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[PMID]:29367479
[Au] Autor:Pornputtapitak W; Pantakitcharoenkul J; Panpakdee R; Teeranachaideekul V; Sinchaipanid N
[Ad] Endereço:Department of Chemical Engineering, Faculty of Engineering, Mahidol University.
[Ti] Título:Development of γ-Oryzanol Rich Extract from Leum Pua Glutinous Rice Bran Loaded Nanostructured Lipid Carriers for Topical Delivery.
[So] Source:J Oleo Sci;67(2):125-133, 2018 Feb 01.
[Is] ISSN:1347-3352
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Leum Pua is native Thai glutinous rice that contains antioxidants higher than white rice and other colored rice. One of the major antioxidants in rice brans is γ-oryzanol (GO). In this study, Leum Pua glutinous rice bran was extracted by different solvents. Oleic acid (~40 g/100 g extract), linoleic acid (~30 g/100 g extract), and palmitic acid (~20 g/100 g extract) were found to be major lipid components in the extracts. Methanol extract showed less variety of lipid components compared to the others. However, hexane extract showed the highest percent of γ-oryzanol compared to other solvents. Therefore, the hexane extract was selected to prepare nanostructured lipid carriers (NLC). The prepared NLC had small particles in the size range of 142.9 ± 0.4 nm for extract-loaded NLC and 137.1 ± 0.5 nm for GO-loaded NLC with narrow size distribution (PI < 0.1) in both formulations. The release profile of extract-loaded NLC formulation was slightly higher than GO-loaded NLC formulation. However, they did not follow the Higuchi model because of small amounts of γ-oryzanol loaded in NLC particles.
[Mh] Termos MeSH primário: Antioxidantes/isolamento & purificação
Portadores de Fármacos
Nanoestruturas
Oryza/química
Fenilpropionatos/isolamento & purificação
Extratos Vegetais/análise
Extratos Vegetais/isolamento & purificação
[Mh] Termos MeSH secundário: Hexanos
Ácido Linoleico/análise
Ácido Oleico/análise
Ácido Palmítico/análise
Tamanho da Partícula
Fenilpropionatos/análise
Solventes
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (Drug Carriers); 0 (Hexanes); 0 (Phenylpropionates); 0 (Plant Extracts); 0 (Solvents); 2UMI9U37CP (Oleic Acid); 2V16EO95H1 (Palmitic Acid); 9KJL21T0QJ (Linoleic Acid); SST9XCL51M (gamma-oryzanol)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180126
[St] Status:MEDLINE
[do] DOI:10.5650/jos.ess17113


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[PMID]:29180863
[Au] Autor:Liu K; Chen W; Yang T; Wen B; Ding D; Keidar M; Tang J; Zhang W
[Ad] Endereço:College of Pharmacy, Weifang Medical University, Weifang.
[Ti] Título:Paclitaxel and quercetin nanoparticles co-loaded in microspheres to prolong retention time for pulmonary drug delivery.
[So] Source:Int J Nanomedicine;12:8239-8255, 2017.
[Is] ISSN:1178-2013
[Cp] País de publicação:New Zealand
[La] Idioma:eng
[Ab] Resumo:High drug resistance, poor water solubility, short half-life, and low local drug concentration are obstacles for successful delivery of chemotherapeutic drugs for lung cancer. A new method involving the use of nanoparticles (NPs) for pulmonary delivery is proposed. However, use of NPs is limited by the particle size range for pulmonary drug delivery considering that NPs cannot be deposited directly into the lungs. NPs polymerized into microspheres (polymeric microspheres, PMs) will result in suitable particle sizes and retain the advantages of nanodrugs after redispersion when applied in pulmonary delivery. We report the development of novel NPs in the form of PMs loaded with paclitaxel (PTX) and quercetin (QUE) double drugs based on the synthesis of oleic acid-conjugated chitosan (OA-CTS) for pulmonary delivery. This approach is aimed toward prolonging PTX retention time in the presence of QUE and bypassing P-glycoprotein drug efflux pumps. NPs loaded with PTX or QUE were prepared with 11% substitution degree using OA-CTS as the carrier by ionic cross-linking method, which NPs loaded with PTX or QUE were used in the preparation of PMs by spray-drying. The diameters of the PMs ranged from 1 to 5 µm which had uniform size range. Scanning electron microscopy showed that PMs were polymers formed by a large number of NPs and readily redispersed (after redispersion, size of NPs ranged between 250 and 350 nm) in water within 1 h. PMs displayed slow-release characteristics at pH 4.5 and 7.4. The in vivo pharmacokinetic and biodistribution studies suggested that PMs exhibit prolonged circulation time and a markedly high accumulation in the lung. The obtained results indicate that PMs can serve as a promising pulmonary delivery system for combined pharmacotherapy using hydrophobic anticancer drugs.
[Mh] Termos MeSH primário: Pulmão/efeitos dos fármacos
Nanopartículas/química
Paclitaxel/administração & dosagem
Quercetina/administração & dosagem
[Mh] Termos MeSH secundário: Subfamília B de Transportador de Cassetes de Ligação de ATP/metabolismo
Membro 1 da Subfamília B de Cassetes de Ligação de ATP/metabolismo
Animais
Antineoplásicos/administração & dosagem
Quitosana/química
Sistemas de Liberação de Medicamentos
Liberação Controlada de Fármacos
Feminino
Meia-Vida
Masculino
Microesferas
Ácido Oleico/química
Paclitaxel/farmacocinética
Tamanho da Partícula
Quercetina/farmacocinética
Ratos Wistar
Distribuição Tecidual
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ATP Binding Cassette Transporter, Sub-Family B); 0 (ATP-Binding Cassette, Sub-Family B, Member 1); 0 (Antineoplastic Agents); 2UMI9U37CP (Oleic Acid); 9012-76-4 (Chitosan); 9IKM0I5T1E (Quercetin); P88XT4IS4D (Paclitaxel)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171129
[St] Status:MEDLINE
[do] DOI:10.2147/IJN.S147028


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[PMID]:28449683
[Au] Autor:Wang LF; Wang XN; Huang CC; Hu L; Xiao YF; Guan XH; Qian YS; Deng KY; Xin HB
[Ad] Endereço:Institute of Translational Medicine, Nanchang University, 999 Xuefu Load, Honggutan District, Nanchang, 330031, China.
[Ti] Título:Inhibition of NAMPT aggravates high fat diet-induced hepatic steatosis in mice through regulating Sirt1/AMPKα/SREBP1 signaling pathway.
[So] Source:Lipids Health Dis;16(1):82, 2017 Apr 27.
[Is] ISSN:1476-511X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Nonalcoholic fatty liver disease is one of the most common liver diseases in the world and is a typical hepatic manifestation of metabolic syndrome which is characterized with lipid accumulation in liver. Nicotinamide phosphoribosyltransferase (NAMPT) has been recently identified as an enzyme involved in nicotinamide adenine dinucleotide (NAD ) biosynthesis and plays an important role in cellular metabolism in variety of organs in mammals. The aim of this study was to investigate the effects of NAMPT on high fat diet-induced hepatic steatosis. METHODS: Hepatic steatosis model was induced by high fat diet (HFD) in C57BL/6 mice in vivo. HepG2 and Hep1-6 hepatocytes were transfected with NAMPT vector plasmid or treated with NAMPT inhibitor FK866 and then incubated with oleic acid. Lipids accumulation was examined by HE staining or oil red staining. Quantitative RT-PCR and Western blot were used to measure expressions of the genes involved in lipogenic synthesis. RESULTS: FK866 significantly promoted liver steatosis in the mice fed with HFD and hepatic lipid accumulation in vitro, accompanied by the increases of the expressions of lipogenic genes such as sterol regulatory element-binding protein 1 (SREBP1) and fatty acid synthase (FASN). Nicotinamide mononucleotide (NMN) and NAD significantly rescued the actions of FK866 in vitro. In contrast, overexpression of NAMPT in HepG2 and Hep1-6 hepatocytes ameliorated hepatic lipid accumulation. In addition, FK866 decreased the protein levels of Sirt1 and phospho-AMPKα in liver of the HFD fed mice. Furthermore, Resveratrol, a Sirt1 activator, significantly reduced lipogenic gene expressions, while EX-527, a Sirt1 specific inhibitor, had the opposite effects. CONCLUSION: Our results demonstrated that inhibition of NAMPT aggravated the HFD- or oleic acid-induced hepatic steatosis through suppressing Sirt1-mediated signaling pathway. On the one hand, the inhibition of NAMPT reduced the production of NAD through inhibiting the NAD salvage pathway, resulting in the decrease of Sirt1 activity, and then attenuated the deacetylation of SREBP1 in which the inhibition of SREBP1 activity promoted the expressions of FASN and ACC. On the other hand, the reduced Sirt1 activity alleviated the activation of AMPKα to further enhance SREBP1 activities.
[Mh] Termos MeSH primário: Proteínas Quinases Ativadas por AMP/genética
Citocinas/genética
Fígado/enzimologia
Nicotinamida Fosforribosiltransferase/genética
Hepatopatia Gordurosa não Alcoólica/genética
Sirtuína 1/genética
Proteína de Ligação a Elemento Regulador de Esterol 1/genética
[Mh] Termos MeSH secundário: Proteínas Quinases Ativadas por AMP/metabolismo
Acrilamidas/farmacologia
Animais
Carbazóis/farmacologia
Linhagem Celular
Citocinas/antagonistas & inibidores
Citocinas/metabolismo
Dieta Hiperlipídica/efeitos adversos
Inibidores Enzimáticos/farmacologia
Regulação da Expressão Gênica
Células Hep G2
Hepatócitos/efeitos dos fármacos
Hepatócitos/enzimologia
Hepatócitos/patologia
Seres Humanos
Fígado/efeitos dos fármacos
Fígado/patologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
NAD/farmacologia
Mononucleotídeo de Nicotinamida/farmacologia
Nicotinamida Fosforribosiltransferase/antagonistas & inibidores
Nicotinamida Fosforribosiltransferase/metabolismo
Hepatopatia Gordurosa não Alcoólica/enzimologia
Hepatopatia Gordurosa não Alcoólica/etiologia
Hepatopatia Gordurosa não Alcoólica/patologia
Ácido Oleico/farmacologia
Piperidinas/farmacologia
Transdução de Sinais
Sirtuína 1/antagonistas & inibidores
Sirtuína 1/metabolismo
Proteína de Ligação a Elemento Regulador de Esterol 1/metabolismo
Estilbenos/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (6-chloro-2,3,4,9-tetrahydro-1H-carbazole-1-carboxamide); 0 (Acrylamides); 0 (Carbazoles); 0 (Cytokines); 0 (Enzyme Inhibitors); 0 (N-(4-(1-benzoylpiperidin-4-yl)butyl)-3-(pyridin-3-yl)acrylamide); 0 (Piperidines); 0 (Srebf1 protein, mouse); 0 (Sterol Regulatory Element Binding Protein 1); 0 (Stilbenes); 0U46U6E8UK (NAD); 1094-61-7 (Nicotinamide Mononucleotide); 2UMI9U37CP (Oleic Acid); EC 2.4.2.12 (Nicotinamide Phosphoribosyltransferase); EC 2.4.2.12 (nicotinamide phosphoribosyltransferase, mouse); EC 2.7.11.1 (AMPK alpha1 subunit, mouse); EC 2.7.11.31 (AMP-Activated Protein Kinases); EC 3.5.1.- (Sirt1 protein, mouse); EC 3.5.1.- (Sirtuin 1); Q369O8926L (resveratrol)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180219
[Lr] Data última revisão:
180219
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1186/s12944-017-0464-z


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[PMID]:28461456
[Au] Autor:Zhao H; Matsuzaka T; Nakano Y; Motomura K; Tang N; Yokoo T; Okajima Y; Han SI; Takeuchi Y; Aita Y; Iwasaki H; Yatoh S; Suzuki H; Sekiya M; Yahagi N; Nakagawa Y; Sone H; Yamada N; Shimano H
[Ad] Endereço:Department of Internal Medicine (Endocrinology and Metabolism), Faculty of Medicine, University of Tsukuba, Tsukuba, Ibaraki, Japan.
[Ti] Título:Elovl6 Deficiency Improves Glycemic Control in Diabetic / Mice by Expanding ß-Cell Mass and Increasing Insulin Secretory Capacity.
[So] Source:Diabetes;66(7):1833-1846, 2017 07.
[Is] ISSN:1939-327X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Dysfunctional fatty acid (FA) metabolism plays an important role in the pathogenesis of ß-cell dysfunction and loss of ß-cell mass in type 2 diabetes (T2D). Elovl6 is a microsomal enzyme that is responsible for converting C16 saturated and monounsaturated FAs into C18 species. We previously showed that Elovl6 played a critical role in the development of obesity-induced insulin resistance by modifying FA composition. To further define its role in T2D development, we assessed the effects of deletion in leptin receptor-deficient C57BL/KsJ / mice, a model of T2D. The / ; mice had a markedly increased ß-cell mass with increased proliferation and decreased apoptosis, an adaptive increase in insulin, and improved glycemic control. / islets were characterized by a prominent elevation of oleate (C18:1n-9), cell stress, and inflammation, which was completely suppressed by Elovl6 deletion. As a mechanistic ex vivo experiment, isolated islets from mice exhibited reduced susceptibility to palmitate-induced inflammation, endoplasmic reticulum stress, and ß-cell apoptosis. In contrast, oleate-treated islets resulted in impaired glucose-stimulated insulin secretion with suppressed related genes irrespective of the Elovl6 gene. Taken together, Elovl6 is a fundamental factor linking dysregulated lipid metabolism to ß-cell dysfunction, islet inflammation, and ß-cell apoptosis in T2D, highlighting oleate as the potential culprit of ß-cell lipotoxicity.
[Mh] Termos MeSH primário: Acetiltransferases/deficiência
Acetiltransferases/genética
Diabetes Mellitus Experimental/genética
Diabetes Mellitus Tipo 2/genética
Células Secretoras de Insulina/secreção
Insulina/secreção
[Mh] Termos MeSH secundário: Acetiltransferases/fisiologia
Animais
Apoptose/genética
Glicemia/metabolismo
Diabetes Mellitus Experimental/metabolismo
Diabetes Mellitus Tipo 2/metabolismo
Estresse do Retículo Endoplasmático
Ácidos Graxos não Esterificados/metabolismo
Feminino
Imuno-Histoquímica
Técnicas In Vitro
Inflamação/induzido quimicamente
Inflamação/genética
Células Secretoras de Insulina/efeitos dos fármacos
Células Secretoras de Insulina/patologia
Ilhotas Pancreáticas/efeitos dos fármacos
Ilhotas Pancreáticas/patologia
Ilhotas Pancreáticas/secreção
Metabolismo dos Lipídeos/genética
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Ácido Oleico/farmacologia
Tamanho do Órgão
Palmitatos/efeitos adversos
Reação em Cadeia da Polimerase em Tempo Real
Receptores para Leptina/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Fatty Acids, Nonesterified); 0 (Insulin); 0 (Palmitates); 0 (Receptors, Leptin); 0 (leptin receptor, mouse); 2UMI9U37CP (Oleic Acid); EC 2.3.1.- (Acetyltransferases); EC 2.3.1.- (fatty acid elongases)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.2337/db16-1277


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[PMID]:29206239
[Au] Autor:Jones Iv AR; Coleman EL; Husni NR; Deeney JT; Raval F; Steenkamp D; Dooms H; Nikolajczyk BS; Corkey BE
[Ad] Endereço:Obesity Research Center, Evans Department of Medicine, Boston University School of Medicine, Boston, MA, United States of America.
[Ti] Título:Type 1 diabetes alters lipid handling and metabolism in human fibroblasts and peripheral blood mononuclear cells.
[So] Source:PLoS One;12(12):e0188474, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Triggers of the autoimmune response that leads to type 1 diabetes (T1D) remain poorly understood. A possibility is that parallel changes in both T cells and target cells provoke autoimmune attack. We previously documented greater Ca2+ transients in fibroblasts from T1D subjects than non-T1D after exposure to fatty acids (FA) and tumor necrosis factor α (TNFα). These data indicate that metabolic and signal transduction defects present in T1D can be elicited ex vivo in isolated cells. Changes that precede T1D, including inflammation, may activate atypical responses in people that are genetically predisposed to T1D. To identify such cellular differences in T1D, we quantified a panel of metabolic responses in fibroblasts and peripheral blood cells (PBMCs) from age-matched T1D and non-T1D subjects, as models for non-immune and immune cells, respectively. Fibroblasts from T1D subjects accumulated more lipid, had higher LC-CoA levels and converted more FA to CO2, with less mitochondrial proton leak in response to oleate alone or with TNFα, using the latter as a model of inflammation. T1D-PBMCs contained and also accumulated more lipid following FA exposure. In addition, they formed more peroxidized lipid than controls following FA exposure. We conclude that both immune and non-immune cells in T1D subjects differ from controls in terms of responses to FA and TNFα. Our results suggest a differential sensitivity to inflammatory insults and FA that may precede and contribute to T1D by priming both immune cells and their targets for autoimmune reactions.
[Mh] Termos MeSH primário: Diabetes Mellitus Tipo 1/metabolismo
Leucócitos Mononucleares/metabolismo
Metabolismo dos Lipídeos
[Mh] Termos MeSH secundário: Trifosfato de Adenosina/metabolismo
Fibroblastos/metabolismo
Seres Humanos
Peroxidação de Lipídeos
Ácido Oleico
Oxirredução
Consumo de Oxigênio
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Tumor Necrosis Factor-alpha); 2UMI9U37CP (Oleic Acid); 8L70Q75FXE (Adenosine Triphosphate)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171226
[Lr] Data última revisão:
171226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171206
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188474


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[PMID]:28460356
[Au] Autor:de Moraes MM; Treptow TGM; Teixeira WKO; Piovesan LA; D'Oca MGM; Votto APS
[Ad] Endereço:Laboratório de Cultura Celular, Programa de Pós-graduação em Ciências Fisiológicas, Instituto de Ciências Biológicas, Universidade Federal do Rio Grande - FURG, Rio Grande do Sul, Brazil.
[Ti] Título:Fatty-monastrol derivatives and its cytotoxic effect against melanoma cell growth.
[So] Source:Bioorg Chem;72:148-155, 2017 06.
[Is] ISSN:1090-2120
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Melanoma is the most dangerous type of skin cancer due to the occurrence of metastases. This work is aimed at studying the effects of the insertion of palmitic and oleic acid chain into monastrol in the melanoma cell line, B16F10. Cells were treated with monastrol, palmitic-monastrol or oleic-monastrol for periods of 0, 24, 48 and 72 h, and the cytotoxic effect was observed for palmitic-monastrol and oleic-monastrol after 24 h. For monastrol the effects were observed in 48 h on B16F10 cells, and in 24 h for a non-tumour cell line, melan-a. In this cell line, fatty-monastrol derivatives were cytotoxic after 24 h of exposure in the same concentrations as B16F10. However, oleic-monastrol inhibited cell growth at 20µM only after 72 h, in contrast to the B16F10 cell line, in which oleic-monastrol inhibited cell growth at 48 h, showing that at least in this structural modification, melan-a was less sensitive than B16F10. The ability of compounds to induce apoptosis and/or necrosis was measured, and it was observed that monastrol induces apoptosis within 24 h. However, the cells treated with fatty-monastrol derivatives did not remain adhered on the well plate after 3 h of treatment. At this time point, these cells still emitted fluorescence indicating viable cells, suggesting a possible effect of palmitic- and oleic-monastrol in the adhesion proteins found on the cell membrane.
[Mh] Termos MeSH primário: Melanoma/tratamento farmacológico
Ácido Oleico/farmacologia
Ácido Palmítico/farmacologia
Pirimidinas/farmacologia
Tionas/farmacologia
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Relação Dose-Resposta a Droga
Ensaios de Seleção de Medicamentos Antitumorais
Seres Humanos
Melanoma/patologia
Estrutura Molecular
Ácido Oleico/química
Ácido Palmítico/química
Pirimidinas/química
Relação Estrutura-Atividade
Tionas/química
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Pyrimidines); 0 (Thiones); 2UMI9U37CP (Oleic Acid); 2V16EO95H1 (Palmitic Acid); 6BSM97YZ8G (monastrol)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171214
[Lr] Data última revisão:
171214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE


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[PMID]:28949782
[Au] Autor:Uversky VN; El-Fakharany EM; Abu-Serie MM; Almehdar HA; Redwan EM
[Ad] Endereço:a Department of Biological Sciences, Faculty of Sciences , King Abdulaziz University , Jeddah , Saudi Arabia.
[Ti] Título:Divergent Anticancer Activity of Free and Formulated Camel Milk α-Lactalbumin.
[So] Source:Cancer Invest;35(9):610-623, 2017 Oct 21.
[Is] ISSN:1532-4192
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Alpha-lactalbumin (α-LA), a small milk calcium-binding globular protein, is known to possess noticeable anticancer activity, which is determined by the ability of this protein to form complexes with oleic acid (OA). To date, in addition to human and bovine α-LA, the ability to form such anti-tumor complexes with OA was described for goat and camel α-LA. Although the mechanisms of the anticancer activity of human and bovine α-LA are already well-studied, little is currently known about the anticancer action of this camel protein. The goal of this study was to fill this gap and to analyze the anticancer and pro-apoptotic activities of camel α-LA in its free form (α-cLA) and as an OA-containing complex (OA-α-cLA) using four human cancer cell lines, including Caco-2 colon cancer cells, PC-3 prostate cancer cells, HepG-2 hepatoma cells, and MCF-7 breast cancer cells as targets. The anti-tumor activities of OA-α-cLA and α-cLA were analyzed using MTT test, annexin/PI staining, cell cycle analysis, nuclear staining, and tyrosine kinase (TK) inhibition methods. We show here that the OA-α-cLA complex does not affect normal cells but has noticeable anti-cancer activity, especially against MCF-7 cells, thus boosting the anticancer activity of α-cLA and improving the selectivity of OA. The OA-α-cLA complex mediated cancer cell death via selective induction of apoptosis and cell-cycle arrest at lower IC than that of free α-cLA by more than two folds. However, OA induced apoptosis at higher extent than OA-α-cLA and α-cLA. OA also caused unselective apoptosis-dependent cell death in both normal and cancer cells to a similar degree. The apoptosis and cell-cycle arresting effect of OA-α-cLA may be attributed to the TK inhibition activity of OA. Therefore, OA-α-cLA serves as efficient anticancer complex with two functional components, α-cLA and OA, possessing different activities. This study declared the effectiveness of OA-α-cLA complex as a promising entity with anticancer activity, and these formulated OA-camel protein complexes constitute an auspicious approach for cancer remedy, particularly for breast cancer.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Camelus
Lactalbumina/farmacologia
Leite/química
Neoplasias/tratamento farmacológico
Ácido Oleico/farmacologia
Inibidores de Proteínas Quinases/farmacologia
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/toxicidade
Apoptose/efeitos dos fármacos
Células CACO-2
Pontos de Checagem do Ciclo Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Cercopithecus aethiops
Composição de Medicamentos
Feminino
Células Hep G2
Seres Humanos
Lactalbumina/isolamento & purificação
Lactalbumina/toxicidade
Células MCF-7
Masculino
Neoplasias/enzimologia
Neoplasias/patologia
Ácido Oleico/toxicidade
Inibidores de Proteínas Quinases/toxicidade
Proteínas Tirosina Quinases/antagonistas & inibidores
Proteínas Tirosina Quinases/metabolismo
Células Vero
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Protein Kinase Inhibitors); 2UMI9U37CP (Oleic Acid); 9013-90-5 (Lactalbumin); EC 2.7.10.1 (Protein-Tyrosine Kinases)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171113
[Lr] Data última revisão:
171113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170927
[St] Status:MEDLINE
[do] DOI:10.1080/07357907.2017.1373783


  8 / 6803 MEDLINE  
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[PMID]:28935810
[Au] Autor:Chen S; Huang Y; Liu Z; Yu W; Zhang H; Li K; Yu X; Tang C; Zhao B; Du J; Jin H
[Ad] Endereço:Department of Pediatrics, Peking University First Hospital, Beijing 100034, P.R. China.
[Ti] Título:Sulphur dioxide suppresses inflammatory response by sulphenylating NF-κB p65 at Cys in a rat model of acute lung injury.
[So] Source:Clin Sci (Lond);131(21):2655-2670, 2017 Nov 01.
[Is] ISSN:1470-8736
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The present study was designed to investigate whether endogenous sulphur dioxide (SO ) controlled pulmonary inflammation in a rat model of oleic acid (OA)-induced acute lung injury (ALI). In this model, adenovirus expressing aspartate aminotransferase (AAT) 1 was delivered to the lungs, and the levels of SO and proinflammatory cytokines in rat lung tissues were measured. In the human alveolar epithelial cell line A549, the nuclear translocation and DNA binding activities of wild-type (wt) and C38S (cysteine-to-serine mutation at p65 Cys ) NF-κB p65 were detected. GFP-tagged C38S p65 was purified from HEK 293 cells and the sulphenylation of NF-κB p65 was studied. OA caused a reduction in SO /AAT pathway activity but increased pulmonary inflammation and ALI. However, either the presence of SO donor, a combination of Na SO and NaHSO , or AAT1 overexpression successfully blocked OA-induced pulmonary NF-κB p65 phosphorylation and consequent inflammation and ALI. Either treatment with an SO donor or overexpression of AAT1 down-regulated OA-induced p65 activity, but AAT1 knockdown in alveolar epithelial cells mimicked OA-induced p65 phosphorylation and inflammation Mechanistically, OA promoted NF-κB nuclear translocation, DNA binding activity, recruitment to the intercellular cell adhesion molecule (ICAM)-1 promoter, and consequent inflammation in epithelial cells; these activities were reduced in the presence of an SO donor. Furthermore, SO induced sulphenylation of p65, which was blocked by the C38S mutation on p65 in epithelial cells. Hence, down-regulation of SO /AAT is involved in pulmonary inflammation during ALI. Furthermore, SO suppressed inflammation by sulphenylating NF-κB p65 at Cys .
[Mh] Termos MeSH primário: Lesão Pulmonar Aguda/tratamento farmacológico
Anti-Inflamatórios/farmacologia
Pulmão/efeitos dos fármacos
Pneumonia/prevenção & controle
Processamento de Proteína Pós-Traducional/efeitos dos fármacos
Sulfitos/farmacologia
Dióxido de Enxofre/metabolismo
Fator de Transcrição RelA/metabolismo
[Mh] Termos MeSH secundário: Células A549
Lesão Pulmonar Aguda/genética
Lesão Pulmonar Aguda/metabolismo
Lesão Pulmonar Aguda/patologia
Adenoviridae/genética
Animais
Anti-Inflamatórios/metabolismo
Aspartato Aminotransferases/genética
Aspartato Aminotransferases/metabolismo
Sítios de Ligação
Quimiocina CCL2/metabolismo
Cisteína
Modelos Animais de Doenças
Técnicas de Transferência de Genes
Vetores Genéticos
Molécula 1 de Adesão Intercelular/genética
Molécula 1 de Adesão Intercelular/metabolismo
Pulmão/metabolismo
Pulmão/patologia
Ácido Oleico
Fosforilação
Pneumonia/genética
Pneumonia/metabolismo
Pneumonia/patologia
Regiões Promotoras Genéticas
Interferência de RNA
Ratos Wistar
Sulfitos/metabolismo
Fator de Transcrição RelA/genética
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (CCL2 protein, human); 0 (Ccl2 protein, rat); 0 (Chemokine CCL2); 0 (ICAM1 protein, human); 0 (ICAM1 protein, rat); 0 (RELA protein, human); 0 (Rela protein, rat); 0 (Sulfites); 0 (Transcription Factor RelA); 0UZA3422Q4 (Sulfur Dioxide); 126547-89-5 (Intercellular Adhesion Molecule-1); 2UMI9U37CP (Oleic Acid); 91829-63-9 (sodium hydrogen sulfite); EC 2.6.1.1 (Aspartate Aminotransferases); K848JZ4886 (Cysteine); VTK01UQK3G (sodium sulfite)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170923
[St] Status:MEDLINE
[do] DOI:10.1042/CS20170274


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[PMID]:28821178
[Au] Autor:Heinze JM; Costanzo A; Baselier I; Fritsche A; Lidolt M; Hinrichs J; Frank-Podlech S; Keast R
[Ad] Endereço:Institute for Diabetes Research and Metabolic Diseases of the Helmholtz Center Munich at the University of Tübingen, Otfried Müller Str. 47, 72076 Tübingen, Germany.
[Ti] Título:Oil Perception-Detection Thresholds for Varying Fatty Stimuli and Inter-individual Differences.
[So] Source:Chem Senses;42(7):585-592, 2017 Sep 01.
[Is] ISSN:1464-3553
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Multiple lines of research have demonstrated that humans can perceive fat in the form of free fatty acids (FFAs). However, the dietary concentration of FFAs is generally very low and fat is mainly consumed as triacylglycerol (TAG). The aim of this study was to examine the perception of different fatty stimuli and possible associations between them. Therefore, detection thresholds for 4 fatty stimuli (oleic acid [FFA], paraffin oil [mixture of hydrocarbon molecules], canola oil [TAG-rich], and canola oil spiked with oleic acid [rich in TAGs and FFAs]) were determined in 30 healthy participants. Additionally, inter-individual differences in fat perception were examined. It was observed that oleic acid was perceivable at significantly lower concentrations than all other stimuli (P < 0.001). Similarly, canola oil with oleic acid was detectable at lower concentrations than canola oil alone (P < 0.001). Moreover, canola oil detection thresholds were significantly lower than paraffin oil detection thresholds (P = 0.017). Participants who were sensitive for low concentrations for oleic acid showed lower detection thresholds for canola oil with and without oleic acid, compared with participants that were less sensitive for oleic acid. The results of this study demonstrate that the higher the concentrations of FFAs in the stimuli, the lower the individual fat detection threshold. Moreover, participants being sensitive for lower concentrations of FFAs are also more likely to detect low concentrations of TAG-rich fats as it is found in the human diet.
[Mh] Termos MeSH primário: Óleos/farmacologia
Ácido Oleico/farmacologia
Parafina/farmacologia
Óleos Vegetais/farmacologia
Limiar Gustativo/efeitos dos fármacos
Paladar/efeitos dos fármacos
[Mh] Termos MeSH secundário: Adolescente
Adulto
Óleo de Canola
Ácidos Graxos não Esterificados/química
Ácidos Graxos não Esterificados/farmacologia
Feminino
Voluntários Saudáveis
Seres Humanos
Masculino
Meia-Idade
Óleos/química
Ácido Oleico/química
Parafina/química
Óleos Vegetais/química
Triglicerídeos/química
Triglicerídeos/farmacologia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Canola Oil); 0 (Fatty Acids, Nonesterified); 0 (Oils); 0 (Plant Oils); 0 (Triglycerides); 2UMI9U37CP (Oleic Acid); 8002-74-2 (Paraffin); 8012-95-1 (paraffin oils)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170820
[St] Status:MEDLINE
[do] DOI:10.1093/chemse/bjx039


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[PMID]:28786227
[Au] Autor:Zhang H; Luo X; Shi K; Wu T; He F; Zhou S; Chen GZ; Peng C
[Ad] Endereço:School of Resource and Environmental Sciences, Hubei International Scientific and Technological Cooperation Base, of Sustainable Resource and Energy, Wuhan University, Wuhan, 430072, P. R. China.
[Ti] Título:Highly Efficient Sulfonic/Carboxylic Dual-Acid Synergistic Catalysis for Esterification Enabled by Sulfur-Rich Graphene Oxide.
[So] Source:ChemSusChem;10(17):3352-3357, 2017 Sep 11.
[Is] ISSN:1864-564X
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:A new sulfonic/carboxylic dual-acid catalyst based on sulfur-rich graphene oxide (GO-S) was readily prepared and used as a highly efficient and reusable solid acid catalyst toward the esterification of oleic acid with methanol for biodiesel production. Higher yields of methyl oleate (98 %) and over 3 times higher turnover frequencies (TOFs) were observed for the GO-S dual-acid catalyst, compared to liquid sulfuric acid or other carbon-based solid acid catalysts. The "acidity" of sulfonic acid groups was enhanced by the addition of carboxylic acid groups as the combination of the two acids enhances their inherent activity by associative interaction.
[Mh] Termos MeSH primário: Ácidos Carboxílicos/química
Grafite/química
Óxidos/química
Ácidos Sulfônicos/química
Enxofre/química
[Mh] Termos MeSH secundário: Catálise
Esterificação
Metanol/química
Ácido Oleico/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Carboxylic Acids); 0 (Oxides); 0 (Sulfonic Acids); 2UMI9U37CP (Oleic Acid); 70FD1KFU70 (Sulfur); 7782-42-5 (Graphite); Y4S76JWI15 (Methanol)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170918
[Lr] Data última revisão:
170918
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170809
[St] Status:MEDLINE
[do] DOI:10.1002/cssc.201700950



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