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[PMID]:24387161
[Au] Autor:Li CL; Yang XL; Wang JJ; Du GH; Yang WM; Zhang HP
[Ad] Endereço:Family Planning Research Institute, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
[Ti] Título:Effects of intracavernous injection of P2X3 and NK1 receptor antagonists on erectile dysfunction induced by spinal cord transection in rats.
[So] Source:Andrologia;47(1):25-9, 2015 Feb.
[Is] ISSN:1439-0272
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:This study aimed to explore the effects of intracavernous injection (ICI) of P2X3 and NK1 receptor antagonists on erectile dysfunction (ED) induced by spinal cord transection in rats. Sixty male Sprague-Dawley (SD) rats were randomly divided into the following three groups (20 rats each group): sham operation group (C group), thoracic spinal cord transection group (T group) and sacral spinal cord transection group (S group). An ED model was established through complete transection of the thoracic or sacral spinal cord. Intracavernous pressure (ICP) with and without injection of P2X3 (Suramin) or NK1 (GR82334) receptor antagonists was recorded 3 weeks after surgery. Immunohistochemistry was employed to detect the expression of P2X3 and NK1 receptors in the dorsal root ganglion (DRG) and smooth muscle of corpus cavernosum. Data were processed with SPSS 17.0. ICI with Suramin (0.1, 0.3 and 1 mm) or GR82334 (0.1, 0.3 and 1 mm) increased ICP dose dependently in the T and S groups. The expression of P2X3 and NK1 receptors in DRG and smooth muscle of corpus cavernosum was up-regulated in the T and S groups. It is concluded that ICI of P2X3 and NK1 receptor antagonists may improve the recovery of erectile function in a rat model with ED after spinal cord transection.
[Mh] Termos MeSH primário: Disfunção Erétil/etiologia
Antagonistas do Receptor de Neuroquinina-1/farmacologia
Ereção Peniana/efeitos dos fármacos
Pênis/efeitos dos fármacos
Fisalemina/análogos & derivados
Antagonistas do Receptor Purinérgico P2X/farmacologia
Traumatismos da Medula Espinal/complicações
Suramina/farmacologia
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Gânglios Espinais/metabolismo
Imuno-Histoquímica
Injeções
Masculino
Pênis/metabolismo
Fisalemina/farmacologia
Ratos
Ratos Sprague-Dawley
Receptores da Neurocinina-1/metabolismo
Receptores Purinérgicos P2X3/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Neurokinin-1 Receptor Antagonists); 0 (Purinergic P2X Receptor Antagonists); 0 (Receptors, Neurokinin-1); 0 (Receptors, Purinergic P2X3); 129623-01-4 (GR 82334); 2507-24-6 (Physalaemin); 6032D45BEM (Suramin)
[Em] Mês de entrada:1509
[Cu] Atualização por classe:150117
[Lr] Data última revisão:
150117
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140107
[St] Status:MEDLINE
[do] DOI:10.1111/and.12217


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[PMID]:24356854
[Au] Autor:Gozal D; Kim J; Bhattacharjee R; Goldman JL; Kheirandish-Gozal L
[Ad] Endereço:Section of Sleep Medicine, Department of Pediatrics, Pritzker School of Medicine, Biological Sciences Division, The University of Chicago, Chicago, IL.
[Ti] Título:Substance P and neurokinin 1 receptors as potential therapeutic targets in children with OSA.
[So] Source:Chest;145(5):1039-1045, 2014 May.
[Is] ISSN:1931-3543
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Increased substance P (SP) levels and abundant expression of neurokinin (NK) 1 receptor in adenotonsillar tissues of children with OSA but not recurrent tonsillar infection (RI) suggest that NK1 antagonists could be useful in treating OSA. METHODS: The effects of SP and the NK1 antagonist GR-82334 were examined on mixed cell cultures prepared from dissociated tonsils harvested intraoperatively from children with OSA and RI. Proliferation was assessed by [3H]-thymidine or 5-ethynyl-2'-deoxyuridine incorporation, and inflammatory cytokine production (tumor necrosis factor [TNF]-α, IL-6, IL-1ß) was assessed in supernatants by enzyme-linked immunosorbent assay. RESULTS: SP elicited dose-dependent increases in tonsillar cell proliferation in mixed cell cultures from children with OSA but not with RI (P < .0001). The NK1 antagonist exhibited dose-dependent reductions in cellular proliferative rates in OSA-derived cell cultures but not in RI-derived mixed cell cultures (P < .00001). SP treatment was associated with increased TNF-α and IL-6 production, and GR-82334 abrogated SP effects, as well as reduced basal cytokine release (P < .0001). CONCLUSIONS: SP pathways appear to underlie intrinsic proliferative and inflammatory signaling pathways in tonsillar tissues from children with OSA but not with RI. Selective disruption of these pathways may provide nonsurgical alternatives for prevention and treatment of pediatric OSA.
[Mh] Termos MeSH primário: Fisalemina/análogos & derivados
Receptores da Neurocinina-1/metabolismo
Apneia Obstrutiva do Sono/tratamento farmacológico
Substância P/metabolismo
[Mh] Termos MeSH secundário: Técnicas de Cultura de Células
Proliferação Celular/efeitos dos fármacos
Criança
Citocinas/metabolismo
Relação Dose-Resposta a Droga
Ensaio de Imunoadsorção Enzimática
Seres Humanos
Antagonistas do Receptor de Neuroquinina-1/uso terapêutico
Tonsila Palatina/efeitos dos fármacos
Tonsila Palatina/metabolismo
Tonsila Palatina/patologia
Fisalemina/administração & dosagem
Fisalemina/uso terapêutico
Receptores da Neurocinina-1/efeitos dos fármacos
Transdução de Sinais/efeitos dos fármacos
Apneia Obstrutiva do Sono/metabolismo
Apneia Obstrutiva do Sono/patologia
Substância P/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cytokines); 0 (Neurokinin-1 Receptor Antagonists); 0 (Receptors, Neurokinin-1); 129623-01-4 (GR 82334); 2507-24-6 (Physalaemin); 33507-63-0 (Substance P)
[Em] Mês de entrada:1406
[Cu] Atualização por classe:170603
[Lr] Data última revisão:
170603
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:131221
[St] Status:MEDLINE


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[PMID]:23666265
[Au] Autor:Zhang HP; Li CL; Lu P; Zheng JC; Yu LL; Yang WM; Xiong F; Zeng XY
[Ad] Endereço:Family Planning Research Institute, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, Hubei, China.
[Ti] Título:The function of P2X3 receptor and NK1 receptor antagonists on cyclophosphamide-induced cystitis in rats.
[So] Source:World J Urol;32(1):91-7, 2014 Feb.
[Is] ISSN:1433-8726
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:PURPOSE: The purpose of the study is to explore the function of P2X3 and NK1 receptors antagonists on cyclophosphamide (CYP)-induced cystitis in rats. METHODS: Sixty female Sprague-Dawley (SD) rats were randomly divided into three groups. The rats in the control group were intraperitoneally (i.p.) injected with 0.9% saline (4 ml/kg); the rats in the model group were i.p. injected with CYP (150 mg/kg); and the rats in the intervention group were i.p. injected with CYP with subsequently perfusion of bladder with P2X3 and NK1 receptors' antagonists, Suramin and GR 82334. Spontaneous pain behaviors following the administration of CYP were observed. Urodynamic parameters, bladder pressure-volume curve, maximum voiding pressure (MVP), and maximum cystometric capacity (MCC), were recorded. Pathological changes in bladder tissue were observed. Immunofluorescence was used to detect the expression of P2X3 and NK1 receptors in bladder. RESULTS: Cyclophosphamide treatment increased the spontaneous pain behaviors scores. The incidence of bladder instability during urine storage period of model group was significantly higher than intervention group (χ(2) = 7.619, P = 0.007) and control group (χ(2) = 13.755, P = 0.000). MCC in the model group was lower than the control and intervention groups (P < 0.01). Histological changes evident in model and intervention groups rats' bladder included edema, vasodilation, and infiltration of inflammatory cells. In model group, the expression of P2X3 receptor increased in urothelium and suburothelium, and NK1 receptor increased in suburothelium, while the expression of them in intervention group was lower. CONCLUSIONS: In CYP-induced cystitis, the expression of P2X3 and NK1 receptors increased in urothelium and/or suburothelium. Perfusion of bladder with P2X3 and NK1 receptors antagonists ameliorated the bladder function.
[Mh] Termos MeSH primário: Ciclofosfamida/efeitos adversos
Cistite/induzido quimicamente
Cistite/tratamento farmacológico
Antagonistas do Receptor de Neuroquinina-1/uso terapêutico
Fisalemina/análogos & derivados
Antagonistas do Receptor Purinérgico P2/uso terapêutico
Suramina/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Cistite/patologia
Modelos Animais de Doenças
Feminino
Antagonistas do Receptor de Neuroquinina-1/farmacologia
Dor/tratamento farmacológico
Fisalemina/farmacologia
Fisalemina/uso terapêutico
Antagonistas do Receptor Purinérgico P2/farmacologia
Ratos
Ratos Sprague-Dawley
Receptores da Neurocinina-1/efeitos dos fármacos
Receptores da Neurocinina-1/metabolismo
Receptores Purinérgicos P2X3/efeitos dos fármacos
Receptores Purinérgicos P2X3/metabolismo
Transdução de Sinais/efeitos dos fármacos
Transdução de Sinais/fisiologia
Suramina/farmacologia
Bexiga Urinária/efeitos dos fármacos
Bexiga Urinária/metabolismo
Bexiga Urinária/patologia
Micção/efeitos dos fármacos
Micção/fisiologia
Urodinâmica/efeitos dos fármacos
Urodinâmica/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Neurokinin-1 Receptor Antagonists); 0 (Purinergic P2 Receptor Antagonists); 0 (Receptors, Neurokinin-1); 0 (Receptors, Purinergic P2X3); 129623-01-4 (GR 82334); 2507-24-6 (Physalaemin); 6032D45BEM (Suramin); 8N3DW7272P (Cyclophosphamide)
[Em] Mês de entrada:1410
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130514
[St] Status:MEDLINE
[do] DOI:10.1007/s00345-013-1098-z


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[PMID]:22628076
[Au] Autor:Singh PK; Maji SK
[Ad] Endereço:Department of Biosciences and Bioengineering and Wadhwani Research Centre for Biosciences and Bioengineering, IIT Bombay, Powai, Mumbai 400076, India.
[Ti] Título:Amyloid-like fibril formation by tachykinin neuropeptides and its relevance to amyloid ß-protein aggregation and toxicity.
[So] Source:Cell Biochem Biophys;64(1):29-44, 2012 Sep.
[Is] ISSN:1559-0283
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Protein aggregation and amyloid formation are associated with both pathological conditions in humans such as Alzheimer's disease and native functions such as peptide hormone storage in the pituitary secretory granules in mammals. Here, we studied amyloid fibrils formation by three neuropeptides namely physalaemin, kassinin and substance P of tachykinin family using biophysical techniques including circular dichroism, thioflavin T, congo red binding and microscopy. All these neuropeptides under study have significant sequence similarity with Aß(25-35) that is known to form neurotoxic amyloids. We found that all these peptides formed amyloid-like fibrils in vitro in the presence of heparin, and these amyloids were found to be nontoxic in neuronal cells. However, the extent of amyloid formation, structural transition, and morphology were different depending on the primary sequences of peptide. When Aß(25-35) and Aß40 were incubated with each of these neuropeptides in 1:1 ratio, a drastic increase in amyloid growths were observed compared to that of individual peptides suggesting that co-aggregation of Aß and these neuropeptides. The electron micrographs of these co-aggregates were dissimilar when compared with individual peptide fibrils further supporting the possible incorporation of these neuropeptides in Aß amyloid fibrils. Further, the fibrils of these neuropeptides can seed the fibrils formation of Aß40 and reduced the toxicity of preformed Aß fibrils. The present study of amyloid formation by tachykinin neuropeptides is not only providing an understanding of the mechanism of amyloid fibril formation in general, but also offering plausible explanation that why these neuropeptide might reduce the cytotoxicity associated with Alzheimer's disease related amyloids.
[Mh] Termos MeSH primário: Peptídeos beta-Amiloides/química
Amiloide/química
Cassinina/química
Fragmentos de Peptídeos/química
Fisalemina/química
[Mh] Termos MeSH secundário: Algoritmos
Sequência de Aminoácidos
Amiloide/farmacologia
Amiloide/ultraestrutura
Peptídeos beta-Amiloides/ultraestrutura
Linhagem Celular Tumoral
Dicroísmo Circular
Vermelho Congo/química
Heparina/química
Seres Humanos
Cassinina/farmacologia
Microscopia Eletrônica
Neurônios/química
Neurônios/efeitos dos fármacos
Fragmentos de Peptídeos/ultraestrutura
Fisalemina/farmacologia
Ligação Proteica
Estrutura Secundária de Proteína
Substância P/química
Substância P/farmacologia
Tiazóis/química
Testes de Toxicidade/métodos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Amyloid); 0 (Amyloid beta-Peptides); 0 (Peptide Fragments); 0 (Thiazoles); 0 (amyloid beta-protein (25-35)); 2390-54-7 (thioflavin T); 2507-24-6 (Physalaemin); 33507-63-0 (Substance P); 3U05FHG59S (Congo Red); 63968-82-1 (Kassinin); 9005-49-6 (Heparin)
[Em] Mês de entrada:1212
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:120526
[St] Status:MEDLINE
[do] DOI:10.1007/s12013-012-9364-z


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[PMID]:21749865
[Au] Autor:Uematsu T; Sakai A; Ito H; Suzuki H
[Ad] Endereço:Department of Orthopedics, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku, Tokyo 113-8602, Japan. s7013@nms.ac.jp
[Ti] Título:Intra-articular administration of tachykinin NK1 receptor antagonists reduces hyperalgesia and cartilage destruction in the inflammatory joint in rats with adjuvant-induced arthritis.
[So] Source:Eur J Pharmacol;668(1-2):163-8, 2011 Oct 01.
[Is] ISSN:1879-0712
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Persistent pain associated with inflammatory arthritis is an aggravating factor that decreases patients' quality of life. Current therapies for joint pain have limited effectiveness and produce unwanted negative side effects. Although the involvement of substance P and its cognate tachykinin receptor, NK(1), in joint inflammation has been extensively documented through animal experiments, the development of oral tachykinin NK(1) receptor antagonists against arthritis-induced pain has been unsuccessful in humans to date. To explore the possibility of using tachykinin NK(1) receptor antagonists as local therapeutic agents for inflammatory arthritis, we examined the effects of tachykinin NK(1) receptor antagonists administered into the rat ankle joint on hyperalgesia in complete Freund's adjuvant (CFA)-induced inflammatory monoarthritis. Administration of the tachykinin NK(1) receptor antagonist WIN 51708 or GR 82334 into the affected ankle joint at day 3 following intra-articular CFA injection reduced the mechanical hyperalgesia 12 h after the tachykinin NK(1) receptor antagonist injection and their analgesic effects persisted for at least 2 days. Histological examinations revealed that intra-articular WIN 51708 reduced the CFA-induced destructive changes in the cartilage. These findings suggest that intra-articular injection of tachykinin NK(1) receptor antagonists is a promising strategy for relieving the hyperalgesia that occurs in inflammatory arthritis.
[Mh] Termos MeSH primário: Analgésicos/farmacologia
Articulação do Tornozelo
Artrite Experimental/complicações
Cartilagem/efeitos dos fármacos
Hiperalgesia/complicações
Hiperalgesia/tratamento farmacológico
Receptores de Taquicininas/antagonistas & inibidores
[Mh] Termos MeSH secundário: Analgésicos/administração & dosagem
Analgésicos/uso terapêutico
Androstanos/administração & dosagem
Androstanos/farmacologia
Androstanos/uso terapêutico
Animais
Benzimidazóis/administração & dosagem
Benzimidazóis/farmacologia
Benzimidazóis/uso terapêutico
Cartilagem/patologia
Adjuvante de Freund/efeitos adversos
Indometacina/administração & dosagem
Indometacina/farmacologia
Indometacina/uso terapêutico
Inflamação/complicações
Inflamação/tratamento farmacológico
Inflamação/patologia
Injeções Subcutâneas
Masculino
Fisalemina/administração & dosagem
Fisalemina/análogos & derivados
Fisalemina/farmacologia
Fisalemina/uso terapêutico
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Analgesics); 0 (Androstanes); 0 (Benzimidazoles); 0 (Receptors, Tachykinin); 0 (WIN 51708); 129623-01-4 (GR 82334); 2507-24-6 (Physalaemin); 9007-81-2 (Freund's Adjuvant); XXE1CET956 (Indomethacin)
[Em] Mês de entrada:1112
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:110714
[St] Status:MEDLINE
[do] DOI:10.1016/j.ejphar.2011.06.037


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[PMID]:20632396
[Au] Autor:Grace CR; Cowsik SM
[Ad] Endereço:School of Life Sciences, Jawaharlal Nehru University, New Delhi 110 067, India.
[Ti] Título:Solution conformation of non-mammalian tachykinin physalaemin in lipid micelles by nuclear magnetic resonance.
[So] Source:Biopolymers;96(3):252-9, 2011.
[Is] ISSN:0006-3525
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Physalaemin (PHY), a non-mammalian tachykinin, binds selectively to neurokinin-1 (NK1) receptor with high affinity. Both the aqueous and lipid-induced conformations of PHY have been studied using two-dimensional nuclear magnetic resonance techniques. These data show that in water PHY prefers to be in an extended conformation and that in the presence of perdeuterated dodecylphosphocholine micelles, a membrane model system, a helical conformation is observed from Pro4 to the C-terminus. Comparison of the structures ofPHYand other NK ligands along with structure activity studies reported on these peptide ligands suggests that helical backbone structural motif is necessary for the binding of these NK ligands to the various NK receptors. Furthermore, consensus in the structures of these ligands suggests that these ligands must be binding along the highly hydrophobic face of the helix that contains the important hydrophobic residues, Phe7, Leu10, and Met11, that are highly conserved in most of the ligands.
[Mh] Termos MeSH primário: Proteínas de Anfíbios/química
Micelas
Fosforilcolina/análogos & derivados
Fisalemina/química
[Mh] Termos MeSH secundário: Motivos de Aminoácidos
Proteínas de Anfíbios/metabolismo
Animais
Ressonância Magnética Nuclear Biomolecular
Fosforilcolina/química
Fisalemina/metabolismo
Ranidae
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Amphibian Proteins); 0 (Micelles); 107-73-3 (Phosphorylcholine); 2507-24-6 (Physalaemin); 53949-18-1 (dodecylphosphocholine)
[Em] Mês de entrada:1109
[Cu] Atualização por classe:110829
[Lr] Data última revisão:
110829
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:100716
[St] Status:MEDLINE
[do] DOI:10.1002/bip.21519


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[PMID]:20651096
[Au] Autor:Park CK; Bae JH; Kim HY; Jo HJ; Kim YH; Jung SJ; Kim JS; Oh SB
[Ad] Endereço:National Research Laboratory for Pain, Dental Research Institute and Department of Physiology, School of Dentistry, Seoul National University, 28-2 Yeongeon-Dong Chongno-Ku, Seoul 110-749, Republic of Korea.
[Ti] Título:Substance P sensitizes P2X3 in nociceptive trigeminal neurons.
[So] Source:J Dent Res;89(10):1154-9, 2010 Oct.
[Is] ISSN:1544-0591
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:UNLABELLED: Peripheral inflammation produces pain hypersensitivity by sensitizing nociceptors. Potentiation of P2X3 receptor activity in nociceptors may play an important role in this peripheral sensitization. However, we do not fully understand how P2X3 activity is elevated in inflammation. Thus, we investigated whether P2X3 activity in trigeminal nociceptive neurons is regulated by the neurokinin-1 (NK-1) receptor that is activated by an inflammatory mediator, substance P. Single-cell RT-PCR and immunohistochemistry revealed that NK-1 in nociceptive neurons was mainly co-expressed with P2X3. Ca(2+) imaging and whole-cell patch-clamp recordings indicated that both substance P and Sar-substance P, a selective NK-1 agonist, significantly potentiated α,ß-meATP-induced currents and [Ca(2+)](i) responses in nociceptive neurons. These potentiating effects were completely blocked by GR82334, a specific NK-1 antagonist. Our results demonstrate that substance P sensitizes P2X3 receptor through the activation of NK-1, thus warranting these receptors as possible targets for pain therapy in the orofacial region. ABBREVIATIONS: α,ß-methylene adenosine 5'-triphosphate (ATP), α,ß-meATP; neurokinin-1, NK-1; single-cell reverse-transcription polymerase chain-reaction, single-cell RT-PCR; [Sar(9),Met(O(2))(11)]-substance P, Sar-substance P.
[Mh] Termos MeSH primário: Neurônios/efeitos dos fármacos
Nociceptores/efeitos dos fármacos
Receptores Purinérgicos P2/efeitos dos fármacos
Substância P/farmacologia
Nervo Trigêmeo/efeitos dos fármacos
[Mh] Termos MeSH secundário: Trifosfato de Adenosina/análogos & derivados
Trifosfato de Adenosina/metabolismo
Animais
Animais Recém-Nascidos
Sinalização do Cálcio/efeitos dos fármacos
Citofotometria
Imuno-Histoquímica
Mediadores da Inflamação/farmacologia
Antagonistas do Receptor de Neuroquinina-1
Técnicas de Patch-Clamp
Fisalemina/análogos & derivados
Fisalemina/farmacologia
Ratos
Ratos Sprague-Dawley
Receptores da Neurocinina-1/agonistas
Receptores da Neurocinina-1/efeitos dos fármacos
Receptores Purinérgicos P2X3
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Substância P/análogos & derivados
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Inflammation Mediators); 0 (Neurokinin-1 Receptor Antagonists); 0 (Receptors, Neurokinin-1); 0 (Receptors, Purinergic P2); 0 (Receptors, Purinergic P2X3); 110880-55-2 (substance P, Sar(9)-Met(O2)(11)-); 129623-01-4 (GR 82334); 2507-24-6 (Physalaemin); 33507-63-0 (Substance P); 8L70Q75FXE (Adenosine Triphosphate); NYX13NT29D (alpha,beta-methyleneadenosine 5'-triphosphate)
[Em] Mês de entrada:1011
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:D; IM
[Da] Data de entrada para processamento:100724
[St] Status:MEDLINE
[do] DOI:10.1177/0022034510377094


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[PMID]:19958761
[Au] Autor:Shiina T; Shima T; Hirayama H; Kuramoto H; Takewaki T; Shimizu Y
[Ad] Endereço:Department of Basic Veterinary Science, Laboratory of Physiology, The United Graduated School of Veterinary Sciences, Gifu University, Yanagido, Gifu, Japan.
[Ti] Título:Contractile responses induced by physalaemin, an analogue of substance P, in the rat esophagus.
[So] Source:Eur J Pharmacol;628(1-3):202-6, 2010 Feb 25.
[Is] ISSN:1879-0712
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:We examined the effects of physalaemin, an agonist of tachykinin receptors, on mechanical responses in the rat esophagus to clarify possible regulatory roles of tachykinins in esophageal motility. Exogenous application of physalaemin caused tonic contractions in rat esophageal segments when tension was recorded in the longitudinal direction but not when tension was recorded in the circular direction. The physalaemin-evoked contractions were blocked by pretreatment with nifedipine, a blocker of L-type calcium channels in both striated and smooth muscle cells. However, tetrodotoxin, a blocker of voltage-dependent sodium channels in striated muscle cells and neurons, did not affect the physalaemin-induced contractions. These results indicate that physalaemin might induce contractile responses in longitudinal smooth muscle of the muscularis mucosa via direct actions on muscle cells but not on neurons. Although pretreatment with a tachykinin NK(1) receptor antagonist, N-acetyl-l-tryptophan 3,5-bis (trifluoromethyl) benzyl ester (L-732,138), did not significantly affect the physalaemin-evoked contractions in rat esophageal segments, a tachykinin NK(2) receptor antagonist, (S)-N-methyl-N[4-(4-acetylamino-4-phenylpiperidino)-2-(3,4-dichlorophenyl) butyl] benzamide (SR48968), and a tachykinin NK(3) receptor antagonist, (S)-(N)-(1-(3-(1-benzoyl-3-(3,4-dichlorophenyl) piperidin-3-yl)propyl)-4-phenylpiperidin-4-yl)-N-methylacetamide (SR142801), significantly inhibited the physalaemin-evoked contractions. These results suggest that tachykinins can activate longitudinal contraction of smooth muscle in the muscularis mucosa, mediated via tachykinin NK(2) and NK(3) receptors on muscle cells, in the rat esophagus.
[Mh] Termos MeSH primário: Esôfago/efeitos dos fármacos
Esôfago/fisiologia
Contração Muscular/efeitos dos fármacos
Fisalemina/farmacologia
Substância P/análogos & derivados
[Mh] Termos MeSH secundário: Animais
Atropina/farmacologia
Esôfago/metabolismo
Masculino
Membrana Mucosa/efeitos dos fármacos
Membrana Mucosa/metabolismo
Membrana Mucosa/fisiologia
Tono Muscular/efeitos dos fármacos
Músculo Liso/efeitos dos fármacos
Músculo Liso/metabolismo
Músculo Liso/fisiologia
Músculo Estriado/efeitos dos fármacos
Músculo Estriado/metabolismo
Músculo Estriado/fisiologia
Nifedipino/farmacologia
Fisalemina/análogos & derivados
Ratos
Ratos Wistar
Receptores de Taquicininas/agonistas
Receptores de Taquicininas/antagonistas & inibidores
Receptores de Taquicininas/metabolismo
Tetrodotoxina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Receptors, Tachykinin); 2507-24-6 (Physalaemin); 33507-63-0 (Substance P); 4368-28-9 (Tetrodotoxin); 7C0697DR9I (Atropine); I9ZF7L6G2L (Nifedipine)
[Em] Mês de entrada:1004
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:091205
[St] Status:MEDLINE
[do] DOI:10.1016/j.ejphar.2009.11.039


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[PMID]:19446555
[Au] Autor:Ko JA; Yanai R; Nishida T
[Ad] Endereço:Department of Ophthalmology, Yamaguchi University Graduate School of Medicine, Ube City, Yamaguchi, Japan. jiae0831@yamaguchi-u.ac.jp
[Ti] Título:Up-regulation of ZO-1 expression and barrier function in cultured human corneal epithelial cells by substance P.
[So] Source:FEBS Lett;583(12):2148-53, 2009 Jun 18.
[Is] ISSN:1873-3468
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The effects of the sensory neurotransmitter substance P on the expression of tight junction proteins and on barrier function in human corneal epithelial cells were investigated. The expression of ZO-1, but not that of occludin or claudin-1, was increased by substance P in a concentration- and time-dependent manner. This effect was inhibited by the NK-1 receptor antagonist GR82334 and by KN62, an inhibitor of Ca(2+)- and calmodulin-dependent protein kinase II. Substance P also increased the transepithelial electrical resistance of a cell monolayer in a manner sensitive to GR82334. Substance P may therefore play a role in maintenance of tight junctions in the corneal epithelium.
[Mh] Termos MeSH primário: Epitélio Anterior/efeitos dos fármacos
Epitélio Anterior/metabolismo
Proteínas de Membrana/genética
Proteínas de Membrana/metabolismo
Fosfoproteínas/genética
Fosfoproteínas/metabolismo
Substância P/farmacologia
[Mh] Termos MeSH secundário: 1-(5-Isoquinolinasulfonil)-2-Metilpiperazina/análogos & derivados
1-(5-Isoquinolinasulfonil)-2-Metilpiperazina/farmacologia
Sequência de Bases
Proteína Quinase Tipo 2 Dependente de Cálcio-Calmodulina/antagonistas & inibidores
Células Cultivadas
Claudina-1
Primers do DNA/genética
Impedância Elétrica
Epitélio Anterior/citologia
Seres Humanos
Antagonistas do Receptor de Neuroquinina-1
Ocludina
Fisalemina/análogos & derivados
Fisalemina/farmacologia
Substância P/metabolismo
Junções Íntimas/efeitos dos fármacos
Junções Íntimas/metabolismo
Regulação para Cima/efeitos dos fármacos
Proteína da Zônula de Oclusão-1
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CLDN1 protein, human); 0 (Claudin-1); 0 (DNA Primers); 0 (Membrane Proteins); 0 (Neurokinin-1 Receptor Antagonists); 0 (OCLN protein, human); 0 (Occludin); 0 (Phosphoproteins); 0 (TJP1 protein, human); 0 (Zonula Occludens-1 Protein); 129623-01-4 (GR 82334); 2507-24-6 (Physalaemin); 33507-63-0 (Substance P); 63HM46XPOW (KN 62); 84477-87-2 (1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine); EC 2.7.11.17 (Calcium-Calmodulin-Dependent Protein Kinase Type 2)
[Em] Mês de entrada:0907
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:090519
[St] Status:MEDLINE
[do] DOI:10.1016/j.febslet.2009.05.010


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[PMID]:19165819
[Au] Autor:Smaniotto A; Bertazzo A; Comai S; Traldi P
[Ad] Endereço:Consiglio Nazionale delle Ricerche, ISTM, Corso Stati Uniti, 4, 35127 Padova, Italy.
[Ti] Título:The role of peptides and proteins in melanoidin formation.
[So] Source:J Mass Spectrom;44(3):410-8, 2009 Mar.
[Is] ISSN:1096-9888
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:High-molecular-weight (HMW) coloured compounds called melanoidins are widely distributed, particularly in foods. It has been proposed that they originate through the Maillard reaction, a non-enzymatic browning reaction, due to the interaction between protein or peptide amino groups and carbohydrates. The melanoidin structure is not definitively known, and they have been generally defined as HMW nitrogen-containing brown polymers.In order to gain information on the nature of melanoidins, a simple in vitro model was chosen to investigate the products of the reactions between sugars and peptide/proteins. This approach would elucidate whether melanoidin formation is due to the binding of different sugar units to a peptide/protein or vice versa. With this aim, the reactivity of two different peptides, EPK177 and physalaemin, and a low-molecular-weight (LMW) protein, lysozyme, was tested towards different saccharides (glucose, maltotriose (MT), maltopentaose and dextran 1000) in aqueous solutions at different temperatures. The incubation mixtures were analysed at different reaction times by MALDI/MS. Furthermore, in order to verify the possible role of sugar pyrolysis products in melanoidin formation, the products arising from the thermal treatment at 200 degrees C of MT were incubated with lysozyme, and the reaction products were analysed by the same MS approach.The obtained results allowed the establishment of some general views: melanoidins cannot simply originate by reactions of sugar moieties with proteins. In fact, the reaction easily occurs, but it does not lead to any coloured product, as melanoidins have been described to be; melanoidins cannot originate from the thermal degradation products of glycated proteins. In fact, the thermal treatment of glycated lysozyme leads to a severe degradation of the protein with the formation of LMW species, far from the view of melanoidins as HMW compounds; experimental evidence has been gained on the melanoidin formation through reaction of intact protein with the pyrolysis products of MT. This hypothesis has been supported either from MALDI measurements or from spectroscopic data that show an absorption band in the range 300-600 nm, typical of melanoidins.
[Mh] Termos MeSH primário: Oligossacarídeos/química
Peptídeos/química
Polímeros/química
Proteínas/química
Espectrometria de Massas por Ionização e Dessorção a Laser Assistida por Matriz
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Galinhas
Dextranos/química
Dextranos/metabolismo
Glucose/química
Glucose/metabolismo
Modelos Químicos
Dados de Sequência Molecular
Muramidase/química
Muramidase/metabolismo
Oligossacarídeos/metabolismo
Peptídeos/metabolismo
Fisalemina/química
Fisalemina/metabolismo
Polímeros/metabolismo
Proteínas/metabolismo
Temperatura Ambiente
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Dextrans); 0 (Oligosaccharides); 0 (Peptides); 0 (Polymers); 0 (Proteins); 0 (melanoidin polymers); 2507-24-6 (Physalaemin); EC 3.2.1.17 (Muramidase); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:0908
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:090124
[St] Status:MEDLINE
[do] DOI:10.1002/jms.1519



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