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[PMID]:28536272
[Au] Autor:Manninen S; Tuominen L; Dunbar RI; Karjalainen T; Hirvonen J; Arponen E; Hari R; Jääskeläinen IP; Sams M; Nummenmaa L
[Ad] Endereço:Turku PET Centre, University of Turku, 20520 Turku, Finland.
[Ti] Título:Social Laughter Triggers Endogenous Opioid Release in Humans.
[So] Source:J Neurosci;37(25):6125-6131, 2017 Jun 21.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The size of human social networks significantly exceeds the network that can be maintained by social grooming or touching in other primates. It has been proposed that endogenous opioid release after social laughter would provide a neurochemical pathway supporting long-term relationships in humans (Dunbar, 2012), yet this hypothesis currently lacks direct neurophysiological support. We used PET and the µ-opioid-receptor (MOR)-specific ligand [ C]carfentanil to quantify laughter-induced endogenous opioid release in 12 healthy males. Before the social laughter scan, the subjects watched laughter-inducing comedy clips with their close friends for 30 min. Before the baseline scan, subjects spent 30 min alone in the testing room. Social laughter increased pleasurable sensations and triggered endogenous opioid release in thalamus, caudate nucleus, and anterior insula. In addition, baseline MOR availability in the cingulate and orbitofrontal cortices was associated with the rate of social laughter. In a behavioral control experiment, pain threshold-a proxy of endogenous opioidergic activation-was elevated significantly more in both male and female volunteers after watching laughter-inducing comedy versus non-laughter-inducing drama in groups. Modulation of the opioidergic activity by social laughter may be an important neurochemical pathway that supports the formation, reinforcement, and maintenance of human social bonds. Social contacts are vital to humans. The size of human social networks significantly exceeds the network that can be maintained by social grooming in other primates. Here, we used PET to show that endogenous opioid release after social laughter may provide a neurochemical mechanism supporting long-term relationships in humans. Participants were scanned twice: after a 30 min social laughter session and after spending 30 min alone in the testing room (baseline). Endogenous opioid release was stronger after laughter versus the baseline scan. Opioid receptor density in the frontal cortex predicted social laughter rates. Modulation of the opioidergic activity by social laughter may be an important neurochemical mechanism reinforcing and maintaining social bonds between humans.
[Mh] Termos MeSH primário: Química Encefálica/fisiologia
Endorfinas/metabolismo
Riso/fisiologia
Meio Social
[Mh] Termos MeSH secundário: Adulto
Mapeamento Encefálico
Feminino
Seres Humanos
Masculino
Apego ao Objeto
Prazer
Tomografia por Emissão de Pósitrons
Receptores Opioides mu/efeitos dos fármacos
Receptores Opioides mu/metabolismo
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Endorphins); 0 (OPRM1 protein, human); 0 (Receptors, Opioid, mu)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170814
[Lr] Data última revisão:
170814
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170525
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.0688-16.2017


  2 / 10019 MEDLINE  
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[PMID]:27744679
[Au] Autor:Johnson TA; Milan-Lobo L; Che T; Ferwerda M; Lambu E; McIntosh NL; Li F; He L; Lorig-Roach N; Crews P; Whistler JL
[Ad] Endereço:Department of Chemistry and Biochemistry, University of California , Santa Cruz, California 95064, United States.
[Ti] Título:Identification of the First Marine-Derived Opioid Receptor "Balanced" Agonist with a Signaling Profile That Resembles the Endorphins.
[So] Source:ACS Chem Neurosci;8(3):473-485, 2017 Mar 15.
[Is] ISSN:1948-7193
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Opioid therapeutics are excellent analgesics, whose utility is compromised by dependence. Morphine (1) and its clinically relevant derivatives such as OxyContin (2), Vicodin (3), and Dilaudid (4) are "biased" agonists at the µ opioid receptor (OR), wherein they engage G protein signaling but poorly engage ß-arrestin and the endocytic machinery. In contrast, endorphins, the endogenous peptide agonists for ORs, are potent analgesics, show reduced liability for tolerance and dependence, and engage both G protein and ß-arrestin pathways as "balanced" agonists. We set out to determine if marine-derived alkaloids could serve as novel OR agonist chemotypes with a signaling profile distinct from morphine and more similar to the endorphins. Screening of 96 sponge-derived extracts followed by LC-MS-based purification to pinpoint the active compounds and subsequent evaluation of a mini library of related alkaloids identified two structural classes that modulate the ORs. These included the following: aaptamine (10), 9-demethyl aaptamine (11), demethyl (oxy)-aaptamine (12) with activity at the δ-OR (EC : 5.1, 4.1, 2.3 µM, respectively) and fascaplysin (17), and 10-bromo fascaplysin (18) with activity at the µ-OR (EC : 6.3, 4.2 µM respectively). An in vivo evaluation of 10 using δ-KO mice indicated its previously reported antidepressant-like effects are dependent on the δ-OR. Importantly, 17 functioned as a balanced agonist promoting both G protein signaling and ß-arrestin recruitment along with receptor endocytosis similar to the endorphins. Collectively these results demonstrate the burgeoning potential for marine natural products to serve as novel lead compounds for therapeutic targets in neuroscience research.
[Mh] Termos MeSH primário: Analgésicos Opioides
Endorfinas/farmacologia
Naftiridinas
Receptores Opioides delta/metabolismo
Transdução de Sinais/efeitos dos fármacos
[Mh] Termos MeSH secundário: Analgésicos Opioides/química
Analgésicos Opioides/isolamento & purificação
Analgésicos Opioides/farmacologia
Animais
Simulação por Computador
AMP Cíclico/metabolismo
Endocitose/efeitos dos fármacos
Endorfinas/química
Proteínas de Ligação ao GTP/metabolismo
Células HEK293
Seres Humanos
Indóis/química
Indóis/isolamento & purificação
Indóis/farmacologia
Locomoção/efeitos dos fármacos
Locomoção/genética
Masculino
Camundongos
Camundongos Transgênicos
Modelos Moleculares
Naftiridinas/química
Naftiridinas/isolamento & purificação
Naftiridinas/farmacologia
Poríferos/química
Receptores Opioides delta/genética
Transdução de Sinais/genética
Espectrometria de Massas por Ionização por Electrospray
Natação/psicologia
beta-Arrestinas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Analgesics, Opioid); 0 (Endorphins); 0 (Indoles); 0 (Naphthyridines); 0 (Receptors, Opioid, delta); 0 (beta-Arrestins); 114719-57-2 (fascaplysine); E0399OZS9N (Cyclic AMP); EC 3.6.1.- (GTP-Binding Proteins); FGW9D01COE (aaptamine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171025
[Lr] Data última revisão:
171025
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161018
[St] Status:MEDLINE
[do] DOI:10.1021/acschemneuro.6b00167


  3 / 10019 MEDLINE  
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[PMID]:27664661
[Au] Autor:Cattaneo S; Stuknyte M; Masotti F; De Noni I
[Ad] Endereço:Dipartimento di Scienze per gli Alimenti, la Nutrizione e l'Ambiente, Università degli Studi di Milano, via G. Celoria 2, 20133 Milan, Italy. Electronic address: stefano.cattaneo@unimi.it.
[Ti] Título:Protein breakdown and release of ß-casomorphins during in vitro gastro-intestinal digestion of sterilised model systems of liquid infant formula.
[So] Source:Food Chem;217:476-482, 2017 Feb 15.
[Is] ISSN:0308-8146
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Protein modifications occurring during sterilisation of infant formulas can affect protein digestibility and release of bioactive peptides. The effect of glycation and cross-linking on protein breakdown and release of ß-casomorphins was evaluated during in vitro gastro-intestinal digestion (GID) of six sterilised model systems of infant formula. Protein degradation during in vitro GID was evaluated by SDS-PAGE and by measuring the nitrogen content of ultrafiltration (3kDa) permeates before and after in vitro GID of model IFs. Glycation strongly hindered protein breakdown, whereas cross-linking resulting from ß-elimination reactions had a negligible effect. Only ß-casomorphin 7 (ß-CM7) was detected (0.187-0.858mgL(-1)) at the end of the intestinal digestion in all untreated IF model systems. The level of ß-CM7 in the sterilised model systems prepared without addition of sugars ranged from 0.256 to 0.655mgL(-1). The release of this peptide during GID was hindered by protein glycation.
[Mh] Termos MeSH primário: Digestão/fisiologia
Endorfinas/metabolismo
Fórmulas Infantis
Esterilização/métodos
[Mh] Termos MeSH secundário: Eletroforese em Gel de Poliacrilamida
Seres Humanos
Lactente
Modelos Biológicos
Fragmentos de Peptídeos/metabolismo
Peptídeos/metabolismo
Proteólise
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Endorphins); 0 (Peptide Fragments); 0 (Peptides); 72122-62-4 (beta-casomorphin 7); 79805-24-6 (beta-casomorphins)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:170902
[Lr] Data última revisão:
170902
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160925
[St] Status:MEDLINE


  4 / 10019 MEDLINE  
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[PMID]:27784644
[Au] Autor:Zhang J; He C; Pi X; Wang Y; Zhou L; Dong S
[Ad] Endereço:Institute of Biochemistry and Molecular Biology, School of Life Sciences, 222 Tianshui South Road, Lanzhou 730000, China.
[Ti] Título:MCRT, a chimeric peptide based on morphiceptin and PFRTic-NH , regulates the depressor effects induced by endokinin A/B.
[So] Source:Eur J Pharmacol;792:33-37, 2016 Dec 05.
[Is] ISSN:1879-0712
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The interactions of the chimeric peptide MCRT (YPFPFRTic-NH ), based on morphiceptin and neuropeptide FF derivative PFRTic-NH , on the effects of endokinin A/B (EKA/B) on mean arterial blood pressure of the urethane-anaesthetized rat have been investigated in the absence and presence of tachykinin receptor antagonists, naloxone and NO synthase inhibitors. While MCRT produced dose dependent decreases in mean arterial pressure, in its presence only a small but statistically insignificant decreases in the magnitude and the time course of the depressor effect of EKA/B (10nmol/kg) were observed. MCRT had little influence on the depressor effect of EKA/B (1 nmol/kg), but strongly potentiated that of EKA/B (100nmol/kg). The tachykinin NK receptor antagonist SR140333B (1mg/kg) and the NK antagonist SR142891 (2.79mg/kg) both reduced the hypotensive effects of EKA/B and MCRT alone and blocked those of the two peptides in combination. The NK antagonist GR159897 (4mg/kg) partially blocked the depressor effects of EKA/B and MCRT alone. Naloxone (2mg/kg) completely blocked the depressor effect of MCTR, but partially blocked that of EKA/B. The NO synthase inhibitor l-NAME (50mg/kg) partially blocked the depressor effects of EKA/B, MCRT, and EKA/B + MCRT. These results could help to better understand the role of tachykinin receptors, opioid receptors and neuropeptide FF receptors in cardiovascular system.
[Mh] Termos MeSH primário: Sistema Cardiovascular/efeitos dos fármacos
Endorfinas/química
Endorfinas/farmacologia
Oligopeptídeos/química
Taquicininas/farmacologia
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Relação Dose-Resposta a Droga
Indóis/farmacologia
Masculino
Óxido Nítrico Sintase/antagonistas & inibidores
Piperidinas/farmacologia
Ratos
Ratos Wistar
Receptores de Neuropeptídeos/metabolismo
Receptores Opioides/metabolismo
Receptores de Taquicininas/antagonistas & inibidores
Tropanos/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Endorphins); 0 (GR 159897); 0 (Indoles); 0 (Oligopeptides); 0 (Piperidines); 0 (Receptors, Neuropeptide); 0 (Receptors, Opioid); 0 (Receptors, Tachykinin); 0 (SR 142801); 0 (SR140333B); 0 (Tachykinins); 0 (Tropanes); 0 (neuropeptide FF receptor); 97TZA8ANPC (morphiceptin); 99566-27-5 (phenylalanyl-leucyl-phenylalanyl-glutaminyl-prolyl-glutaminyl-arginyl-phenylalaninamide); EC 1.14.13.39 (Nitric Oxide Synthase)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170321
[Lr] Data última revisão:
170321
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161107
[St] Status:MEDLINE


  5 / 10019 MEDLINE  
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[PMID]:27662391
[Au] Autor:Wang R; Wang J; Xue Q; Tan L; Cai J; Wang H
[Ad] Endereço:Key Laboratory of Marine Chemistry Theory and Technology, Ministry of Education, Ocean University of China, Qingdao 266100, China.
[Ti] Título:Preliminary analysis of allelochemicals produced by the diatom Phaeodactylum tricornutum.
[So] Source:Chemosphere;165:298-303, 2016 Dec.
[Is] ISSN:1879-1298
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Marine diatom Phaeodactylum tricornutum is known to exude allelochemicals with negative effects on Heterosigma akashiwo according to our previous study, while the information about the allelochemical compounds remains unknown. The present study dealt with isolation and analysis of the active substances released by P. tricornutum into the culture medium. Filtrate of P. tricornutum was extracted using ethyl acetate and chloroform respectively. The anti-algal fractions were isolated using high performance liquid chromatography (HPLC) and screened using activity-guided fraction methods. Results demonstrated that fraction â…¡ and â…¥ showed significant allelopathic effect on H. akashiwo growth. Then the anti-algal activity fractions were analyzed preliminary using gas chromatography-mass spectrometry (GC-MS) and high performance liquid chromatography-electrospray time-of-flight mass spectrometry (HPLC-ESI-TOF-MS). An active compound was derived from fraction â…¥ with the molecular weight of 578 and possible molecular formula of C H N O , which was speculated to be TYR-PRO-PHE-PRO-GLY-NH . a kind of glycinamides.
[Mh] Termos MeSH primário: Diatomáceas/metabolismo
Dinoflagelados/efeitos dos fármacos
Endorfinas/análise
Fragmentos de Peptídeos/análise
Feromônios/análise
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Cromatografia Líquida de Alta Pressão
Diatomáceas/química
Endorfinas/metabolismo
Cromatografia Gasosa-Espectrometria de Massas
Peso Molecular
Fragmentos de Peptídeos/metabolismo
Feromônios/metabolismo
Espectrometria de Massas por Ionização por Electrospray
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Endorphins); 0 (Peptide Fragments); 0 (Pheromones); 72122-63-5 (beta-casomorphin 5)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:171008
[Lr] Data última revisão:
171008
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160924
[St] Status:MEDLINE


  6 / 10019 MEDLINE  
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[PMID]:27611101
[Au] Autor:Trivedi M; Zhang Y; Lopez-Toledano M; Clarke A; Deth R
[Ad] Endereço:Department of Pharmaceutical Sciences, Nova Southeastern University, 3200 South University Drive, Fort Lauderdale, FL, USA. Electronic address: mtrivedi@nova.edu.
[Ti] Título:Differential neurogenic effects of casein-derived opioid peptides on neuronal stem cells: implications for redox-based epigenetic changes.
[So] Source:J Nutr Biochem;37:39-46, 2016 11.
[Is] ISSN:1873-4847
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Food-derived peptides, such as ß-casomorphin BCM7, have potential to cross the gastrointestinal tract and blood-brain barrier and are associated with neurological disorders and neurodevelopmental disorders. We previously established a novel mechanism through which BCM7 affects the antioxidant levels in neuronal cells leading to inflammatory consequences. In the current study, we elucidated the effects of casein-derived peptides on neuronal development by using the neurogenesis of neural stem cells (NSCs) as an experimental model. First, the transient changes in intracellular thiol metabolites during NSC differentiation (neurogenesis) were investigated. Next, the neurogenic effects of food-derived opioid peptides were measured, along with changes in intracellular thiol metabolites, redox status and global DNA methylation levels. We observed that the neurogenesis of NSCs was promoted by human BCM7 to a greater extent, followed by A2-derived BCM9 in contrast to bovine BCM7, which induced increased astrocyte formation. The effect was most apparent when human BCM7 was administered for 1day starting on 3days postplating, consistent with immunocytochemistry. Furthermore, neurogenic changes regulated by bovine BCM7 and morphine were associated with an increase in the glutathione/glutathione disulfide ratio and a decrease in the S-adenosylmethionine/S-adenosylhomocysteine ratio, indicative of changes in the redox and the methylation states. Finally, bovine BCM7 and morphine decreased DNA methylation in differentiating NSCs. In conclusion, these results suggest that food-derived opioid peptides and morphine regulated neurogenesis and differentiation of NSCs through changes in the redox state and epigenetic regulation.
[Mh] Termos MeSH primário: Caseínas/metabolismo
Metilação de DNA
Endorfinas/metabolismo
Epigênese Genética
Células-Tronco Neurais/metabolismo
Neurogênese
Peptídeos Opioides/metabolismo
Fragmentos de Peptídeos/metabolismo
[Mh] Termos MeSH secundário: Analgésicos Opioides/farmacologia
Animais
Apoptose/efeitos dos fármacos
Astrócitos/citologia
Astrócitos/efeitos dos fármacos
Astrócitos/imunologia
Astrócitos/metabolismo
Caseínas/efeitos adversos
Caseínas/química
Bovinos
Proliferação Celular/efeitos dos fármacos
Células Cultivadas
Metilação de DNA/efeitos dos fármacos
Endorfinas/efeitos adversos
Endorfinas/química
Epigênese Genética/efeitos dos fármacos
Glutationa/química
Glutationa/metabolismo
Seres Humanos
Metilação
Morfina/farmacologia
Células-Tronco Neurais/citologia
Células-Tronco Neurais/efeitos dos fármacos
Células-Tronco Neurais/imunologia
Neurogênese/efeitos dos fármacos
Peptídeos Opioides/efeitos adversos
Peptídeos Opioides/química
Oxirredução
Fragmentos de Peptídeos/efeitos adversos
Fragmentos de Peptídeos/química
Processamento de Proteína Pós-Traducional
S-Adenosil-Homocisteína/química
S-Adenosil-Homocisteína/metabolismo
S-Adenosilmetionina/química
S-Adenosilmetionina/metabolismo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Analgesics, Opioid); 0 (Caseins); 0 (Endorphins); 0 (Opioid Peptides); 0 (Peptide Fragments); 72122-62-4 (beta-casomorphin 7); 76I7G6D29C (Morphine); 79805-24-6 (beta-casomorphins); 7LP2MPO46S (S-Adenosylmethionine); 979-92-0 (S-Adenosylhomocysteine); GAN16C9B8O (Glutathione)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171109
[Lr] Data última revisão:
171109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160910
[St] Status:MEDLINE


  7 / 10019 MEDLINE  
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[PMID]:27410528
[Au] Autor:Pain S
[Ti] Título:Painful progress.
[So] Source:Nature;535(7611):S18-9, 2016 07 14.
[Is] ISSN:1476-4687
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Manejo da Dor/história
Dor/história
[Mh] Termos MeSH secundário: Anestesia/história
Anestesia/métodos
Animais
Aspirina/história
Encéfalo/patologia
Encéfalo/fisiopatologia
Cocaína/administração & dosagem
Cocaína/história
Cocaína/uso terapêutico
Síndromes da Dor Regional Complexa/história
Cárie Dentária/história
Cárie Dentária/terapia
Terapia por Estimulação Elétrica/história
Endorfinas/história
Endorfinas/metabolismo
Feminino
História do Século XVII
História do Século XVIII
História do Século XIX
História do Século XX
História do Século XXI
História Antiga
Seres Humanos
Hyoscyamus
Isoquinolinas/história
Isoquinolinas/metabolismo
Masculino
Camundongos
Microglia/fisiologia
Modelos Psicológicos
Morfina/história
Morfina/farmacologia
Morfina/uso terapêutico
Bloqueio Nervoso/história
Neuroimagem/história
Óxido Nitroso/administração & dosagem
Óxido Nitroso/história
Óxido Nitroso/farmacologia
Nociceptores/metabolismo
Ópio/história
Dor/fisiopatologia
Receptores Dopaminérgicos/metabolismo
Caracteres Sexuais
Punção Espinal
Linfócitos T/fisiologia
[Pt] Tipo de publicação:HISTORICAL ARTICLE; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Endorphins); 0 (Isoquinolines); 0 (Receptors, Dopamine); 0 (dehydrocorybulbine); 76I7G6D29C (Morphine); 8008-60-4 (Opium); I5Y540LHVR (Cocaine); K50XQU1029 (Nitrous Oxide); R16CO5Y76E (Aspirin)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:161216
[Lr] Data última revisão:
161216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160714
[St] Status:MEDLINE
[do] DOI:10.1038/535S18a


  8 / 10019 MEDLINE  
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[PMID]:27410526
[Au] Autor:Marchant J
[Ti] Título:Placebos: Honest fakery.
[So] Source:Nature;535(7611):S14-5, 2016 07 14.
[Is] ISSN:1476-4687
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Dor Crônica/tratamento farmacológico
Dor Crônica/psicologia
Efeito Placebo
Placebos/uso terapêutico
[Mh] Termos MeSH secundário: Apomorfina/administração & dosagem
Apomorfina/uso terapêutico
Condicionamento (Psicologia)/efeitos dos fármacos
Condicionamento (Psicologia)/fisiologia
Dopamina/metabolismo
Endocanabinoides/metabolismo
Endorfinas/metabolismo
Endorfinas/secreção
Seres Humanos
Síndrome do Intestino Irritável/tratamento farmacológico
Síndrome do Intestino Irritável/psicologia
Imagem por Ressonância Magnética
Doença de Parkinson/tratamento farmacológico
Doença de Parkinson/psicologia
Placebos/administração & dosagem
Placebos/farmacologia
Prostaglandinas/metabolismo
Receptores Opioides/metabolismo
Autorrelato
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Endocannabinoids); 0 (Endorphins); 0 (Placebos); 0 (Prostaglandins); 0 (Receptors, Opioid); N21FAR7B4S (Apomorphine); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:161216
[Lr] Data última revisão:
161216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160714
[St] Status:MEDLINE
[do] DOI:10.1038/535S14a


  9 / 10019 MEDLINE  
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[PMID]:27382769
[Au] Autor:Wang K; Han D; Zhang Y; Rong C; Zhang Y
[Ti] Título:[Protective effect and mechanism of ß-CM7 on renin angiotensin system & diabetic cardiomyopathy].
[So] Source:Sheng Wu Gong Cheng Xue Bao;32(2):195-203, 2016 Feb.
[Is] ISSN:1000-3061
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:This article aimed at exploring the effects and protective mechanism of ß-CM7 on renin angiotensin system (RAS) in diabetic rats myocardial tissue. We divided 32 male SD rats into 4 groups: control group, diabetic model control group, insulin (3.7x10(-8) mol/d) treatment group and ß-CM7 (7.5x10(-8) mol/d) treatment group. After 30 days, all rats were decapitated and myocardical tissues were collected immediately. After injection, ß-CM7 could decrease the content of Ang II, increase the content of Angl-7. And ß-CM7 could improve the mRNA of AT1 receptor and Mas receptor. ß-CM7 also could improve the mRNA of ACE and ACE2, enhance the activity of ACE and ACE2. These data confirmed tli ß-CM7 could activate ACE2-Angl-7-Mas axis, negative passage in RAS, to inhibit the expression ACE mnRiJA and protein in rat myocardium, alleviate the myocardial tissue damage induced by Ang II. The effect of ß-CM7 on inhibiting myocardium damage might be related to ACE/ACE2 passageway.
[Mh] Termos MeSH primário: Cardiomiopatias Diabéticas/tratamento farmacológico
Endorfinas/farmacologia
Fragmentos de Peptídeos/farmacologia
Sistema Renina-Angiotensina
[Mh] Termos MeSH secundário: Angiotensina II/metabolismo
Animais
Diabetes Mellitus Experimental/tratamento farmacológico
Masculino
Miocárdio/metabolismo
Miocárdio/patologia
Peptidil Dipeptidase A/metabolismo
RNA Mensageiro
Ratos
Ratos Sprague-Dawley
Receptor Tipo 1 de Angiotensina/metabolismo
Receptores Acoplados a Proteínas-G/metabolismo
[Pt] Tipo de publicação:ENGLISH ABSTRACT; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Endorphins); 0 (Peptide Fragments); 0 (RNA, Messenger); 0 (Receptor, Angiotensin, Type 1); 0 (Receptors, G-Protein-Coupled); 11128-99-7 (Angiotensin II); 72122-62-4 (beta-casomorphin 7); EC 3.4.15.1 (Peptidyl-Dipeptidase A)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:160706
[Lr] Data última revisão:
160706
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160708
[St] Status:MEDLINE


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[PMID]:27365337
[Au] Autor:Lay J; Carbone SE; DiCello JJ; Bunnett NW; Canals M; Poole DP
[Ad] Endereço:Monash Institute of Pharmaceutical Sciences, Monash University, Parkville, Victoria, Australia;
[Ti] Título:Distribution and trafficking of the µ-opioid receptor in enteric neurons of the guinea pig.
[So] Source:Am J Physiol Gastrointest Liver Physiol;311(2):G252-66, 2016 Aug 01.
[Is] ISSN:1522-1547
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The µ-opioid receptor (MOR) is a major regulator of gastrointestinal motility and secretion and mediates opiate-induced bowel dysfunction. Although MOR is of physiological and therapeutic importance to gut function, the cellular and subcellular distribution and regulation of MOR within the enteric nervous system are largely undefined. Herein, we defined the neurochemical coding of MOR-expressing neurons in the guinea pig gut and examined the effects of opioids on MOR trafficking and regulation. MOR expression was restricted to subsets of enteric neurons. In the stomach MOR was mainly localized to nitrergic neurons (∼88%), with some overlap with neuropeptide Y (NPY) and no expression by cholinergic neurons. These neurons are likely to have inhibitory motor and secretomotor functions. MOR was restricted to noncholinergic secretomotor neurons (VIP-positive) of the ileum and distal colon submucosal plexus. MOR was mainly detected in nitrergic neurons of the colon (nitric oxide synthase positive, 87%), with some overlap with choline acetyltransferase (ChAT). No expression of MOR by intrinsic sensory neurons was detected. [d-Ala(2), MePhe(4), Gly(ol)(5)]enkephalin (DAMGO), morphiceptin, and loperamide induced MOR endocytosis in myenteric neurons. After stimulation with DAMGO and morphiceptin, MOR recycled, whereas MOR was retained within endosomes following loperamide treatment. Herkinorin or the δ-opioid receptor agonist [d-Ala(2), d-Leu(5)]enkephalin (DADLE) did not evoke MOR endocytosis. In summary, we have identified the neurochemical coding of MOR-positive enteric neurons and have demonstrated differential trafficking of MOR in these neurons in response to established and putative MOR agonists.
[Mh] Termos MeSH primário: Colo/inervação
Sistema Nervoso Entérico/metabolismo
Íleo/inervação
Receptores Opioides mu/metabolismo
Estômago/inervação
[Mh] Termos MeSH secundário: Analgésicos Opioides/farmacologia
Animais
Neurônios Colinérgicos/metabolismo
Endocitose
Endorfinas/farmacologia
Ala(2)-MePhe(4)-Gly(5)-Encefalina/farmacologia
Sistema Nervoso Entérico/efeitos dos fármacos
Cobaias
Loperamida/farmacologia
Masculino
Neurônios Motores/metabolismo
Neurônios Nitrérgicos/metabolismo
Transporte Proteico
Receptores Opioides mu/agonistas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Analgesics, Opioid); 0 (Endorphins); 0 (Receptors, Opioid, mu); 100929-53-1 (Enkephalin, Ala(2)-MePhe(4)-Gly(5)-); 6X9OC3H4II (Loperamide); 97TZA8ANPC (morphiceptin)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170619
[Lr] Data última revisão:
170619
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160702
[St] Status:MEDLINE
[do] DOI:10.1152/ajpgi.00184.2016



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