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[PMID]:28346885
[Au] Autor:Cao FR; Xiao BX; Wang LS; Tao X; Yan MZ; Pan RL; Liao YH; Liu XM; Chang Q
[Ad] Endereço:Key Laboratory of Bioactive Substances and Resources Utilization of Chinese Herbal Medicine, Ministry of Education, Institute of Medicinal Plant Development, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100193, PR China.
[Ti] Título:Plasma and brain pharmacokinetics of ganoderic acid A in rats determined by a developed UFLC-MS/MS method.
[So] Source:J Chromatogr B Analyt Technol Biomed Life Sci;1052:19-26, 2017 May 01.
[Is] ISSN:1873-376X
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Ganoderic acid A (GAA), an active triterpenoid of the traditional Chinese herbal medicine Lingzhi, has been reported to exhibit antinociceptive, antioxidative, and anti-cancer activities. The present study aims to establish a sensitive and rapid UPLC-MS/MS method for studying the plasma and brain pharmacokinetics of GAA in rats. The analytes were separated on a C18 column eluted with a gradient mobile phase consisting of acetonitrile and 0.1% aqueous formic acid at 0.3mL/min. The eluate was monitored by a mass detector using an MRM (m/z, 515.3-285.1) model in negative electrospray ionization. The calibration curve showed good linearity (r >0.99), with limits of detection and quantification of 0.25 and 2.00 nmol/L, respectively. The intra- and inter-day precision and accuracy were less than 9.99% and ranged from 97.45% to 114.62%, respectively. The extraction recovery from plasma was between 92.89% and 98.87%. GAA was found to be stable in treated samples at room temperature (22°C) for 12h and in plasma at -20°C for 7d. The developed method was successfully applied to a pharmacokinetic study of GAA in rats. GAA could be rapidly absorbed into the circulation (T , 0.15h) and eliminated relatively slowly (t , 2.46h) after orally dosing, and could also be detected in the brain lateral ventricle (T , 0.25h and t , 1.40h) after intravenously dosing. The absolute oral bioavailability and brain permeability of GAA were estimated to be 8.68% and 2.96%, respectively.
[Mh] Termos MeSH primário: Encéfalo/metabolismo
Cromatografia Líquida de Alta Pressão/métodos
Medicamentos de Ervas Chinesas/farmacocinética
Ácidos Heptanoicos/sangue
Ácidos Heptanoicos/líquido cefalorraquidiano
Lanosterol/análogos & derivados
Espectrometria de Massas em Tandem/métodos
[Mh] Termos MeSH secundário: Analgésicos/sangue
Analgésicos/líquido cefalorraquidiano
Animais
Antineoplásicos Fitogênicos/sangue
Antineoplásicos Fitogênicos/líquido cefalorraquidiano
Antioxidantes/farmacocinética
Lanosterol/sangue
Lanosterol/líquido cefalorraquidiano
Limite de Detecção
Masculino
Microdiálise/métodos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE; VALIDATION STUDIES
[Nm] Nome de substância:
0 (Analgesics); 0 (Antineoplastic Agents, Phytogenic); 0 (Antioxidants); 0 (Drugs, Chinese Herbal); 0 (Heptanoic Acids); 1J05Z83K3M (Lanosterol); 548G37DF65 (ganoderic acid A)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170328
[St] Status:MEDLINE


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[PMID]:28035464
[Au] Autor:El-Tanbouly GS; El-Awady MS; Megahed NA; El-Kashef HA; Salem HA
[Ad] Endereço:Department of Pharmacology and Biochemistry, Faculty of Pharmacy, Delta University for Science and Technology, Gamasa, Egypt.
[Ti] Título:The lipoxin A agonist BML-111 attenuates acute hepatic dysfunction induced by cecal ligation and puncture in rats.
[So] Source:Naunyn Schmiedebergs Arch Pharmacol;390(4):361-368, 2017 Apr.
[Is] ISSN:1432-1912
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Sepsis is a systemic inflammatory response associating severe infection leading to multi-organ failure, such as hepatic dysfunction. This study investigates the possible hepatoprotective effect of the lipoxin A agonist (BML-111) in cecal ligation and puncture (CLP) model in rats. Pretreatment with BML-111 (1 mg/kg, i.p., 1 h before CLP) protected against CLP-induced mortality after 24 h. BML-111 prevented marked inflammatory cells in liver tissues and decreased elevation in serum hepatic biomarkers [alanine aminotransferase (ALT), aspartate aminotransferase (AST), total bilirubin (TB), gamma-glutamyl transferase (γ-GT)] induced by CLP. Additionally, BML-111 attenuated elevated serum level of interleukin-6 (IL-6) and downregulated hepatic IL-6 mRNA expression. Meanwhile, BML-111 further increased serum IL-10 and upregulated hepatic IL-10 mRNA expression, while it downregulated hepatic mRNA expression of nuclear factor inhibitory protein kappa-B alpha (NFκBia), toll-like receptor-4 (TLR-4), and 5-lipooxygenase (5-LOX). Moreover, BML-111 prevented NF-κB/p65 nuclear translocation and activation. In conclusion, BML-111 attenuated CLP-induced acute hepatic dysfunction through its anti-inflammatory effect by decreasing NF-κB activity, TLR-4, and 5-LOX expression with subsequent decrease in pro-inflammatory IL-6 and elevation in anti-inflammatory IL-10.
[Mh] Termos MeSH primário: Ácidos Heptanoicos/uso terapêutico
Lipoxinas/agonistas
Hepatopatias/tratamento farmacológico
Substâncias Protetoras/uso terapêutico
[Mh] Termos MeSH secundário: Alanina Transaminase/sangue
Animais
Araquidonato 5-Lipoxigenase/genética
Aspartato Aminotransferases/sangue
Bilirrubina/sangue
Ceco/lesões
Ceco/cirurgia
Ácidos Heptanoicos/farmacologia
Interleucina-10/sangue
Interleucina-10/genética
Interleucina-6/sangue
Interleucina-6/genética
Ligadura
Fígado/efeitos dos fármacos
Fígado/metabolismo
Fígado/patologia
Hepatopatias/etiologia
Hepatopatias/metabolismo
Hepatopatias/patologia
Masculino
NF-kappa B/genética
NF-kappa B/metabolismo
Substâncias Protetoras/farmacologia
RNA Mensageiro/metabolismo
Ratos Sprague-Dawley
Receptor 4 Toll-Like/genética
gama-Glutamiltransferase/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (5(S),6(R)-7-trihydroxyheptanoic acid, methyl ester); 0 (Heptanoic Acids); 0 (Interleukin-6); 0 (Lipoxins); 0 (NF-kappa B); 0 (Protective Agents); 0 (RNA, Messenger); 0 (Tlr4 protein, rat); 0 (Toll-Like Receptor 4); 0 (lipoxin A4); 130068-27-8 (Interleukin-10); EC 1.13.11.34 (Arachidonate 5-Lipoxygenase); EC 2.3.2.2 (gamma-Glutamyltransferase); EC 2.6.1.1 (Aspartate Aminotransferases); EC 2.6.1.2 (Alanine Transaminase); RFM9X3LJ49 (Bilirubin)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170920
[Lr] Data última revisão:
170920
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161231
[St] Status:MEDLINE
[do] DOI:10.1007/s00210-016-1335-2


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[PMID]:27884962
[Au] Autor:Tucci S; Floegel U; Beermann F; Behringer S; Spiekerkoetter U
[Ad] Endereço:Department of General Pediatrics, Center for Pediatrics and Adolescent Medicine, University Hospital Freiburg, Freiburg, Germany sara.tucci@uniklinik-freiburg.de.
[Ti] Título:Triheptanoin: long-term effects in the very long-chain acyl-CoA dehydrogenase-deficient mouse.
[So] Source:J Lipid Res;58(1):196-207, 2017 Jan.
[Is] ISSN:1539-7262
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A rather new approach in the treatment of long-chain fatty acid oxidation disorders is represented by triheptanoin, a triglyceride with three medium-odd-chain heptanoic acids (C7), due to its anaplerotic potential. We here investigate the effects of a 1-year triheptanoin-based diet on the clinical phenotype of very long-chain-acyl-CoA-dehydrogenase-deficient (VLCAD ) mice. The cardiac function was assessed in VLCAD mice by in vivo MRI. Metabolic adaptations were identified by the expression of genes regulating energy metabolism and anaplerotic processes using real-time PCR, and the results were correlated with the measurement of the glycolytic enzymes pyruvate dehydrogenase and pyruvate kinase. Finally, the intrahepatic lipid accumulation and oxidative stress in response to the long-term triheptanoin diet were assessed. Triheptanoin was not able to prevent the development of systolic dysfunction in VLCAD mice despite an upregulation of cardiac glucose oxidation. Strikingly, the anaplerotic effects of triheptanoin were restricted to the liver. Despite this, the hepatic lipic content was increased upon triheptanoin supplementation. Our data demonstrate that the concept of anaplerosis does not apply to all tissues equally.
[Mh] Termos MeSH primário: Acil-CoA Desidrogenase de Cadeia Longa/genética
Cardiomiopatias/tratamento farmacológico
Erros Inatos do Metabolismo Lipídico/tratamento farmacológico
Triglicerídeos/administração & dosagem
[Mh] Termos MeSH secundário: Animais
Cardiomiopatias/genética
Cardiomiopatias/metabolismo
Cardiomiopatias/patologia
Metabolismo Energético/efeitos dos fármacos
Metabolismo Energético/genética
Ácidos Graxos/metabolismo
Ácidos Heptanoicos/metabolismo
Seres Humanos
Erros Inatos do Metabolismo Lipídico/genética
Erros Inatos do Metabolismo Lipídico/metabolismo
Erros Inatos do Metabolismo Lipídico/patologia
Fígado/metabolismo
Fígado/patologia
Camundongos
Oxirredução/efeitos dos fármacos
Estresse Oxidativo/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fatty Acids); 0 (Heptanoic Acids); 0 (Triglycerides); 2P6O7CFW5K (triheptanoin); EC 1.3.8.8 (Acyl-CoA Dehydrogenase, Long-Chain)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170824
[Lr] Data última revisão:
170824
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161126
[St] Status:MEDLINE
[do] DOI:10.1194/jlr.M072033


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[PMID]:27832512
[Au] Autor:Zhang K; Li H; Chen W; Zhao M; Cui H; Min Q; Wang H; Chen S; Li D
[Ad] Endereço:Tianjin Key Laboratory for Industrial BioSystems and Bioprocessing Engineering, Tianjin Institute of Industrial Biotechnology, Chinese Academy of Sciences, Tianjin, 300308, China.
[Ti] Título:Regulation of the Docosapentaenoic Acid/Docosahexaenoic Acid Ratio (DPA/DHA Ratio) in Schizochytrium limacinum B4D1.
[So] Source:Appl Biochem Biotechnol;182(1):67-81, 2017 May.
[Is] ISSN:1559-0291
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Docosapentaenoic acid/docosahexaenoic acid ratio (DPA/DHA ratio) in Schizochytrium was relatively stable. But ideally the ratio of DPA/DHA will vary according to the desired end use. This study reports several ways of modulating the DPA/DHA ratio. Incubation times changed the DPA/DHA ratio, and changes in this ratio were associated with the variations in the saturated fatty acid (SFAs) content. Propionic acid sharply increased the SFAs content in lipids, dramatically decreased the even-chain SFAs content, and reduced the DPA/DHA ratio. Pentanoic acid (C5:0) and heptanoic acid (C7:0) had similar effects as propionic acid, whereas butyric acid (C4:0), hexanoic acid (C6:0), and octanoic acid (C8:0) did not change the fatty acid profile and the DPA/DHA ratio. Transcription analyses show that ß-oxidation might be responsible for this phenomenon. Iodoacetamide upregulated polyunsaturated fatty acid (PUFA) synthase genes, reduced the DHA content, and improved the DPA content, causing the DPA/DHA ratio to increase. These results present new insights into the regulation of the DPA/DHA ratio.
[Mh] Termos MeSH primário: Ácidos Docosa-Hexaenoicos/biossíntese
Ácido Graxo Sintases/genética
Ácidos Graxos Insaturados/biossíntese
Estramenópilas/efeitos dos fármacos
Transcrição Genética/efeitos dos fármacos
[Mh] Termos MeSH secundário: Ácido Butírico/metabolismo
Ácido Butírico/farmacologia
Caproatos/metabolismo
Caproatos/farmacologia
Caprilatos/metabolismo
Caprilatos/farmacologia
Ácido Graxo Sintases/metabolismo
Ácidos Graxos/biossíntese
Ácidos Heptanoicos/metabolismo
Ácidos Heptanoicos/farmacologia
Iodoacetamida/farmacologia
Ácidos Pentanoicos/metabolismo
Ácidos Pentanoicos/farmacologia
Propionatos/metabolismo
Propionatos/farmacologia
Estramenópilas/enzimologia
Estramenópilas/genética
Estramenópilas/crescimento & desenvolvimento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Caproates); 0 (Caprylates); 0 (Fatty Acids); 0 (Fatty Acids, Unsaturated); 0 (Heptanoic Acids); 0 (Pentanoic Acids); 0 (Propionates); 107-92-6 (Butyric Acid); 1F8SN134MX (hexanoic acid); 25167-62-8 (Docosahexaenoic Acids); EC 2.3.1.85 (Fatty Acid Synthases); JHU490RVYR (propionic acid); NS3OZT14QT (docosapentaenoic acid); OBL58JN025 (octanoic acid); ZRH8M27S79 (Iodoacetamide)
[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:161111
[St] Status:MEDLINE
[do] DOI:10.1007/s12010-016-2311-5


  5 / 5722 MEDLINE  
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[PMID]:28294872
[Au] Autor:Mikhin VP; Zhilyaeva YA; Gromnaky NI
[Ad] Endereço:Kursk State Medical University, Kursk, Russia.
[Ti] Título:[Pleotropic Effects of Atorvastatin in Patients With Chronic Ischemic Heart Disease].
[So] Source:Kardiologiia;56(5):42-46, 2016 May.
[Is] ISSN:0022-9040
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:Examined 52 patients with a diagnosis Ischemic heart disease: stable angina II-III FC CHF I-IIA stage, in combination with hypercholesterolemia aged 53-65 years (58,2+/-6,5), receiving together with traditional antianginal therapy generic atorvastatin Torvakard in the dose of 10 mg/day (20 people) with the level of total cholesterol from 5.0 to 6.50 mmol/l, patients with cholesterol levels from is 6.51 to 8.0 mmol/l was taking Torvakard 20 mg/day (32 person). As a result of 3 months therapy with low doses of Torvakarda decreased level of CRP, endothelin-1, IMT, improving the parameters of endothelium-dependent vasodilation, which shows the positive impact of the drug on morphological and functional parameters of the vascular wall.
[Mh] Termos MeSH primário: Isquemia Miocárdica
[Mh] Termos MeSH secundário: Idoso
Anticolesterolemiantes
Atorvastatina Cálcica
LDL-Colesterol
Ácidos Heptanoicos
Seres Humanos
Inibidores de Hidroximetilglutaril-CoA Redutases
Hipercolesterolemia
Meia-Idade
Pirróis
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anticholesteremic Agents); 0 (Cholesterol, LDL); 0 (Heptanoic Acids); 0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors); 0 (Pyrroles); 48A5M73Z4Q (Atorvastatin Calcium)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170914
[Lr] Data última revisão:
170914
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170316
[St] Status:MEDLINE


  6 / 5722 MEDLINE  
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[PMID]:28087914
[Au] Autor:Yan L; Ye L; Wang K; Zhou J; Zhu C
[Ad] Endereço:Department of Cardiology, Tongling People's Hospital of Anhui Province, Tongling 244000, China.
[Ti] Título:[Atorvastatin improves reflow after percutaneous coronary intervention in patients with acute ST-segment elevation myocardial infarction by decreasing serum uric acid level].
[So] Source:Zhejiang Da Xue Xue Bao Yi Xue Ban;45(5):530-535, 2016 May 25.
[Is] ISSN:1008-9292
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:To investigate the effect of atorvastatin on reflow in patients with acute ST-segment elevation myocardial infarction (STEMI) after percutaneous coronary intervention (PCI) and its relation to serum uric acid levels. One hundred and fourteen STEMI patients undergoing primary PCI were enrolled and randomly divided into two groups:55 cases received oral atorvastatin 20 mg before PCI (routine dose group) and 59 cases received oral atorvastatin 80 mg before PCI (high dose group). According to the initial serum uric acid level, patients in two groups were further divided into normal uric acid subgroup and hyperuricemia subgroup. The changes of uric acid level and coronary artery blood flow after PCI were observed. Correlations between the decrease of uric acid, the dose of atorvastatin and the blood flow of coronary artery after PCI were analyzed. Serum uric acid levels were decreased after treatment in both groups (all <0.05), and patients with hyperuricemia showed more significant decrease in serum uric acid level ( <0.05). Compared with the routine dose group, serum uric acid level in patients with hyperuricemia decreased more significantly in the high dose group ( <0.05), but no significant difference was observed between patients with normal serum uric acid levels in two groups ( >0.05). Among 114 patients, there were 19 cases without reflow after PCI (16.7%). In the routine dose group, there were 12 patients without reflow, in which 3 had normal uric acid and 9 had high uric acid levels ( <0.01). In the high dose group, there were 7 patients without reflow, in which 2 had normal uric acid and 5 had high uric acid ( <0.05). Logistic regression analysis showed that hyperuricemia was one of independent risk factors for no-reflow after PCI ( =1.01, 95% :1.01-1.11, <0.01). The incidence of no-flow after PCI in the routine dose group was 21.8% (12/55), and that in the high dose group was 11.9% (7/59) ( <0.01). High dose atorvastatin can decrease serum uric acid levels and improve reflow after PCI in patients with STEMI.
[Mh] Termos MeSH primário: Atorvastatina Cálcica/uso terapêutico
Hiperuricemia/complicações
Hiperuricemia/tratamento farmacológico
Reperfusão Miocárdica/métodos
Intervenção Coronária Percutânea/efeitos adversos
Infarto do Miocárdio com Supradesnível do Segmento ST/cirurgia
Ácido Úrico/metabolismo
[Mh] Termos MeSH secundário: Doença Aguda
Feminino
Ácidos Heptanoicos
Seres Humanos
Masculino
Pirróis
Fatores de Risco
Ácido Úrico/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Heptanoic Acids); 0 (Pyrroles); 268B43MJ25 (Uric Acid); 48A5M73Z4Q (Atorvastatin Calcium)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170115
[St] Status:MEDLINE


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[PMID]:27749253
[Au] Autor:Hassan SA; Elzanfaly ES; El-Zeany SB; Salem MY
[Ti] Título:Development and validation of HPLC and CE methods for simultaneous determination of amlodipine and atorvastatin in the presence of their acidic degradation products in tablets.
[So] Source:Acta Pharm;66(4):479-490, 2016 Dec 01.
[Is] ISSN:1846-9558
[Cp] País de publicação:Croatia
[La] Idioma:eng
[Ab] Resumo:Two methods were developed for separation and quantitation of amlodipine (AML) and atorvastatin (ATV) in the presence of their acidic degradation products. The first method was a simple isocratic RP-HPLC method while the second was capillary electrophoresis (CE). Degradation products were obtained by acidic hydrolysis of the two drugs and their structures were elucidated for the first time by IR and MS spectra. Degradation products did not interfere with the determination of either drug and the assays were therefore stability-indicating. The linearity of the proposed methods was established over the ranges 1-50 µg mL-1 for AML and ATV in the HPLC method and in the range of 3-50 and 4-50 µg mL-1 for AML and ATV, respectively, in the CE method. The proposed methods were validated according to ICH guidelines. The methods were successfully applied to estimation of AML and ATV in combined tablets.
[Mh] Termos MeSH primário: Anlodipino/análise
Anticolesterolemiantes/análise
Anti-Hipertensivos/análise
Atorvastatina Cálcica/análise
Bloqueadores dos Canais de Cálcio/análise
Química Farmacêutica/métodos
Inibidores de Hidroximetilglutaril-CoA Redutases/análise
[Mh] Termos MeSH secundário: Anlodipino/análogos & derivados
Anlodipino/química
Anticolesterolemiantes/química
Anti-Hipertensivos/química
Atorvastatina Cálcica/análogos & derivados
Atorvastatina Cálcica/química
Bloqueadores dos Canais de Cálcio/química
Calibragem
Cromatografia Líquida de Alta Pressão
Cromatografia de Fase Reversa
Combinação de Medicamentos
Estabilidade de Medicamentos
Eletroforese Capilar
Ácidos Heptanoicos/química
Ácido Clorídrico/química
Hidrólise/efeitos dos fármacos
Inibidores de Hidroximetilglutaril-CoA Redutases/química
Limite de Detecção
Estrutura Molecular
Pirróis/química
Reprodutibilidade dos Testes
Comprimidos
[Pt] Tipo de publicação:JOURNAL ARTICLE; VALIDATION STUDIES
[Nm] Nome de substância:
0 (Anticholesteremic Agents); 0 (Antihypertensive Agents); 0 (Calcium Channel Blockers); 0 (Drug Combinations); 0 (Heptanoic Acids); 0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors); 0 (Pyrroles); 0 (Tablets); 0 (amlodipine, atorvastatin drug combination); 1J444QC288 (Amlodipine); 48A5M73Z4Q (Atorvastatin Calcium); QTT17582CB (Hydrochloric Acid)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170124
[Lr] Data última revisão:
170124
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161018
[St] Status:MEDLINE


  8 / 5722 MEDLINE  
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[PMID]:27640015
[Au] Autor:Gill BS; Kumar S; Navgeet
[Ad] Endereço:Centre for Biosciences, Central University of Punjab, Bathinda, India.
[Ti] Título:Evaluating anti-oxidant potential of ganoderic acid A in STAT 3 pathway in prostate cancer.
[So] Source:Mol Biol Rep;43(12):1411-1422, 2016 Dec.
[Is] ISSN:1573-4978
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Evaluating anti-oxidant potential of Ganoderic acid A in STAT 3 pathway in Prostate cancer. Molecular docking and ADMET activities of different isoforms of ganoderic acid on STAT 3 pathway were performed by Maestro 9.6 (Schrödinger Inc). The ganoderic acid A is best-docked among isoforms which analyses the expression level of antioxidant and STAT 3 pathway in PC-3 cells. The receptor-based molecular docking reveals the best binding interaction of SH2 domain of STAT3 and ganoderic acid A with GScore (-6.134), kcal/mol, Lipophilic EvdW (-1.83), Electro (-1.1), Glide emodel (-31.857), H bond (1.98), MM-GBSA (-69.555). The molecular docking QikProp analyzed the absorption, distribution, metabolism, excretion, and toxicity (ADME/T). The ganoderic acid A is best-docked among isoforms which downregulates the expression of STAT 3 in PC-3 cells. Moreover, ganoderic acid A inhibits proliferation, viability, ROS, DPPH, and analyzed the expression of SOD1, SOD2, and SOD3 by Real time PCR in a PC-3 cell in a dose-dependent manner. Molecular docking revealed the mechanistic binding of Ganoderic acid A in STAT3 signaling, which inhibits the proliferation, viability, and ROS in PC-3 cells.
[Mh] Termos MeSH primário: Antineoplásicos/química
Depuradores de Radicais Livres/química
Ácidos Heptanoicos/química
Lanosterol/análogos & derivados
Neoplasias da Próstata/tratamento farmacológico
Fator de Transcrição STAT3/química
[Mh] Termos MeSH secundário: Antineoplásicos/farmacologia
Sítios de Ligação
Linhagem Celular Tumoral
Proliferação Celular
Ensaios de Seleção de Medicamentos Antitumorais
Expressão Gênica/efeitos dos fármacos
Ácidos Heptanoicos/farmacologia
Seres Humanos
Ligações de Hidrogênio
Lanosterol/química
Lanosterol/farmacologia
Masculino
Simulação de Acoplamento Molecular
Terapia de Alvo Molecular
Ligação Proteica
Termodinâmica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Free Radical Scavengers); 0 (Heptanoic Acids); 0 (STAT3 Transcription Factor); 0 (STAT3 protein, human); 1J05Z83K3M (Lanosterol); 548G37DF65 (ganoderic acid A)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160919
[St] Status:MEDLINE


  9 / 5722 MEDLINE  
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[PMID]:27618287
[Au] Autor:Guo J; Hong L; West XZ; Wang H; Salomon RG
[Ad] Endereço:Department of Chemistry, Case Western Reserve University , Cleveland, Ohio 44106, United States.
[Ti] Título:Bioactive 4-Oxoheptanedioic Monoamide Derivatives of Proteins and Ethanolaminephospholipids: Products of Docosahexaenoate Oxidation.
[So] Source:Chem Res Toxicol;29(10):1706-1719, 2016 Oct 17.
[Is] ISSN:1520-5010
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Oxidative stress causes lipid-derived oxidative modification of biomolecules that has been implicated in many pathological states. Phospholipids containing polyunsaturated fatty acids are major targets of free radical-initiated oxidation. Phospholipids that incorporate docosahexaenoate (DHA) are highly enriched in important neural structures including the brain and retina, where DHA comprises 40% and 60% of total fatty acids, respectively. Oxidative fragmentation of 2-docosahexaenoyl-1-palmityl-sn-glycerophosphocholine generates esters of 4-hydroxy-7-oxohept-5-enoic acid (HOHA) and 4-keto-7-oxohept-5-enoic acid (KOHA) with 2-lysophosphatidylcholine, HOHA-PC, and KOHA-PC. Covalent HOHA adducts that incorporate the primary amino groups of proteins and ethanolamine phospholipids in carboxyethylpyrrole (CEP) derivatives were detected immunologically with anti-CEP antibodies in human tumors, retina, and blood. Now, we generated an anti-OHdiA antibody to test the hypothesis that KOHA adducts, which incorporate the primary amino groups of proteins or ethanolamine phospholipids in 4-oxo-heptanedioic (OHdiA) monoamide derivatives, are present in vivo. However, whereas the anti-CEP antibody is highly specific and does not cross-react with the OHdiA monoamide epitope, the anti-OHdiA monoamide antibody cross-reacted with CEP epitopes making it of little value as an analytical tool for OHdiA monoamides but suggesting the possibility that OHdiA monoamides would exhibit receptor-mediated biological activity similar to that of CEP. An LC-MS/MS method was developed that allows quantification of OHdiA derivatives in biological samples. We now find that KOHA-PC forms OHdiA monoamide adducts of proteins and ethanolamine phospholipids and that OHdiA-protein levels are significantly higher than OHdiA-ethanloamine phospholipid levels in blood from healthy human subjects, 0.45 µM and 0.18 µM, respectively (n = 3, and p = 0.027). OHdiA monoamide epitopes are angiogenic, causing TLR2-dependent adhesion and tube formation by human umbilical vein endothelial cells. OHdiA monoamide epitopes are only slightly less potent than CEP epitopes that contribute to the pathological angiogenesis of age-related macular degeneration and tumor growth.
[Mh] Termos MeSH primário: Ácidos Dicarboxílicos/metabolismo
Ácidos Docosa-Hexaenoicos/metabolismo
Etanolamina/metabolismo
Ácidos Heptanoicos/metabolismo
Fosfolipídeos/metabolismo
Albumina Sérica/metabolismo
[Mh] Termos MeSH secundário: Animais
Bovinos
Ácidos Dicarboxílicos/química
Ácidos Docosa-Hexaenoicos/química
Etanolamina/sangue
Etanolamina/química
Ácidos Heptanoicos/química
Células Endoteliais da Veia Umbilical Humana/citologia
Células Endoteliais da Veia Umbilical Humana/metabolismo
Seres Humanos
Estrutura Molecular
Oxirredução
Fosfolipídeos/sangue
Fosfolipídeos/química
Albumina Sérica/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Dicarboxylic Acids); 0 (Heptanoic Acids); 0 (Phospholipids); 0 (Serum Albumin); 25167-62-8 (Docosahexaenoic Acids); 5KV86114PT (Ethanolamine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171017
[Lr] Data última revisão:
171017
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160913
[St] Status:MEDLINE


  10 / 5722 MEDLINE  
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Texto completo
[PMID]:27575328
[Au] Autor:Sakamoto S; Kikkawa N; Kohno T; Shimizu K; Tanaka H; Morimoto S
[Ad] Endereço:Department of Pharmacognosy, Graduate School of Pharmaceutical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan.
[Ti] Título:Immunochromatographic strip assay for detection of bioactive Ganoderma triterpenoid, ganoderic acid A in Ganoderma lingzhi.
[So] Source:Fitoterapia;114:51-55, 2016 Oct.
[Is] ISSN:1873-6971
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Ganoderic acid A (GAA) is one of the major Ganoderma triterpenes produced by medicinal mushroom belonging to the genus Ganoderma (Ganodermataceae). Due to its interesting pharmacological activities, Ganoderma species have been traditionally used in China for the treatment of various diseases. Herein, we developed a colloidal gold-based immunochromatographic strip assay (ICA) for the rapid detection of GAA using highly specific monoclonal antibody against GAA (MAb 12A) conjugated with gold nanoparticles. Using the developed ICA, the detection of GAA can be completed within 15min after dipping the test strip into an analyte solution with the limit of detection (LOD) for GAA of ~500ng/mL. In addition, this system makes it possible to perform a semi-quantitative analysis of GAA in Ganoderma lingzhi, where high reliability was evaluated by enzyme-linked immunosorbent assay (ELISA). The newly developed ICA can potentially be applied to the standardization of Ganoderma using GAA as an index because GAA is major triterpenoid present much in the mushroom.
[Mh] Termos MeSH primário: Ganoderma/química
Ácidos Heptanoicos/isolamento & purificação
Imunocromatografia
Lanosterol/análogos & derivados
[Mh] Termos MeSH secundário: Anticorpos Monoclonais
Ensaio de Imunoadsorção Enzimática
Lanosterol/isolamento & purificação
Limite de Detecção
Reprodutibilidade dos Testes
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Heptanoic Acids); 1J05Z83K3M (Lanosterol); 548G37DF65 (ganoderic acid A)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160831
[St] Status:MEDLINE



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