Base de dados : MEDLINE
Pesquisa : D12.125.068.330.700 [Categoria DeCS]
Referências encontradas : 786 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 79 ir para página                         

  1 / 786 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28370133
[Au] Autor:Suarez-Mendez S; Tovilla-Zarate CA; Ortega-Varela LF; Bermudez-Ocaña DY; Blé-Castillo JL; González-Castro TB; Zetina-Esquivel AM; Diaz-Zagoya JC; Esther Juárez-Rojop I
[Ad] Endereço:Division Académica de Ciencias de la Salud, Universidad Juárez Autónoma de Tabasco, Villahermosa, Tabasco, México.
[Ti] Título:Isobolographic Analyses of Proglumide-Celecoxib Interaction in Rats with Painful Diabetic Neuropathy.
[So] Source:Drug Dev Res;78(2):116-123, 2017 Mar.
[Is] ISSN:1098-2299
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Preclinical Research The aim of the present study was to analyze the antihyperalgesic and antiallodynic interaction between the non-selective cholecystokinin (CCK) antagonist receptor, proglumide, and the selective cyclooxygenase-2 inhibitor, celecoxib in streptozotocin (STZ)-induced diabetic rats. Hyperalgesia was evaluated in the formalin test and tactile allodynia using von Frey filaments. Isobolographic analyses were employed to define the nature of the compound interactions, using a fixed dose ratio (0.5:0.5). Proglumide (20-160 mg/kg) and celecoxib (0.3-30 mg/kg) in these fixed dose ratio combinations induced dose-dependent antihyperalgesia and an antiallodynic effect in diabetic rats. ED values were calculated for the treatments and an isobologram was constructed. Theoretical ED values for combination proglumide-celecoxib estimated from the isobolograms for antihyperalgesic and antiallodynic activity (30.50 ± 1.90 mg/kg and 45.81 ± 4.55 mg/kg, respectively) were obtained, while experimental ED values for this antihyperalgesic and antiallodynic combined effect (13.83 ± 0.65 mg/kg and 17.74 ± 3.57 mg/kg; respectively) were significantly different. Coadministration of proglumide-celecoxib showed an interaction index value of 0.45 ± 0.03 for the antihyperalgesic effect and 0.39 ± 0.08 for the antiallodynic activity, indicating a synergistic interaction. These data suggest that proglumide and celecoxib can interact synergistically to reduce hyperalgesic and allodynic behaviors in diabetic neuropathy. This combination could be useful to treat neuropathic pain in diabetic patients. Drug Dev Res 78 : 116-123, 2017. ©2017 Wiley Periodicals, Inc.
[Mh] Termos MeSH primário: Celecoxib/administração & dosagem
Diabetes Mellitus Experimental/complicações
Neuropatias Diabéticas/tratamento farmacológico
Hiperalgesia/tratamento farmacológico
Proglumida/administração & dosagem
[Mh] Termos MeSH secundário: Animais
Celecoxib/uso terapêutico
Diabetes Mellitus Experimental/induzido quimicamente
Neuropatias Diabéticas/etiologia
Relação Dose-Resposta a Droga
Combinação de Medicamentos
Sinergismo Farmacológico
Hiperalgesia/etiologia
Masculino
Proglumida/uso terapêutico
Ratos
Ratos Wistar
Estreptozocina
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Drug Combinations); 5W494URQ81 (Streptozocin); EPL8W5565D (Proglumide); JCX84Q7J1L (Celecoxib)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171106
[Lr] Data última revisão:
171106
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170404
[St] Status:MEDLINE
[do] DOI:10.1002/ddr.21382


  2 / 786 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:27573516
[Au] Autor:Yin K; Deuis JR; Lewis RJ; Vetter I
[Ad] Endereço:Centre for Pain Research, Institute for Molecular Bioscience, University of Queensland, Queensland, Australia.
[Ti] Título:Transcriptomic and behavioural characterisation of a mouse model of burn pain identify the cholecystokinin 2 receptor as an analgesic target.
[So] Source:Mol Pain;12, 2016.
[Is] ISSN:1744-8069
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Burn injury is a cause of significant mortality and morbidity worldwide and is frequently associated with severe and long-lasting pain that remains difficult to manage throughout recovery. We characterised a mouse model of burn-induced pain using pharmacological and transcriptomic approaches. Mechanical allodynia elicited by burn injury was partially reversed by meloxicam (5 mg/kg), gabapentin (100 mg/kg) and oxycodone (3 and 10 mg/kg), while thermal allodynia and gait abnormalities were only significantly improved by amitriptyline (3 mg/kg) and oxycodone (10 mg/kg). The need for relatively high opioid doses to elicit analgesia suggested a degree of opioid resistance, similar to that shown clinically in burn patients. We thus assessed the gene expression changes in dorsal root ganglion neurons and pathophysiological mechanisms underpinning burn injury-induced pain using a transcriptomic approach. Burn injury was associated with significantly increased expression of genes associated with axon guidance, neuropeptide signalling, behavioural defence response and extracellular signalling, confirming a mixed neuropathic and inflammatory aetiology. Notably, among the pain-related genes that were upregulated post-injury was the cholecystokinin 2 receptor (Cckbr), a G protein-coupled receptor known as a pain target involved in reducing opioid effectiveness. Indeed, the clinically used cholecystokinin receptor antagonist proglumide (30 mg/kg) was effective at reversing mechanical allodynia, with additional analgesia evident in combination with low-dose oxycodone (1 mg/kg), including significant reversal of thermal allodynia. These findings highlight the complex pathophysiological mechanisms underpinning burn injury-induced pain and suggest that cholecystokinin-2 receptor antagonists may be useful clinically as adjuvants to decrease opioid requirements and improve analgesic management.
[Mh] Termos MeSH primário: Transtornos Neurológicos da Marcha/etiologia
Regulação da Expressão Gênica/fisiologia
Hiperalgesia/etiologia
Dor
Receptor de Colecistocinina B/metabolismo
Transcriptoma
[Mh] Termos MeSH secundário: Aminas/farmacologia
Aminas/uso terapêutico
Amitriptilina/farmacologia
Amitriptilina/uso terapêutico
Animais
Ácidos Cicloexanocarboxílicos/farmacologia
Ácidos Cicloexanocarboxílicos/uso terapêutico
Modelos Animais de Doenças
Transtornos Neurológicos da Marcha/tratamento farmacológico
Gânglios Espinais/citologia
Regulação da Expressão Gênica/efeitos dos fármacos
Hiperalgesia/tratamento farmacológico
Masculino
Metacarpo/patologia
Camundongos
Camundongos Endogâmicos C57BL
Atividade Motora/efeitos dos fármacos
Oxicodona/farmacologia
Oxicodona/uso terapêutico
Dor/complicações
Dor/tratamento farmacológico
Dor/metabolismo
Limiar da Dor/efeitos dos fármacos
Proglumida/farmacologia
Proglumida/uso terapêutico
Receptor de Colecistocinina B/antagonistas & inibidores
Receptor de Colecistocinina B/genética
Células Receptoras Sensoriais/efeitos dos fármacos
Suporte de Carga/fisiologia
Ácido gama-Aminobutírico/farmacologia
Ácido gama-Aminobutírico/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amines); 0 (Cyclohexanecarboxylic Acids); 0 (Receptor, Cholecystokinin B); 1806D8D52K (Amitriptyline); 56-12-2 (gamma-Aminobutyric Acid); 6CW7F3G59X (gabapentin); CD35PMG570 (Oxycodone); EPL8W5565D (Proglumide)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171018
[Lr] Data última revisão:
171018
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160831
[St] Status:MEDLINE


  3 / 786 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:26400945
[Au] Autor:Crosby KM; Baimoukhametova DV; Bains JS; Pittman QJ
[Ad] Endereço:Hotchkiss Brain Institute and Department of Physiology and Pharmacology, University of Calgary, Calgary, Alberta T2N 4N1, Canada, and Biology Department, Mount Allison University, Sackville, New Brunswick E4L 1G7, Canada.
[Ti] Título:Postsynaptic Depolarization Enhances GABA Drive to Dorsomedial Hypothalamic Neurons through Somatodendritic Cholecystokinin Release.
[So] Source:J Neurosci;35(38):13160-70, 2015 Sep 23.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Somatodendritically released peptides alter synaptic function through a variety of mechanisms, including autocrine actions that liberate retrograde transmitters. Cholecystokinin (CCK) is a neuropeptide expressed in neurons in the dorsomedial hypothalamic nucleus (DMH), a region implicated in satiety and stress. There are clear demonstrations that exogenous CCK modulates food intake and neuropeptide expression in the DMH, but there is no information on how endogenous CCK alters synaptic properties. Here, we provide the first report of somatodendritic release of CCK in the brain in male Sprague Dawley rats. CCK is released from DMH neurons in response to repeated postsynaptic depolarizations, and acts in an autocrine fashion on CCK2 receptors to enhance postsynaptic NMDA receptor function and liberate the retrograde transmitter, nitric oxide (NO). NO subsequently acts presynaptically to enhance GABA release through a soluble guanylate cyclase-mediated pathway. These data provide the first demonstration of synaptic actions of somatodendritically released CCK in the hypothalamus and reveal a new form of retrograde plasticity, depolarization-induced potentiation of inhibition. Significance statement: Somatodendritic signaling using endocannabinoids or nitric oxide to alter the efficacy of afferent transmission is well established. Despite early convincing evidence for somatodendritic release of neurohypophysial peptides in the hypothalamus, there is only limited evidence for this mode of release for other peptides. Here, we provide the first evidence for somatodendritic release of the satiety peptide cholecystokinin (CCK) in the brain. We also reveal a new form of synaptic plasticity in which postsynaptic depolarization results in enhancement of inhibition through the somatodendritic release of CCK.
[Mh] Termos MeSH primário: Colecistocinina/metabolismo
Núcleo Hipotalâmico Dorsomedial/citologia
Potenciais Pós-Sinápticos Inibidores/efeitos dos fármacos
Plasticidade Neuronal/efeitos dos fármacos
Neurônios/efeitos dos fármacos
Ácido gama-Aminobutírico/metabolismo
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Colecistocinina/farmacologia
GABAérgicos/farmacologia
Guanosina Difosfato/análogos & derivados
Guanosina Difosfato/farmacologia
Técnicas In Vitro
Masculino
Técnicas de Patch-Clamp
Peptídeos/farmacologia
Proglumida/análogos & derivados
Proglumida/farmacologia
Quinazolinonas/farmacologia
Ratos
Ratos Sprague-Dawley
Receptor de Colecistocinina B/antagonistas & inibidores
Receptor de Colecistocinina B/metabolismo
Transdução de Sinais/efeitos dos fármacos
Proteína 25 Associada a Sinaptossoma/antagonistas & inibidores
Proteína 25 Associada a Sinaptossoma/metabolismo
Tionucleotídeos/farmacologia
Ácido gama-Aminobutírico/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (2-(2-(5-bromo-1H-indol-3-yl)ethyl)-3-(1-methylethoxyphenyl)-4-(3H)-quinazolinone); 0 (GABA Agents); 0 (Peptides); 0 (Quinazolinones); 0 (Receptor, Cholecystokinin B); 0 (Snap25 protein, rat); 0 (Synaptosomal-Associated Protein 25); 0 (Thionucleotides); 146-91-8 (Guanosine Diphosphate); 56-12-2 (gamma-Aminobutyric Acid); 71376-97-1 (guanosine 5'-O-(2-thiodiphosphate)); 9011-97-6 (Cholecystokinin); EPL8W5565D (Proglumide); LAD1UQ73BE (lorglumide)
[Em] Mês de entrada:1512
[Cu] Atualização por classe:150924
[Lr] Data última revisão:
150924
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150925
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.3123-14.2015


  4 / 786 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:26384952
[Au] Autor:Shen L; Wang DQ; Lo CC; Arnold M; Tso P; Woods SC; Liu M
[Ad] Endereço:Department of Pathology and Laboratory Medicine, University of Cincinnati College of Medicine, Cincinnati, OH 45237, USA.
[Ti] Título:Gut vagal afferents are necessary for the eating-suppressive effect of intraperitoneally administered ginsenoside Rb1 in rats.
[So] Source:Physiol Behav;152(Pt A):62-7, 2015 Dec 01.
[Is] ISSN:1873-507X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Ginsenoside Rb1 (Rb1) reduces food intake in both lean and high-fat diet induced-obese rats; however, the sites and/or mediation of the eating-suppressive effect of Rb1 have not previously been identified. We hypothesized that intraperitoneally (ip) administered Rb1 exerts its anorectic action by enhancing sensitivity to satiation signals, such as cholecystokinin (CCK), and/or that it acts through vagal afferent nerves that relay the satiating signaling to the hindbrain. To test these hypotheses, we gave ip bolus doses of Rb1 (2.5-10.0mg/kg) and CCK-8 (0.125-4.0µg/kg) alone or in combination and assessed food intake in rats. Low doses of Rb1 (2.5mg/kg) or CCK-8 (0.125µg/kg) alone had no effect on food intake whereas higher doses did. When these subthreshold doses of Rb1 and CCK-8 were co-administered, the combination significantly reduced food intake relative to saline controls, and this effect was attenuated by lorglumide, a selective CCK1-receptor antagonist. Interestingly, lorglumide blocked food intake induced by an effective dose of CCK-8 alone, but not by Rb1 alone, suggesting that Rb1's anorectic effect is independent of the CCK1 receptor. To determine whether peripherally administered Rb1 suppresses feeding via abdominal vagal nerves, we evaluated the effect of ip Rb1 injection in subdiaphragmatic vagal deafferentation (SDA) and control rats. Rb1's effect on food intake was significantly attenuated in SDA rats, compared with that in SHAM controls. These data indicate that the vagal afferent system is the major pathway conveying peripherally administered Rb1's satiation signal.
[Mh] Termos MeSH primário: Depressores do Apetite/administração & dosagem
Ingestão de Alimentos/efeitos dos fármacos
Ginsenosídeos/administração & dosagem
Neurônios Aferentes/efeitos dos fármacos
Sincalida/administração & dosagem
Nervo Vago/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Relação Dose-Resposta a Droga
Ingestão de Alimentos/fisiologia
Glucose
Antagonistas de Hormônios/farmacologia
Injeções Intraperitoneais
Masculino
Neurônios Aferentes/citologia
Neurônios Aferentes/fisiologia
Proglumida/análogos & derivados
Proglumida/farmacologia
Ratos Long-Evans
Receptor de Colecistocinina A/antagonistas & inibidores
Receptor de Colecistocinina A/metabolismo
Saciação/efeitos dos fármacos
Saciação/fisiologia
Nervo Vago/citologia
Nervo Vago/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Appetite Depressants); 0 (Ginsenosides); 0 (Hormone Antagonists); 0 (Receptor, Cholecystokinin A); 7413S0WMH6 (ginsenoside Rb1); EPL8W5565D (Proglumide); IY9XDZ35W2 (Glucose); LAD1UQ73BE (lorglumide); M03GIQ7Z6P (Sincalide)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150920
[St] Status:MEDLINE


  5 / 786 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:26167074
[Au] Autor:Jia D; Yamamoto M; Otsuki M
[Ad] Endereço:Dongmei Jia, Department of Gastroenterology and Metabolism, University of Occupational and Environmental Health, Japan, School of Medicine, Kitakyushu 807-8555, Japan.
[Ti] Título:Effect of endogenous cholecystokinin on the course of acute pancreatitis in rats.
[So] Source:World J Gastroenterol;21(25):7742-53, 2015 Jul 07.
[Is] ISSN:2219-2840
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:AIM: To examine the effects of pancreatic rest, stimulation and rest/stimulation on the natural course of recovery after acute pancreatitis. METHODS: Acute hemorrhagic pancreatitis (AP) was induced in male rats by intraductal infusion of 40 µL/100 g body weight of 3% sodium taurocholate. All rats took food ad libitum. At 24 h after induction of AP, rats were divided into four groups: control (AP-C), pancreas rest (AP-R), stimulation (AP-S), and rest/stimulation (AP-R/S). Rats in the AP-C, AP-R and AP-S groups received oral administration of 2 mL/kg body weight saline, cholecystokinin (CCK)-1 receptor antagonist, and endogenous CCK release stimulant, respectively, twice daily for 10 d, while those in the AP-R/S group received twice daily CCK-1 receptor antagonist for the first 5 d followed by twice daily CCK release stimulant for 5 d. Rats without any treatment were used as control group (Control). Biochemical and histological changes in the pancreas, and secretory function were evaluated on day 12 at 24 h after the last treatment. RESULTS: Feeding ad libitum (AP-C) delayed biochemical, histological and functional recovery from AP. In AP-C rats, bombesin-stimulated pancreatic secretory function and HOMA-ß-cell score were significantly lower than those in other groups of rats. In AP-R rats, protein per DNA ratio and pancreatic exocrine secretory function were significantly low compared with those in Control rats. In AP-S and AP-R/S rats, the above parameters recovered to the Control levels. Bombesin-stimulated pancreatic exocrine response in AP-R/S rats was higher than in AP-S rats and almost returned to control levels. In the pancreas of AP-C rats, destruction of pancreatic acini, marked infiltration of inflammatory cells, and strong expression of α-smooth muscle actin, tumor necrosis factor-α and interleukin-1ß were seen. Pancreatic rest reversed these histological alterations, but not atrophy of pancreatic acini and mild infiltration of inflammatory cells. In AP-S and AP-R/S rats, the pancreas showed almost normal architecture. CONCLUSION: The favorable treatment strategy for AP is to keep the pancreas at rest during an early stage followed by pancreatic stimulation by promoting endogenous CCK release.
[Mh] Termos MeSH primário: Colecistocinina/metabolismo
Pâncreas/metabolismo
Pancreatite/metabolismo
[Mh] Termos MeSH secundário: Administração Oral
Animais
Biomarcadores/sangue
Bombesina/administração & dosagem
Proliferação Celular
Replicação do DNA
Modelos Animais de Doenças
Gabexato/administração & dosagem
Gabexato/análogos & derivados
Antagonistas de Hormônios/administração & dosagem
Resistência à Insulina
Masculino
Pâncreas/efeitos dos fármacos
Pâncreas/patologia
Pâncreas/fisiopatologia
Testes de Função Pancreática
Pancreatite/induzido quimicamente
Pancreatite/diagnóstico
Pancreatite/tratamento farmacológico
Pancreatite/patologia
Pancreatite/fisiopatologia
Proglumida/administração & dosagem
Proglumida/análogos & derivados
Ratos Wistar
Receptor de Colecistocinina A/antagonistas & inibidores
Receptor de Colecistocinina A/metabolismo
Recuperação de Função Fisiológica
Ácido Taurocólico
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biomarkers); 0 (Hormone Antagonists); 0 (Receptor, Cholecystokinin A); 0FD207WKDU (camostat); 4V7M9137X9 (Gabexate); 5E090O0G3Z (Taurocholic Acid); 77MPX3N42I (loxiglumide); 9011-97-6 (Cholecystokinin); EPL8W5565D (Proglumide); PX9AZU7QPK (Bombesin)
[Em] Mês de entrada:1603
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150714
[St] Status:MEDLINE
[do] DOI:10.3748/wjg.v21.i25.7742


  6 / 786 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:25478062
[Au] Autor:Ahmad M; Abu-Taweel GM; Aboshaiqah AE; Ajarem JS
[Ad] Endereço:Department of Medical Surgical Nursing, College of Nursing, King Saud University, P.O. Box 642, Riyadh 11421, Saudi Arabia.
[Ti] Título:The effects of quinacrine, proglumide, and pentoxifylline on seizure activity, cognitive deficit, and oxidative stress in rat lithium-pilocarpine model of status epilepticus.
[So] Source:Oxid Med Cell Longev;2014:630509, 2014.
[Is] ISSN:1942-0994
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The present data indicate that status epilepticus (SE) induced in adult rats is associated with cognitive dysfunctions and cerebral oxidative stress (OS). This has been demonstrated using lithium-pilocarpine (Li-Pc) model of SE. OS occurring in hippocampus and striatum of mature brain following SE is apparently due to both the increased free radicals production and the limited antioxidant defense. Pronounced alterations were noticed in the enzymatic, glutathione-S transferase (GST), catalase (CAT), and superoxide dismutase (SOD), as well as in the nonenzymatic; thiobarbituric acid (TBARS) and reduced glutathione (GST), indices of OS in the hippocampus and striatum of SE induced animals. Quinacrine (Qcn), proglumide (Pgm), and pentoxifylline (Ptx) administered to animals before inducing SE, were significantly effective in ameliorating the seizure activities, cognitive dysfunctions, and cerebral OS. The findings suggest that all the drugs were effective in the order of Ptx < Pgm < Qcn indicating that these drugs are potentially antiepileptic as well as antioxidant; however, further studies are needed to establish this fact. It can be assumed that these antiepileptic substances with antioxidant properties combined with conventional therapies might provide a beneficial effect in treatment of epilepsy through ameliorating the cerebral OS.
[Mh] Termos MeSH primário: Transtornos Cognitivos/tratamento farmacológico
Estresse Oxidativo/efeitos dos fármacos
Pentoxifilina/farmacologia
Proglumida/farmacologia
Quinacrina/farmacologia
Convulsões/tratamento farmacológico
Estado Epiléptico/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Transtornos Cognitivos/etiologia
Transtornos Cognitivos/metabolismo
Compostos de Lítio
Masculino
Pilocarpina
Distribuição Aleatória
Ratos
Ratos Sprague-Dawley
Convulsões/metabolismo
Convulsões/psicologia
Estado Epiléptico/metabolismo
Estado Epiléptico/psicologia
Superóxido Dismutase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Lithium Compounds); 01MI4Q9DI3 (Pilocarpine); EC 1.15.1.1 (Superoxide Dismutase); EPL8W5565D (Proglumide); H0C805XYDE (Quinacrine); SD6QCT3TSU (Pentoxifylline)
[Em] Mês de entrada:1506
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:141206
[St] Status:MEDLINE
[do] DOI:10.1155/2014/630509


  7 / 786 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:25362597
[Au] Autor:Ahmad M; Wadaan MA
[Ad] Endereço:Department of Medical Surgical Nursing, College of Nursing, Bioproducts Research Chair, King Saud University, Riyadh, Saudi Arabia.
[Ti] Título:Ameliorating effects of proglumide on neurobehavioral and biochemical deficits in animal model of status epilepticus.
[So] Source:Pak J Pharm Sci;27(6):1945-51, 2014 Nov.
[Is] ISSN:1011-601X
[Cp] País de publicação:Pakistan
[La] Idioma:eng
[Ab] Resumo:Status epilepticus (SE) is a recurrent generalized convulsion condition and is regarded as a medical emergency with around 50% of the cases occurring in children. Besides neurobehavioral and motor deficits, SE is reportedly associated with imbalance in a number of neurochemicals in several areas of the brain. Furthermore, neuronal hyperactivity and/or excitotoxicity in such brain areas have been associated with excessive generation of free radicals. Proglumide (Pgm) is a known cholecystokinin (CCK) antagonist and any changes in the level of CCK and in the number of CCK receptors has been linked with SE. The present study was designed to investigate the possible neuroprotective effects of Pgm (0, 250, 500 and 750mg/ml/kg i.p.) on epileptic seizure activities, some neurobehavioral tests, and on some oxidative stress related parameters like lipid peroxides measured as thiobarbituric acid-reactive substance (TBARS) and total glutathione (GSH) in brain (hippocampus and striatum) of young rats that were experimentally induced with SE by lithium (Li) in 3mEq/ml/kg dose, i.p. followed 20h later by pilocarpine (Pc) in 20mg/ml/kg dose, s.c.). Besides significant anti-epileptic effect, Pgm significantly ameliorated SE-induced deterioration in cognitive behavior (in water-maze), motor performance (on rotarod), and biochemical changes in brain. It is concluded from the present study that Pgm has significant neuroprotective effects against SE and this effect may probably be due to its antioxidant activity. Pgm may prove to be a potentially effective antiepileptic drug, however, further studies are needed to ascertain this possibility.
[Mh] Termos MeSH primário: Proglumida/uso terapêutico
Estado Epiléptico/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Cognição/efeitos dos fármacos
Modelos Animais de Doenças
Glutationa/metabolismo
Lítio
Masculino
Atividade Motora/efeitos dos fármacos
Estresse Oxidativo/efeitos dos fármacos
Pilocarpina
Proglumida/farmacologia
Ratos
Ratos Sprague-Dawley
Estado Epiléptico/metabolismo
Estado Epiléptico/psicologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
01MI4Q9DI3 (Pilocarpine); 9FN79X2M3F (Lithium); EPL8W5565D (Proglumide); GAN16C9B8O (Glutathione)
[Em] Mês de entrada:1501
[Cu] Atualização por classe:141103
[Lr] Data última revisão:
141103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:141103
[St] Status:MEDLINE


  8 / 786 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:25253956
[Au] Autor:Mao JD; Wu P; Huang JX; Wu J; Yang G
[Ad] Endereço:Jia-Ding Mao, Pei Wu, Jian-Xiong Huang, Jian Wu, Guang Yang, Department of General Surgery, the First Affiliated Yijishan Hospital of Wannan Medical College, Wuhu 241001, Anhui Province, China.
[Ti] Título:Role of ERK-MAPK signaling pathway in pentagastrin-regulated growth of large intestinal carcinoma.
[So] Source:World J Gastroenterol;20(35):12542-50, 2014 Sep 21.
[Is] ISSN:2219-2840
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:AIM: To explore the role and mechanisms of extracellular signal-regulated protein kinase-mitogen-activated protein kinase (ERK-MAPK) signaling in pentagastrin-regulated growth of large intestinal carcinoma. METHODS: HT-29 cells were incubated in different media and divided into the control group, pentagastrin group, proglumide group, and pentagastrin + proglumide group. No reagent was added to the control group, and other groups were incubated with reagent at different concentrations. Changes in proliferation of HT-29 cells were detected by MTT assay, and the optimal concentrations of pentagastrin and proglumide were determined. The changes in proliferation index (PI) and apoptosis rate (AR) of HT-29 cells were detected by Annexin V-fluorescein isothiocyanate flow cytometry. mRNA expression of pentagastrin receptor/cholecystokinin-B receptor (CCK-BR), ERK1/2 and K-ras were detected by reverse transcriptase polymerase chain reaction. The protein and phosphorylation level of ERK1/2 and K-ras were detected by western blotting. All data were analyzed by analysis of variance and SNK-q test. RESULTS: The proliferation of HT-29 cells was stimulated by pentagastrin at a concentration of 6.25-100 mg/L, and the optimal concentration of pentagastrin was 25.0 mg/L (F = 31.36, P < 0.05). Proglumide had no obvious effect on the proliferation of HT-29 cells, while it significantly inhibited the proliferation of HT-29 cells stimulated by pentagastrin when the concentration of proglumide was 8.0-128.0 mg/L, and the optimal concentration was 32.0 mg/L (F = 24.31, P < 0.05). The PI of the pentagastrin (25.0 mg/L) group was 37.5% ± 5.2%, which was significantly higher than 27.7% ± 5.0% of the control group and 27.3% ± 5.8% of the pentagastrin (25.0 mg/L) + proglumide (32.0 mg/L) group (Q = 4.56-4.75, P < 0.05). The AR of the pentagastrin (25.0 mg/L) group was 1.9% ± 0.4%, which was significantly lower than 2.5% ± 0.4% of the control group and 2.4% ± 0.3% of the pentagastrin (25.0 mg/L) + proglumide (32.0 mg/L) group (Q = 4.23-4.06, P < 0.05). mRNA expression of CCK-BR was detected in HT-29 cells. The phosphorylation levels of ERK1/2 protein and phosphorylated K-ras protein of the pentagastrin group were 0.43% ± 0.04% and 0.45% ± 0.06%, which were significantly higher than 0.32% ± 0.02% and 0.31% ± 0.05% of the control group (Q = 7.78-4.95, P < 0.05), and 0.36% ± 0.01% and 0.35% ± 0.04% of the pentagastrin + proglumide group (Q = 5.72-4.08, P < 0.05). There were no significant differences in the mRNA and protein expression of ERK1/2 and K-ras among the control, pentagastrin, proglumide and pentagastrin + proglumide groups (F = 0.52, 0.72, 0.78, 0.28; P > 0.05). CONCLUSION: Gastrin stimulates proliferation of HT-29 cells and inhibits apoptosis by upregulating phosphorylation of ERK and K-ras through the Ras-Raf-MEK1/2-ERK1/2 pathway, and this is restrained by proglumide.
[Mh] Termos MeSH primário: Adenocarcinoma/enzimologia
Proliferação Celular/efeitos dos fármacos
Neoplasias do Colo/enzimologia
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Proteína Quinase 1 Ativada por Mitógeno/metabolismo
Proteína Quinase 3 Ativada por Mitógeno/metabolismo
Pentagastrina/farmacologia
[Mh] Termos MeSH secundário: Adenocarcinoma/genética
Adenocarcinoma/patologia
Apoptose/efeitos dos fármacos
Neoplasias do Colo/genética
Neoplasias do Colo/patologia
Relação Dose-Resposta a Droga
Ativação Enzimática
Células HT29
Seres Humanos
Proteína Quinase 1 Ativada por Mitógeno/genética
Proteína Quinase 3 Ativada por Mitógeno/genética
Fosforilação
Proglumida/farmacologia
Proteínas Proto-Oncogênicas/genética
Proteínas Proto-Oncogênicas/metabolismo
Proteínas Proto-Oncogênicas p21(ras)
RNA Mensageiro/metabolismo
Receptor de Colecistocinina B/agonistas
Receptor de Colecistocinina B/genética
Receptor de Colecistocinina B/metabolismo
Proteínas ras/genética
Proteínas ras/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (KRAS protein, human); 0 (Proto-Oncogene Proteins); 0 (RNA, Messenger); 0 (Receptor, Cholecystokinin B); EC 2.7.11.24 (MAPK1 protein, human); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3); EC 3.6.5.2 (Proto-Oncogene Proteins p21(ras)); EC 3.6.5.2 (ras Proteins); EF0NX91490 (Pentagastrin); EPL8W5565D (Proglumide)
[Em] Mês de entrada:1505
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140926
[St] Status:MEDLINE
[do] DOI:10.3748/wjg.v20.i35.12542


  9 / 786 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:25058882
[Au] Autor:Smith JP; Cooper TK; McGovern CO; Gilius EL; Zhong Q; Liao J; Molinolo AA; Gutkind JS; Matters GL
[Ad] Endereço:From the *National Institute of Diabetes and Digestive and Kidney Disease, The National Institutes of Health, Bethesda, MD; Departments of †Medicine, ‡Comparative Medicine and Pathology, §Public Health Sciences, and ∥Biochemistry and Molecular Biology, The Pennsylvania State University, College of Medicine, Hershey, PA; and ¶National Institute of Dental and Craniofacial Research, The National Institutes of Health, Bethesda, MD.
[Ti] Título:Cholecystokinin receptor antagonist halts progression of pancreatic cancer precursor lesions and fibrosis in mice.
[So] Source:Pancreas;43(7):1050-9, 2014 Oct.
[Is] ISSN:1536-4828
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: Exogenous administration of cholecystokinin (CCK) induces hypertrophy and hyperplasia of the pancreas with an increase in DNA content. We hypothesized that endogenous CCK is involved in the malignant progression of pancreatic intraepithelial neoplasia (PanIN) lesions and the fibrosis associated with pancreatic cancer. METHODS: The presence of CCK receptors in early PanIN lesions was examined by immunohistochemistry in mouse and human pancreas. Pdx1-Cre/LSL-Kras transgenic mice were randomized to receive either untreated drinking water or water supplemented with a CCK receptor antagonist (proglumide, 0.1 mg/mL). Pancreas from the mice were removed and examined histologically for number and grade of PanINs after 1, 2, or 4 months of antagonist therapy. RESULTS: Both CCK-A and CCK-B receptors were identified in early stage PanINs from mouse and human pancreas. The grade of PanIN lesions was reversed, and progression to advanced lesions arrested in mice treated with proglumide compared with the controls (P = 0.004). Furthermore, pancreatic fibrosis was significantly reduced in antagonist-treated animals compared with vehicle (P < 0.001). CONCLUSIONS: These findings demonstrate that endogenous CCK is in part responsible for the development and progression of pancreatic cancer. The use of CCK receptor antagonists may have a role in cancer prophylaxis in high-risk subjects and may reduce fibrosis in the microenvironment.
[Mh] Termos MeSH primário: Carcinoma in Situ/prevenção & controle
Pâncreas/efeitos dos fármacos
Neoplasias Pancreáticas/prevenção & controle
Lesões Pré-Cancerosas/tratamento farmacológico
Proglumida/uso terapêutico
Receptor de Colecistocinina A/antagonistas & inibidores
Receptor de Colecistocinina B/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Carcinoma in Situ/química
Carcinoma in Situ/tratamento farmacológico
Carcinoma in Situ/patologia
Colecistocinina/fisiologia
Progressão da Doença
Ensaios de Seleção de Medicamentos Antitumorais
Fibrose
Seres Humanos
Camundongos
Camundongos Transgênicos
Pâncreas/química
Pâncreas/patologia
Neoplasias Pancreáticas/química
Neoplasias Pancreáticas/tratamento farmacológico
Neoplasias Pancreáticas/patologia
Pancreatite/prevenção & controle
Lesões Pré-Cancerosas/metabolismo
Lesões Pré-Cancerosas/patologia
Proglumida/farmacologia
Distribuição Aleatória
Receptor de Colecistocinina A/análise
Receptor de Colecistocinina B/análise
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Receptor, Cholecystokinin A); 0 (Receptor, Cholecystokinin B); 9011-97-6 (Cholecystokinin); EPL8W5565D (Proglumide)
[Em] Mês de entrada:1505
[Cu] Atualização por classe:161025
[Lr] Data última revisão:
161025
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140725
[St] Status:MEDLINE
[do] DOI:10.1097/MPA.0000000000000194


  10 / 786 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:24914377
[Au] Autor:Liu JF; Zhang J; Liu XB; Drew PA
[Ad] Endereço:Jun-Feng Liu, Jian Zhang, Xin-Bo Liu, Department of Thoracic Surgery, Fourth Hospital, Hebei Medical University, Shijiazhuang 050011, Hebei Province, China.
[Ti] Título:Investigation of cholecystokinin receptors in the human lower esophageal sphincter.
[So] Source:World J Gastroenterol;20(21):6554-9, 2014 Jun 07.
[Is] ISSN:2219-2840
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:AIM: To compare the binding of cholecystokinin (CCK)-8 to CCK receptors in sling and clasp fibers of the human lower esophageal sphincter. METHODS: Esophageal sling and clasp fibers were isolated from eight esophagectomy specimens, resected for squamous cell carcinoma in the upper two thirds of the esophagus, which had been maintained in oxygenated Kreb's solution. Western blot was used to measure CCK-A and CCK-B receptor subtypes in the two muscles. A radioligand binding assay was used to determine the binding parameters of (3)H-CCK-8S to the CCK receptor subtypes. The specificity of binding was determined by the addition of proglumide, which blocks the binding of CCK to both receptor subtypes. RESULTS: There was no significant difference between the sling and clasp fibers of the human lower esophageal sphincter in the amount of CCK-A [integrated optical density (IOD) value: 22.65 ± 0.642 vs 22.328 ± 1.042, P = 0.806] or CCK-B receptor protein (IOD value: 13.20 ± 0.423 vs 12.45 ± 0.294, P = 0.224) as measured by Western blot. The maximum binding of radio-labeled CCK-8S was higher in the sling fibers than in the clasp fibers (595.75 ± 3.231 cpm vs 500.000 ± 10.087 cpm, P < 0.001) and dissociation constant was lower (K(d): 1.437 ± 0.024 nmol/L vs 1.671 ± 0.024 nmol/L, P < 0.001). The IC50 of the receptor specific antagonists were lower for the CCK-A receptors than for the CCK-B (P < 0.01). CONCLUSION: CCK binding modulates the contractile function of the lower esophageal sphincter through differential binding to the CCK-A receptor on the sling and clasp fibers.
[Mh] Termos MeSH primário: Esfíncter Esofágico Inferior/patologia
Junção Esofagogástrica/patologia
Regulação da Expressão Gênica
Receptor de Colecistocinina A/metabolismo
Receptor de Colecistocinina B/metabolismo
Sincalida/metabolismo
[Mh] Termos MeSH secundário: Idoso
Western Blotting
Esofagectomia
Junção Esofagogástrica/metabolismo
Esôfago/patologia
Feminino
Seres Humanos
Concentração Inibidora 50
Soluções Isotônicas
Masculino
Meia-Idade
Proglumida/química
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Isotonic Solutions); 0 (Krebs-Ringer solution); 0 (Receptor, Cholecystokinin A); 0 (Receptor, Cholecystokinin B); EPL8W5565D (Proglumide); M03GIQ7Z6P (Sincalide)
[Em] Mês de entrada:1504
[Cu] Atualização por classe:151022
[Lr] Data última revisão:
151022
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140611
[St] Status:MEDLINE
[do] DOI:10.3748/wjg.v20.i21.6554



página 1 de 79 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

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