Base de dados : MEDLINE
Pesquisa : D10.251.355.255.100 [Categoria DeCS]
Referências encontradas : 16030 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 1603 ir para página                         

  1 / 16030 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28471490
[Au] Autor:Wang C; Liu W; Yao L; Zhang X; Zhang X; Ye C; Jiang H; He J; Zhu Y; Ai D
[Ad] Endereço:Tianjin Key Laboratory of Metabolic Diseases, Department of Physiology and Pathophysiology, Tianjin Medical University, Tianjin, China.
[Ti] Título:Hydroxyeicosapentaenoic acids and epoxyeicosatetraenoic acids attenuate early occurrence of nonalcoholic fatty liver disease.
[So] Source:Br J Pharmacol;174(14):2358-2372, 2017 Jul.
[Is] ISSN:1476-5381
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND PURPOSE: The ω-3 polyunsaturated fatty acids (PUFAs) mediate protective effects on several metabolic disorders. However, the functions of their metabolites in the early stage of nonalcoholic fatty liver disease (NAFLD) are largely unknown. EXPERIMENTAL APPROACH: Mice were fed a control diet, high-fat diet (HFD) or ω-3 PUFA-enriched HFD (ω3HFD) for 4 days and phenotypes were analysed. LC-MS/MS was used to determine the eicosanoid profiles. Primary hepatocytes and peritoneal macrophages were used for the mechanism study. KEY RESULTS: In short-term HFD-fed mice, the significantly increased lipid accumulation in the liver was reversed by ω-3 PUFA supplementation. Metabolomics showed that the plasma concentrations of hydroxyeicosapentaenoic acids (HEPEs) and epoxyeicosatetraenoic acids (EEQs) were reduced by a short-term HFD and markedly increased by the ω3HFD. However, HEPE/EEQ treatment had no direct protective effect on hepatocytes. ω3HFD also significantly attenuated HFD-induced adipose tissue inflammation. Furthermore, the expression of pro-inflammatory cytokines and activation of the JNK pathway induced by palmitate were suppressed by HEPEs and EEQs in macrophages. 17,18-EEQ, 5-HEPE and 9-HEPE were identified as the effective components among these metabolites, as indicated by their greater suppression of the palmitate-induced expression of inflammatory factors, chemotaxis and JNK activation compared to other metabolites in macrophages. A mixture of 17,18-EEQ, 5-HEPE and 9-HEPE significantly ameliorated the short-term HFD-induced accumulation of macrophages in adipose tissue and hepatic steatosis. CONCLUSION AND IMPLICATIONS: 17,18-EEQ, 5-HEPE and 9-HEPE may be potential approaches to prevent NAFLD in the early stage by inhibiting the inflammatory response in adipose tissue macrophages via JNK signalling.
[Mh] Termos MeSH primário: Ácidos Araquidônicos/farmacologia
Ácido Eicosapentaenoico/análogos & derivados
Hepatopatia Gordurosa não Alcoólica/prevenção & controle
[Mh] Termos MeSH secundário: Animais
Ácidos Araquidônicos/administração & dosagem
Ácidos Araquidônicos/metabolismo
Ácido Eicosapentaenoico/administração & dosagem
Ácido Eicosapentaenoico/metabolismo
Ácido Eicosapentaenoico/farmacologia
Macrófagos/efeitos dos fármacos
Macrófagos/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Hepatopatia Gordurosa não Alcoólica/metabolismo
Hepatopatia Gordurosa não Alcoólica/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Arachidonic Acids); 131339-23-6 (17,18-epoxy-5,8,11,14-eicosatetraenoic acid); 83952-40-3 (5-hydroxy-6,8,11,14,17-eicosapentaenoic acid); AAN7QOV9EA (Eicosapentaenoic Acid)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180216
[Lr] Data última revisão:
180216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1111/bph.13844


  2 / 16030 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29273526
[Au] Autor:Stueber T; Meyer S; Jangra A; Hage A; Eberhardt M; Leffler A
[Ad] Endereço:Department of Anaesthesiology and Intensive Care Medicine, Hannover Medical School, Hannover, Germany.
[Ti] Título:Activation of the capsaicin-receptor TRPV1 by the acetaminophen metabolite N-arachidonoylaminophenol results in cytotoxicity.
[So] Source:Life Sci;194:67-74, 2018 Feb 01.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: The anandamide reuptake inhibitor N-arachidonoylaminophenol (AM404) and the reactive substance N-acetyl-p-benzoquinone imine (NAPQI) are both metabolites of acetaminophen and may contribute to acetaminophen-induced analgesia by acting at TRPV1 expressed in the peripheral or central nervous system. While NAPQI slowly sensitizes and activates TRPV1 by interacting with distinct intracellular cysteine residues, detailed properties of AM404 as an agonist of TRPV1 have not yet been reported on. We explored the effects of AM404 on recombinant human TRPV1 and in rodent dorsal root ganglion (DRG) neurons. MATERIALS AND METHODS: HEK 293 cells expressing different isoforms of recombinant TRPV1 and rodent DRG neurons were employed for patch clamp and calcium imaging experiments. Cytotoxicity was assessed by propidium iodide and Annexin V staining on TRPV1-HEK 293 cells and with trypan blue staining on DRG neurons. KEY FINDINGS: AM404 activates hTRPV1 at concentrations >1µM and in a concentration-dependent manner. AM404 also potentiates TRPV1-mediated currents evoked by heat and anandamide. Moreover, AM404-evoked currents are potentiated by NAPQI. While the partly capsaicin-insensitive rabbit (o) TRPV1 fails to respond to AM404, AM404-sensitivity is restored by insertion of the capsaicin binding-domain of rat TRPV1 into oTRPV1. In DRG neurons, AM404-evoked calcium influx as well as cell death is mediated by TRPV1. SIGNIFICANCE: AM404 gates TRPV1 by interacting with the vanilloid-binding site, and TRPV1 is the main receptor for AM404 in DRG neurons. While direct activation of TRPV1 requires high concentrations of AM404, it is possible that synergistic effects of AM404 with further TRPV1-agonists may occur at clinically relevant concentrations.
[Mh] Termos MeSH primário: Acetaminofen/farmacologia
Analgésicos não Entorpecentes/farmacologia
Ácidos Araquidônicos/farmacologia
Gânglios Espinais/efeitos dos fármacos
Canais de Cátion TRPV/metabolismo
[Mh] Termos MeSH secundário: Acetaminofen/metabolismo
Analgesia
Analgésicos não Entorpecentes/metabolismo
Animais
Ácidos Araquidônicos/metabolismo
Benzoquinonas/metabolismo
Capsaicina/farmacologia
Gânglios Espinais/citologia
Células HEK293
Seres Humanos
Iminas/metabolismo
Camundongos Endogâmicos C57BL
Neurônios/efeitos dos fármacos
Neurônios/metabolismo
Coelhos
Ratos Sprague-Dawley
Fármacos do Sistema Sensorial/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Analgesics, Non-Narcotic); 0 (Arachidonic Acids); 0 (Benzoquinones); 0 (Imines); 0 (Sensory System Agents); 0 (TRPV Cation Channels); 0 (TRPV1 protein, human); 362O9ITL9D (Acetaminophen); G6S9BN13TI (N-acetyl-4-benzoquinoneimine); S07O44R1ZM (Capsaicin); XVJ94H0U21 (N-(4-hydroxyphenyl)arachidonylamide)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171224
[St] Status:MEDLINE


  3 / 16030 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Registro de Ensaios Clínicos
Texto completo
[PMID]:29179781
[Au] Autor:Pei R; DiMarco DM; Putt KK; Martin DA; Gu Q; Chitchumroonchokchai C; White HM; Scarlett CO; Bruno RS; Bolling BW
[Ad] Endereço:1Department of Nutritional Sciences,University of Connecticut,3624 Horsebarn Road Extension,Unit 4017,Storrs,CT 06269,USA.
[Ti] Título:Low-fat yogurt consumption reduces biomarkers of chronic inflammation and inhibits markers of endotoxin exposure in healthy premenopausal women: a randomised controlled trial.
[So] Source:Br J Nutr;118(12):1043-1051, 2017 Dec.
[Is] ISSN:1475-2662
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The anti-inflammatory mechanisms of low-fat dairy product consumption are largely unknown. The objective of this study was to determine whether low-fat yogurt reduces biomarkers of chronic inflammation and endotoxin exposure in women. Premenopausal women (BMI 18·5-27 and 30-40 kg/m2) were randomised to consume 339 g of low-fat yogurt (yogurt non-obese (YN); yogurt obese (YO)) or 324 g of soya pudding (control non-obese; control obese (CO)) daily for 9 weeks (n 30/group). Fasting blood samples were analysed for IL-6, TNF-α/soluble TNF II (sTNF-RII), high-sensitivity C-reactive protein, 2-arachidonoyl glycerol, anandamide, monocyte gene expression, soluble CD14 (sCD14), lipopolysaccharide (LPS), LPS binding protein (LBP), IgM endotoxin-core antibody (IgM EndoCAb), and zonulin. BMI, waist circumference and blood pressure were also determined. After 9-week yogurt consumption, YO and YN had decreased TNF-α/sTNFR-RII. Yogurt consumption increased plasma IgM EndoCAb regardless of obesity status. sCD14 was not affected by diet, but LBP/sCD14 was lowered by yogurt consumption in both YN and YO. Yogurt intervention increased plasma 2-arachidonoylglycerol in YO but not YN. YO peripheral blood mononuclear cells expression of NF-κB inhibitor α and transforming growth factor ß1 increased relative to CO at 9 weeks. Other biomarkers were unchanged by diet. CO and YO gained approximately 0·9 kg in body weight. YO had 3·6 % lower diastolic blood pressure at week 3. Low-fat yogurt for 9 weeks reduced biomarkers of chronic inflammation and endotoxin exposure in premenopausal women compared with a non-dairy control food. This trial was registered as NCT01686204.
[Mh] Termos MeSH primário: Biomarcadores/sangue
Dieta
Endotoxinas/toxicidade
Inflamação/sangue
Inflamação/dietoterapia
Iogurte/análise
[Mh] Termos MeSH secundário: Proteínas da Fase Aguda
Adulto
Antropometria
Ácidos Araquidônicos/sangue
Proteína C-Reativa/metabolismo
Proteínas de Transporte/sangue
Doença Crônica
Citocinas/sangue
Gorduras na Dieta/administração & dosagem
Gorduras na Dieta/análise
Endocanabinoides/sangue
Endotoxemia/sangue
Endotoxemia/dietoterapia
Feminino
Glicerídeos/sangue
Seres Humanos
Imunoglobulina M/sangue
Leucócitos Mononucleares/metabolismo
Glicoproteínas de Membrana/sangue
Meia-Idade
NF-kappa B/metabolismo
Obesidade/metabolismo
Alcamidas Poli-Insaturadas/sangue
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Acute-Phase Proteins); 0 (Arachidonic Acids); 0 (Biomarkers); 0 (Carrier Proteins); 0 (Cytokines); 0 (Dietary Fats); 0 (Endocannabinoids); 0 (Endotoxins); 0 (Glycerides); 0 (Immunoglobulin M); 0 (Membrane Glycoproteins); 0 (NF-kappa B); 0 (Polyunsaturated Alkamides); 0 (lipopolysaccharide-binding protein); 8D239QDW64 (glyceryl 2-arachidonate); 9007-41-4 (C-Reactive Protein); UR5G69TJKH (anandamide)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180207
[Lr] Data última revisão:
180207
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171129
[Cl] Clinical Trial:ClinicalTrial
[St] Status:MEDLINE
[do] DOI:10.1017/S0007114517003038


  4 / 16030 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29223163
[Au] Autor:Novosadova EV; Arsenyeva EL; Manuilova ES; Khaspekov LG; Bobrov MY; Bezuglov VV; Illarioshkin SN; Grivennikov IA
[Ad] Endereço:Institute of Molecular Genetics, Russian Academy of Sciences, Moscow, 123182, Russia. novek-img@mail.ru.
[Ti] Título:Neuroprotective Properties of Endocannabinoids N-Arachidonoyl Dopamine and N-Docosahexaenoyl Dopamine Examined in Neuronal Precursors Derived from Human Pluripotent Stem Cells.
[So] Source:Biochemistry (Mosc);82(11):1367-1372, 2017 Nov.
[Is] ISSN:1608-3040
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Neuroprotective properties of endocannabinoids N-arachidonoyl dopamine (NADA) and N-docosahexaenoyl dopamine (DHDA) were examined in neuronal precursor cells differentiated from human induced pluripotent stem cells and subjected to oxidative stress. Both compounds exerted neuroprotective activity, which was enhanced by elevating the concentration of the endocannabinoids within the 0.1-10 µM range. However, both agents at 10 µM concentration showed a marked toxic effect resulting in death of ~30% of the cells. Finally, antagonists of cannabinoid receptors as well as the receptor of the TRPV1 endovanilloid system did not hamper the neuroprotective effects of these endocannabinoids.
[Mh] Termos MeSH primário: Ácidos Araquidônicos/farmacologia
Dopamina/análogos & derivados
Células-Tronco Neurais/efeitos dos fármacos
Fármacos Neuroprotetores/farmacologia
Células-Tronco Pluripotentes/citologia
[Mh] Termos MeSH secundário: Agonistas de Receptores de Canabinoides/farmacologia
Dopamina/farmacologia
Relação Dose-Resposta a Droga
Endocanabinoides/farmacologia
Seres Humanos
Estresse Oxidativo
Canais de Cátion TRPV/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Arachidonic Acids); 0 (Cannabinoid Receptor Agonists); 0 (Endocannabinoids); 0 (N-docosahexaenoyl dopamine); 0 (Neuroprotective Agents); 0 (TRPV Cation Channels); 0 (TRPV1 protein, human); 0 (arachidonyl dopamine); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180103
[Lr] Data última revisão:
180103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171211
[St] Status:MEDLINE
[do] DOI:10.1134/S0006297917110141


  5 / 16030 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27771531
[Au] Autor:Sartim AG; Moreira FA; Joca SRL
[Ad] Endereço:Department of Physical and Chemical, School of Pharmaceutical Science of Ribeirão Preto, University of São Paulo, Ribeirão Preto, SP, Brazil.
[Ti] Título:Involvement of CB and TRPV1 receptors located in the ventral medial prefrontal cortex in the modulation of stress coping behavior.
[So] Source:Neuroscience;340:126-134, 2017 Jan 06.
[Is] ISSN:1873-7544
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cannabinoid type-1 (CB ) and transient receptor potential vanilloid type-1 (TRPV1) receptors may have opposite roles in modulating neural activity and, consequently, in regulating the stress response. These receptors are widely expressed in several brain structures, including the ventral medial prefrontal cortex (vmPFC). The functional consequences of the interaction between CB and TRPV1, however, have scarcely been explored. Therefore, we investigated if CB and TRPV1 receptors located in the vmPFC would be involved in the behavioral changes induced by the stress of the forced swim test (FST). Rats with cannulae implanted into the vmPFC were given the dual blocker of TRPV1 receptors and fatty acid amide hydrolase (FAAH), Arachidonyl serotonin (AA-5HT, 0.125/0.25/0.5nmol), TRPV1 antagonist, SB366791 (0.5/1/10nmol), FAAH inhibitor, URB597 (0.001/0.01/0.1/1nmol), or vehicle and were submitted to the FST, or to the open-field test. Another group received intra-vmPFC injection of SB366791 or vehicle, followed by a second injection of URB597 or vehicle, and was submitted to the FST. Lastly, a group received intra-vmPFC injection of a CB antagonist, in sub-effective dose or vehicle, followed by AA-5HT, SB366791 or vehicle. The results showed that AA-5HT, SB366791 and URB597 significantly reduced the immobility time without changing the locomotor activity. Furthermore, the co-administration of URB597 and SB366791 in sub-effective doses induced an antidepressant-like effect in the FST. Additionally, the antidepressant-like effect of AA-5HT was prevented by the CB antagonist. Together, these results suggest that both, CB and TRPV1 receptors located in the vmPFC are involved in the behavioral responses to stress, although in opposite ways.
[Mh] Termos MeSH primário: Adaptação Psicológica/fisiologia
Córtex Pré-Frontal/metabolismo
Receptor CB1 de Canabinoide/metabolismo
Estresse Psicológico/metabolismo
Canais de Cátion TRPV/metabolismo
[Mh] Termos MeSH secundário: Adaptação Psicológica/efeitos dos fármacos
Amidoidrolases/antagonistas & inibidores
Amidoidrolases/metabolismo
Anilidas/farmacologia
Animais
Antidepressivos/farmacologia
Ácidos Araquidônicos/farmacologia
Benzamidas/farmacologia
Carbamatos/farmacologia
Cinamatos/farmacologia
Masculino
Atividade Motora/efeitos dos fármacos
Atividade Motora/fisiologia
Neurotransmissores/farmacologia
Córtex Pré-Frontal/efeitos dos fármacos
Ratos Wistar
Serotonina/análogos & derivados
Serotonina/farmacologia
Canais de Cátion TRPV/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anilides); 0 (Antidepressive Agents); 0 (Arachidonic Acids); 0 (Benzamides); 0 (Carbamates); 0 (Cinnamates); 0 (Cnr1 protein, rat); 0 (N-(3-methoxyphenyl)-4-chlorocinnamanilide); 0 (Neurotransmitter Agents); 0 (Receptor, Cannabinoid, CB1); 0 (TRPV Cation Channels); 0 (Trpv1 protein, rat); 0 (arachidonyl serotonin); 0 (cyclohexyl carbamic acid 3'-carbamoylbiphenyl-3-yl ester); 333DO1RDJY (Serotonin); EC 3.5.- (Amidohydrolases); EC 3.5.1.- (fatty-acid amide hydrolase)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171224
[Lr] Data última revisão:
171224
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


  6 / 16030 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28743542
[Au] Autor:Maia J; Almada M; Silva A; Correia-da-Silva G; Teixeira N; Sá SI; Fonseca BM
[Ad] Endereço:UCIBIO, REQUIMTE, Departamento de Ciências Biológicas, Laboratório de Bioquímica, Faculdade de Farmácia, Universidade do Porto, Porto, Portugal.
[Ti] Título:The endocannabinoid system expression in the female reproductive tract is modulated by estrogen.
[So] Source:J Steroid Biochem Mol Biol;174:40-47, 2017 11.
[Is] ISSN:1879-1220
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The endocannabinoid system (ECS) is involved in several physiological events that resulted in a growing interest in its modulation. Moreover, the uterine levels of anandamide (AEA), the major endocannabinoid, must be tightly regulated to create proper embryo implantation conditions. However, there are no evidences about the regulation of AEA in uterus by estrogen. Thus, the aim of this study is to elucidate whether estradiol benzoate (EB) and tamoxifen (TAM) administration to ovariectomized (OVX) rats can induce changes in the expression of cannabinoid receptors and AEA-metabolic enzymes in uterus by evaluating gene transcription and protein levels by qPCR, Western blot and immunohistochemistry. Moreover, the plasmatic and uterine levels of AEA and of prostaglandin E (PGE ) and prostaglandin F α (PGF ), the major cyclooxygenase-2 (COX-2) products, were determined by UPLC-MS/MS. The immunohistochemistry showed that cannabinoid receptors, as well as AEA-metabolic enzymes are mainly located in the epithelial cells of both lumen and glands and, to a lesser extent, in the muscle cells. Moreover, EB administration to OVX rats significantly increased CB1, CB2, NAPE-PLD, FAAH and COX-2 expression and transcription. These effects were absent in TAM and TAM+EB treatments showing that this response is estrogen receptor dependent. Additionally, although uterine levels of AEA remained unchanged in EB or TAM treated animals, they showed a rise with EB treatment in plasma. The latter also produced a decrease in uterine PGE levels. In summary, these data collectively indicate that the expression of ECS components, as well as, the AEA and PGE levels in rat uterus is modulated by EB. Thus, estradiol may have a direct regulatory role in the modulation of ECS in female reproductive tissues.
[Mh] Termos MeSH primário: Estradiol/análogos & derivados
Estrogênios/farmacologia
Tamoxifeno/farmacologia
Útero/efeitos dos fármacos
[Mh] Termos MeSH secundário: Amidoidrolases/genética
Amidoidrolases/metabolismo
Animais
Ácidos Araquidônicos/sangue
Ácidos Araquidônicos/metabolismo
Ciclo-Oxigenase 2/genética
Ciclo-Oxigenase 2/metabolismo
Dinoprosta/sangue
Dinoprostona/sangue
Dinoprostona/metabolismo
Endocanabinoides/sangue
Endocanabinoides/metabolismo
Estradiol/farmacologia
Feminino
Tamanho do Órgão/efeitos dos fármacos
Ovariectomia
Fosfolipase D/genética
Fosfolipase D/metabolismo
Alcamidas Poli-Insaturadas/sangue
Alcamidas Poli-Insaturadas/metabolismo
Ratos Wistar
Receptor CB1 de Canabinoide/genética
Receptor CB1 de Canabinoide/metabolismo
Receptor CB2 de Canabinoide/genética
Receptor CB2 de Canabinoide/metabolismo
Útero/metabolismo
Útero/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Arachidonic Acids); 0 (Endocannabinoids); 0 (Estrogens); 0 (Polyunsaturated Alkamides); 0 (Receptor, Cannabinoid, CB1); 0 (Receptor, Cannabinoid, CB2); 094ZI81Y45 (Tamoxifen); 1S4CJB5ZGN (estradiol 3-benzoate); 4TI98Z838E (Estradiol); B7IN85G1HY (Dinoprost); EC 1.14.99.1 (Cyclooxygenase 2); EC 1.14.99.1 (Ptgs2 protein, rat); EC 3.1.4.4 (NAPE-PLD protein, rat); EC 3.1.4.4 (Phospholipase D); EC 3.5.- (Amidohydrolases); EC 3.5.1.- (fatty-acid amide hydrolase); K7Q1JQR04M (Dinoprostone); UR5G69TJKH (anandamide)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171208
[Lr] Data última revisão:
171208
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE


  7 / 16030 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28938452
[Au] Autor:Forner-Piquer I; Maradonna F; Gioacchini G; Santangeli S; Allarà M; Piscitelli F; Habibi HR; Di Marzo V; Carnevali O
[Ad] Endereço:Dipartimento Scienze della Vita e dell'Ambiente, Università Politecnica delle Marche, 60131 Ancona, Italy.
[Ti] Título:Dose-Specific Effects of Di-Isononyl Phthalate on the Endocannabinoid System and on Liver of Female Zebrafish.
[So] Source:Endocrinology;158(10):3462-3476, 2017 Oct 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Phthalates, used as plasticizers, have become a ubiquitous contaminant and have been reported for their potential to induce toxicity in living organisms. Among them, di-isononyl phthalate (DiNP) has been recently used to replace di(2-ethylhexyl) phthalate (DEHP). Nowadays, there is evidence that DiNP is an endocrine-disrupting chemical; however, little is known about its effects on the endocannabinoid system (ECS) and lipid metabolism. Hence, the aim of our study was to investigate the effects of DiNP on the ECS in zebrafish liver and brain and on hepatic lipid storage. To do so, adult female zebrafish were exposed to three concentrations (0.42 µg/L, 4.2 µg/L, and 42 µg/L) of DiNP via water for 3 weeks. Afterwards, we investigated transcript levels for genes involved in the ECS of the brain and liver as well as liver histology and image analysis, Fourier-transform infrared spectroscopy imaging, and measurement of endocannabinoid levels. Our results demonstrate that DiNP upregulates orexigenic signals and causes hepatosteatosis together with deregulation of the peripheral ECS and lipid metabolism. A decrease in the levels of ECS components at the central level was observed after exposure to the highest DiNP concentration tested. These findings suggest that replacement of DEHP with DiNP should be considered with caution because of observed adverse DiNP effects on aquatic organisms.
[Mh] Termos MeSH primário: Encéfalo/efeitos dos fármacos
Endocanabinoides/metabolismo
Metabolismo dos Lipídeos/efeitos dos fármacos
Fígado/efeitos dos fármacos
Ácidos Ftálicos/farmacologia
Plastificantes/farmacologia
[Mh] Termos MeSH secundário: Animais
Ácidos Araquidônicos/metabolismo
Encéfalo/metabolismo
Relação Dose-Resposta a Droga
Disruptores Endócrinos/farmacologia
Fígado Gorduroso/metabolismo
Feminino
Expressão Gênica/efeitos dos fármacos
Glicerídeos/metabolismo
Lipase Lipoproteica/efeitos dos fármacos
Lipase Lipoproteica/genética
Lipase Lipoproteica/metabolismo
Fosfolipase D/efeitos dos fármacos
Fosfolipase D/genética
Fosfolipase D/metabolismo
Alcamidas Poli-Insaturadas/metabolismo
Receptor CB1 de Canabinoide/efeitos dos fármacos
Receptor CB1 de Canabinoide/genética
Receptor CB1 de Canabinoide/metabolismo
Receptor CB2 de Canabinoide/efeitos dos fármacos
Receptor CB2 de Canabinoide/genética
Receptor CB2 de Canabinoide/metabolismo
Peixe-Zebra
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Arachidonic Acids); 0 (Endocannabinoids); 0 (Endocrine Disruptors); 0 (Glycerides); 0 (Phthalic Acids); 0 (Plasticizers); 0 (Polyunsaturated Alkamides); 0 (Receptor, Cannabinoid, CB1); 0 (Receptor, Cannabinoid, CB2); 4010KIX4CK (diisononyl phthalate); 8D239QDW64 (glyceryl 2-arachidonate); EC 3.1.1.34 (Lipoprotein Lipase); EC 3.1.4.4 (N-acylphosphatidylethanolamine phospholipase D, mouse); EC 3.1.4.4 (Phospholipase D); UR5G69TJKH (anandamide)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170923
[St] Status:MEDLINE
[do] DOI:10.1210/en.2017-00458


  8 / 16030 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28910408
[Au] Autor:Karlsson J; Gouveia-Figueira S; Alhouayek M; Fowler CJ
[Ad] Endereço:Department of Pharmacology and Clinical Neuroscience, Pharmacology Unit, Umeå University, Umeå, Sweden.
[Ti] Título:Effects of tumour necrosis factor α upon the metabolism of the endocannabinoid anandamide in prostate cancer cells.
[So] Source:PLoS One;12(9):e0185011, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Tumour necrosis factor α (TNFα) is involved in the pathogenesis of prostate cancer, a disease where disturbances in the endocannabinoid system are seen. In the present study we have investigated whether treatment of DU145 human prostate cancer cells affects anandamide (AEA) catabolic pathways. Additionally, we have investigated whether cyclooxygenase-2 (COX-2) can regulate the uptake of AEA into cells. Levels of AEA synthetic and catabolic enzymes were determined by qPCR. AEA uptake and hydrolysis in DU145 and RAW264.7 macrophage cells were assayed using AEA labeled in the arachidonic and ethanolamine portions of the molecule, respectively. Levels of AEA, related N-acylethanolamines (NAEs), prostaglandins (PG) and PG-ethanolamines (PG-EA) in DU145 cells and medium were quantitated by ultra-performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS) analysis. TNFα treatment of DU145 cells increased mRNA levels of PTSG2 (gene of COX-2) and decreased the mRNA of the AEA synthetic enzyme N-acyl-phosphatidylethanolamine selective phospholipase D. mRNA levels of the AEA hydrolytic enzymes fatty acid amide hydrolase (FAAH) and N-acylethanolamine-hydrolyzing acid amidase were not changed. AEA uptake in both DU145 and RAW264.7 cells was inhibited by FAAH inhibition, but not by COX-2 inhibition, even in RAW264.7 cells where the expression of this enzyme had greatly been induced by lipopolysaccharide + interferon γ treatment. AEA and related NAEs were detected in DU145 cells, but PGs and PGE2-EA were only detected when the cells had been preincubated with 100 nM AEA. The data demonstrate that in DU145 cells, TNFα treatment changes the relative expression of the enzymes involved in the hydrolytic and oxygenation catabolic pathways for AEA. In RAW264.7 cells, COX-2, in contrast to FAAH, does not regulate the cellular accumulation of AEA. Further studies are necessary to determine the extent to which inflammatory mediators are involved in the abnormal endocannabinoid signalling system in prostate cancer.
[Mh] Termos MeSH primário: Amidoidrolases/genética
Ácidos Araquidônicos/análise
Ciclo-Oxigenase 2/genética
Endocanabinoides/análise
Alcamidas Poli-Insaturadas/análise
Neoplasias da Próstata/metabolismo
Fator de Necrose Tumoral alfa/farmacologia
[Mh] Termos MeSH secundário: Amidoidrolases/metabolismo
Animais
Linhagem Celular Tumoral
Cromatografia Líquida de Alta Pressão
Ciclo-Oxigenase 2/metabolismo
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Lipopolissacarídeos/efeitos adversos
Masculino
Camundongos
Prostaglandinas/análise
Neoplasias da Próstata/genética
Células RAW 264.7
Espectrometria de Massas em Tandem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Arachidonic Acids); 0 (Endocannabinoids); 0 (Lipopolysaccharides); 0 (Polyunsaturated Alkamides); 0 (Prostaglandins); 0 (Tumor Necrosis Factor-alpha); EC 1.14.99.1 (Cyclooxygenase 2); EC 1.14.99.1 (PTGS2 protein, human); EC 3.5.- (Amidohydrolases); EC 3.5.1.- (fatty-acid amide hydrolase); UR5G69TJKH (anandamide)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171012
[Lr] Data última revisão:
171012
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170915
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0185011


  9 / 16030 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28859122
[Au] Autor:Luszczki JJ; Patrzylas P; Zagaja M; Andres-Mach M; Zaluska K; Kondrat-Wrobel MW; Szpringer M; Chmielewski J; Florek-Luszczki M
[Ad] Endereço:Department of Pathophysiology, Medical University of Lublin, Lublin, Poland.
[Ti] Título:Effects of arachidonyl-2'-chloroethylamide (ACEA) on the protective action of various antiepileptic drugs in the 6-Hz corneal stimulation model in mice.
[So] Source:PLoS One;12(8):e0183873, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Accumulating evidence indicates that cannabinoid CB1 receptor ligands play a pivotal role in seizures, not only in preclinical studies on animals, but also in clinical settings. This study was aimed at characterizing the influence of arachidonyl-2'-chloroethylamide (ACEA-a selective cannabinoid CB1 receptor agonist) co-administered with phenylmethylsulfonyl fluoride (PMSF) on the anticonvulsant potency of various antiepileptic drugs (clobazam, lacosamide, levetiracetam, phenobarbital, tiagabine and valproate) in the 6-Hz corneal stimulation model. Psychomotor seizures in male albino Swiss mice were evoked by a current (32 mA, 6 Hz, 3 s stimulus duration) delivered via corneal electrodes. Potential adverse effects produced by the antiepileptic drugs in combination with ACEA+PMSF were assessed using the chimney test (motor performance), passive avoidance task (remembering and acquisition of learning), and grip-strength test (muscular strength). Brain concentrations of antiepileptic drugs were measured by HPLC to exclude any pharmacokinetic contribution to the observed effect. ACEA (5 mg/kg, i.p.) + PMSF (30 mg/kg, i.p.) significantly potentiated the anticonvulsant potency of levetiracetam (P<0.05), but not that of clobazam, lacosamide, phenobarbital, tiagabine or valproate in the 6-Hz corneal stimulation model. Moreover, ACEA+PMSF did not significantly affect total brain concentrations of levetiracetam in mice. No behavioral side effects were observed in animals receiving combinations of the studied antiepileptic drugs with ACEA+PMSF. In conclusion, the combined administration of ACEA+PMSF with levetiracetam is associated with beneficial anticonvulsant pharmacodynamic interaction in the 6-Hz corneal stimulation model. The selective activation of cannabinoid CB1 receptor-mediated neurotransmission in the brain may enhance levetiracetam-related suppression of seizures in epilepsy patients, contributing to the efficacious treatment of epilepsy in future.
[Mh] Termos MeSH primário: Anticonvulsivantes/farmacologia
Ácidos Araquidônicos/farmacologia
Epilepsia Parcial Complexa/tratamento farmacológico
Fluoreto de Fenilmetilsulfonil/farmacologia
Piracetam/análogos & derivados
Receptor CB1 de Canabinoide/agonistas
[Mh] Termos MeSH secundário: Acetamidas/farmacologia
Animais
Aprendizagem da Esquiva/efeitos dos fármacos
Benzodiazepinas/farmacologia
Córnea
Modelos Animais de Doenças
Sinergismo Farmacológico
Quimioterapia Combinada
Eletrochoque/métodos
Epilepsia Parcial Complexa/metabolismo
Epilepsia Parcial Complexa/fisiopatologia
Masculino
Camundongos
Força Muscular/efeitos dos fármacos
Ácidos Nipecóticos/farmacologia
Fenobarbital/farmacologia
Piracetam/farmacologia
Desempenho Psicomotor/efeitos dos fármacos
Ácido Valproico/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Acetamides); 0 (Anticonvulsants); 0 (Arachidonic Acids); 0 (Nipecotic Acids); 0 (Receptor, Cannabinoid, CB1); 0 (arachidonyl-2-chloroethylamide); 12794-10-4 (Benzodiazepines); 230447L0GL (etiracetam); 2MRO291B4U (clobazam); 563KS2PQY5 (lacosamide); 57KD15003I (Phenylmethylsulfonyl Fluoride); 614OI1Z5WI (Valproic Acid); YQE403BP4D (Phenobarbital); Z80I64HMNP (tiagabine); ZH516LNZ10 (Piracetam)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170901
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0183873


  10 / 16030 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28853554
[Au] Autor:Martin GG; Huang H; McIntosh AL; Kier AB; Schroeder F
[Ad] Endereço:Department of Physiology and Pharmacology, Texas A&M University , College Station, Texas 77843-4466, United States.
[Ti] Título:Endocannabinoid Interaction with Human FABP1: Impact of the T94A Variant.
[So] Source:Biochemistry;56(38):5147-5159, 2017 Sep 26.
[Is] ISSN:1520-4995
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Using recombinant human wild-type fatty acid binding protein 1 (WT FABP1 T94T) and a variant (FABP1 T94A) protein, fluorescence binding assays, and circular dichroism, it was shown for the first time that WT FABP1 and the T94A variant each have a single, relatively hydrophobic site for binding fluorescent NBD-labeled analogues of N-arachidonoylethanolamide and 2-arachidonoylglycerol with high affinity. Most native N-acylethanolamides (NAEs) but only one 2-monoacylglycerol [i.e., 2-arachidonoylglycerol (2-AG)] displaced WT FABP1-bound fluorescently labeled endocannabinoids (ECs). While the T94A variant did not differ in affinity for AEA and most other NAEs, it exhibited a modestly higher affinity for OEA, as well as a higher affinity for 2-AG. Binding of AEA and 2-AG altered WT FABP1's secondary structure more extensively than any other previously examined ligand did. The T94A variant without a ligand was more susceptible to temperature-induced unfolding. While the T94A variant was much less sensitive to ligand (i.e., AEA or 2-AG)-induced conformational change, nevertheless binding of AEA and 2-AG significantly stabilized the T94A structure to thermal unfolding. These data provide the first evidence that ECs not only bind to but also alter the secondary structure of the human FABP1, with the latter markedly impacted by the T94A substitution, a variant strongly associated with hepatic accumulation of lipids and non-alcoholic fatty liver disease (NAFLD). Importantly, NAFLD has been associated with elevated hepatic levels of ECs and FABP1.
[Mh] Termos MeSH primário: Endocanabinoides/metabolismo
Proteínas de Ligação a Ácido Graxo/química
Proteínas de Ligação a Ácido Graxo/metabolismo
[Mh] Termos MeSH secundário: Animais
Ácidos Araquidônicos/metabolismo
Sítios de Ligação
Dicroísmo Circular
Endocanabinoides/química
Proteínas de Ligação a Ácido Graxo/genética
Fluorescência
Glicerídeos/metabolismo
Seres Humanos
Alcamidas Poli-Insaturadas/metabolismo
Estrutura Secundária de Proteína
Ratos
Temperatura Ambiente
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Arachidonic Acids); 0 (Endocannabinoids); 0 (FABP1 protein, human); 0 (Fabp1 protein, rat); 0 (Fatty Acid-Binding Proteins); 0 (Glycerides); 0 (Polyunsaturated Alkamides); 8D239QDW64 (glyceryl 2-arachidonate); UR5G69TJKH (anandamide)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170831
[St] Status:MEDLINE
[do] DOI:10.1021/acs.biochem.7b00647



página 1 de 1603 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