-α, CCL5 or CXCL10. This effect of the inactivated-H5N1 was inhibited by sialic acid receptor inhibitor (α-2,3 sialidase), adenosine diphosphatase (apyrase), P2Y receptor (P2YR) inhibitor (suramin), P2Y6R antagonist (MRS2578), phospholipase C inhibitor (U73122), protein kinase C inhibitors (BIM and Gö6976) and cell-permeant Ca2+ chelator (BAPTA-AM). Inhibitors of MAPK signaling, including of ERK1/2 (PD98059), p38 MAPK (SB203580) and JNK (SP600125) significantly suppressed the inactivated-H5N1-induced mRNA expression of CXCL8. On the other hand, the inactivated-H5N1-induced mRNA expression of IL-6 was inhibited by SB203580, but not PD98059 or SP600125, whereas SN-50, an inhibitor of NF-κB, inhibited the effect of virus on mRNA expression of both of IL-6 and CXCL8. Taken together, our data suggest that, without infection, inactivated-H5N1 induces mRNA expression of IL-6 and CXCL8 by a mechanism, or mechanisms, requiring interaction between viral hemagglutinin and α-2,3 sialic acid receptors at the cell membrane of host cells, and involves activation of P2Y6 purinergic receptors.
[Mh] Termos MeSH primário: Regulação da Expressão Gênica
Vírus da Influenza A Subtipo H5N1/fisiologia
Influenza Humana/genética
Interleucina-6/genética
Interleucina-8/genética
Receptores Purinérgicos P2/metabolismo
Mucosa Respiratória/virologia
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Galinhas
Seres Humanos
Influenza Humana/metabolismo
Influenza Humana/virologia
RNA Mensageiro/genética
Mucosa Respiratória/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (IL8 protein, human); 0 (Interleukin-6); 0 (Interleukin-8); 0 (RNA, Messenger); 0 (Receptors, Purinergic P2); 0 (purinoceptor P2Y6)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170919
[Lr] Data última revisão:
170919
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170512
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0176974


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[PMID]:28322086
[Au] Autor:Örçen A; Yilmaz V; Giris M; Akcan U; Tüzün E; Erten G
[Ad] Endereço:Department of Neuroscience, Aziz Sancar Institute of Experimental Medicine, Istanbul University , Istanbul , Turkey.
[Ti] Título:Viability of SH-SY5Y cells is associated with purinergic P2 receptor expression alterations.
[So] Source:Acta Biol Hung;68(1):22-34, 2017 Mar.
[Is] ISSN:0236-5383
[Cp] País de publicação:Hungary
[La] Idioma:eng
[Ab] Resumo:To investigate the role of metabotrophic purinergic P2Y receptors in neuroblastoma cell survival, expression of P2 receptors by normal mouse (C57BL/6) brain and human neuroblastoma SH-SY5Y cells was investigated by Western blot and real time PCR studies. Viability of SH-SY5Y cells treated with purinergic receptor antagonists suramin and pyridoxal-phosphate-6-azophenyl-2',4'-disulfonate (PPADS) was evaluated by MTT assay and flow cytometry. In the brain samples of C57BL/6 mice, expressions of P2Y4 and P2X7 were significantly reduced, whereas that of P2Y1 was significantly elevated in an age-dependent manner. SH-SY5Y cell viability was significantly reduced and necrotic cell rates were mildly increased by 400 µM suramin and 100 µM PPADS treatment. Antagonist treatment downregulated P2Y1, P2Y2 and P2Y4 and upregulated P2Y6, P2Y12 and P2X7 mRNA levels in SH-SY5Y cells on the 24th hour. These alterations were abolished for all P2 receptors except P2Y1 in the 48th hour. P2Y receptors are expressed by both normal mouse brain and human neuroblastoma cells. Purinergic receptor antagonism interferes with neuroblastoma viability through elevation of necrotic cell death and modulation of P2 receptor expression. P2Y receptors might thus be useful targets for future anti-tumor treatment trials.
[Mh] Termos MeSH primário: Regulação Neoplásica da Expressão Gênica/genética
Receptores Purinérgicos P2/genética
[Mh] Termos MeSH secundário: Fatores Etários
Animais
Encéfalo/efeitos dos fármacos
Encéfalo/metabolismo
Linhagem Celular Tumoral
Sobrevivência Celular/efeitos dos fármacos
Sobrevivência Celular/genética
Citometria de Fluxo
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Immunoblotting
Masculino
Camundongos Endogâmicos C57BL
Isoformas de Proteínas/genética
Isoformas de Proteínas/metabolismo
Antagonistas do Receptor Purinérgico P2/farmacologia
Fosfato de Piridoxal/análogos & derivados
Fosfato de Piridoxal/farmacologia
Receptores Purinérgicos P2/metabolismo
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Suramina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Protein Isoforms); 0 (Purinergic P2 Receptor Antagonists); 0 (Receptors, Purinergic P2); 149017-66-3 (pyridoxal phosphate-6-azophenyl-2',4'-disulfonic acid); 5V5IOJ8338 (Pyridoxal Phosphate); 6032D45BEM (Suramin)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170615
[Lr] Data última revisão:
170615
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170322
[St] Status:MEDLINE
[do] DOI:10.1556/018.68.2017.1.3



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