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[PMID]:29199986
[Au] Autor:Tarver CL; Pusey M
[Ad] Endereço:Department of Biological Science, University of Alabama in Huntsville, Huntsville, AL 35899, USA.
[Ti] Título:A low-cost method for visible fluorescence imaging.
[So] Source:Acta Crystallogr F Struct Biol Commun;73(Pt 12):657-663, 2017 Dec 01.
[Is] ISSN:2053-230X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A wide variety of crystallization solutions are screened to establish conditions that promote the growth of a diffraction-quality crystal. Screening these conditions requires the assessment of many crystallization plates for the presence of crystals. Automated systems for screening and imaging are very expensive. A simple approach to imaging trace fluorescently labeled protein crystals in crystallization plates has been devised, and can be implemented at a cost as low as $50. The proteins ß-lactoglobulin B, trypsin and purified concanavalin A (ConA) were trace fluorescently labeled using three different fluorescent probes: Cascade Yellow (CY), Carboxyrhodamine 6G (CR) and Pacific Blue (PB). A crystallization screening plate was set up using ß-lactoglobulin B labeled with CR, trypsin labeled with CY, ConA labeled with each probe, and a mixture consisting of 50% PB-labeled ConA and 50% CR-labeled ConA. The wells of these plates were imaged using a commercially available macro-imaging lens attachment for smart devices that have a camera. Several types of macro lens attachments were tested with smartphones and tablets. Images with the highest quality were obtained with an iPhone 6S and an AUKEY Ora 10× macro lens. Depending upon the fluorescent probe employed and its Stokes shift, a light-emitting diode or a laser diode was used for excitation. An emission filter was used for the imaging of protein crystals labeled with CR and crystals with two-color fluorescence. This approach can also be used with microscopy systems commonly used to observe crystallization plates.
[Mh] Termos MeSH primário: Corantes Fluorescentes/química
Imagem Molecular/instrumentação
Imagem Molecular/métodos
Proteínas/química
[Mh] Termos MeSH secundário: Cor
Concanavalina A/química
Custos e Análise de Custo
Cristalização
Desenho de Equipamento
Fluorescência
Lactoglobulinas/química
Imagem Molecular/economia
Rodaminas/química
Smartphone/economia
Smartphone/instrumentação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (6-carboxyrhodamine-6G); 0 (Fluorescent Dyes); 0 (Lactoglobulins); 0 (Proteins); 0 (Rhodamines); 11028-71-0 (Concanavalin A)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171205
[St] Status:MEDLINE
[do] DOI:10.1107/S2053230X17015941


  2 / 17480 MEDLINE  
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[PMID]:29199979
[Au] Autor:Quirnheim Pais D; Rathmann B; Koepke J; Tomova C; Wurzinger P; Thielmann Y
[Ad] Endereço:Molecular Membrane Biology, Max Planck Institute of Biophysics, Max-von-Laue-Strasse 3, 60438 Frankfurt am Main, Germany.
[Ti] Título:A standardized technique for high-pressure cooling of protein crystals.
[So] Source:Acta Crystallogr D Struct Biol;73(Pt 12):997-1006, 2017 Dec 01.
[Is] ISSN:2059-7983
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cryogenic temperatures slow down secondary radiation damage during data collection from macromolecular crystals. In 1973, cooling at high pressure was identified as a method for cryopreserving crystals in their mother liquor [Thomanek et al. (1973). Acta Cryst. A29, 263-265]. Results from different groups studying different crystal systems indicated that the approach had merit, although difficulties in making the process work have limited its widespread use. Therefore, a simplified and reliable technique has been developed termed high-pressure cooling (HPC). An essential requirement for HPC is to protect crystals in capillaries. These capillaries form part of new sample holders with SPINE standard dimensions. Crystals are harvested with the capillary, cooled at high pressure (220 MPa) and stored in a cryovial. This system also allows the usage of the standard automation at the synchrotron. Crystals of hen egg-white lysozyme and concanavalin A have been successfully cryopreserved and yielded data sets to resolutions of 1.45 and 1.35 Å, respectively. Extensive work has been performed to define the useful working range of HPC in capillaries with 250 µm inner diameter. Three different 96-well crystallization screens that are most frequently used in our crystallization facility were chosen to study the formation of amorphous ice in this cooling setup. More than 89% of the screening solutions were directly suitable for HPC. This achievement represents a drastic improvement for crystals that suffered from cryoprotection or were not previously eligible for cryoprotection.
[Mh] Termos MeSH primário: Cristalização
Cristalografia por Raios X/instrumentação
Síncrotrons
[Mh] Termos MeSH secundário: Animais
Galinhas
Temperatura Baixa
Concanavalina A/química
Criopreservação
Crioprotetores/química
Muramidase/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cryoprotective Agents); 11028-71-0 (Concanavalin A); EC 3.2.1.- (hen egg lysozyme); EC 3.2.1.17 (Muramidase)
[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:171205
[St] Status:MEDLINE
[do] DOI:10.1107/S2059798317016357


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[PMID]:29337673
[Au] Autor:Abu-Rish EY; Elhayek SY; Mohamed YS; Hamad I; Bustanji Y
[Ad] Endereço:1Department of Biopharmaceutics and Clinical Pharmacy, School of Pharmacy The University of Jordan, Amman 11942, Jordan.
[Ti] Título:Evaluation of immunomodulatory effects of lamotrigine in BALB/c mice.
[So] Source:Acta Pharm;67(4):543-555, 2017 Dec 20.
[Is] ISSN:1846-9558
[Cp] País de publicação:Croatia
[La] Idioma:eng
[Ab] Resumo:Modulation of the immune system has recently been shown to be involved in the pharmacological effects of old antiepileptic drugs and in the pathogenesis of epilepsy. Therefore, the most recent guidelines for immunotoxicological evaluation of drugs were consulted to investigate the immunomodulatory effects of lamotrigine, a newer antiepileptic drug, in BALB/c mice. These included the in vivo effects of lamotrigine on delayed-type hypersensitivity (DTH) response to sheep red blood cell (SRBC) antigens, hemagglutination titer assays and hematological changes. In vitro effects of lamotrigine on ConA-induced splenocyte proliferation and cytokine secretion were assessed. The results showed that lamotrigine treatment significantly increased the DTH response to SRBC in the mouse model of this study. This was accompanied by a significant increase in relative monocyte and neutrophil counts and in spleen cellularity. Lamotrigine significantly inhibited ConA-induced splenocyte proliferation in vitro and it significantly inhibited IL-2 and TNF-α secretion in ConA-stimulated splenocytes. In conclusion, the results demonstrated significant immunomodulatory effects of lamotrigine in BALB/c mice. These data could expand the understanding of lamotrigine-induced adverse reactions and its role in modulating the immune system in epilepsy.
[Mh] Termos MeSH primário: Imunomodulação/efeitos dos fármacos
Triazinas/farmacologia
[Mh] Termos MeSH secundário: Animais
Anticonvulsivantes/farmacologia
Proliferação Celular/efeitos dos fármacos
Concanavalina A/farmacologia
Citocinas/metabolismo
Feminino
Hipersensibilidade Tardia/tratamento farmacológico
Camundongos
Camundongos Endogâmicos BALB C/imunologia
Baço/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anticonvulsants); 0 (Cytokines); 0 (Triazines); 11028-71-0 (Concanavalin A); U3H27498KS (lamotrigine)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180131
[Lr] Data última revisão:
180131
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180117
[St] Status:MEDLINE


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[PMID]:28846383
[Au] Autor:Gerlits OO; Coates L; Woods RJ; Kovalevsky A
[Ad] Endereço:UT/ORNL Joint Institute for Biological Sciences, University of Tennessee , Knoxville, Tennessee 37996, United States.
[Ti] Título:Mannobiose Binding Induces Changes in Hydrogen Bonding and Protonation States of Acidic Residues in Concanavalin A As Revealed by Neutron Crystallography.
[So] Source:Biochemistry;56(36):4747-4750, 2017 Sep 12.
[Is] ISSN:1520-4995
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Plant lectins are carbohydrate-binding proteins with various biomedical applications. Concanavalin A (Con A) holds promise in treating cancerous tumors. To better understand the Con A carbohydrate binding specificity, we obtained a room-temperature neutron structure of this legume lectin in complex with a disaccharide Manα1-2Man, mannobiose. The neutron structure afforded direct visualization of the hydrogen bonding between the protein and ligand, showing that the ligand is able to alter both protonation states and interactions for residues located close to and distant from the binding site. An unprecedented low-barrier hydrogen bond was observed forming between the carboxylic side chains of Asp28 and Glu8, with the D atom positioned equidistant from the oxygen atoms having an O···D···O angle of 101.5°.
[Mh] Termos MeSH primário: Concanavalina A/química
Concanavalina A/metabolismo
Mananas/química
Mananas/metabolismo
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Sítios de Ligação
Ligações de Hidrogênio
Conformação Proteica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Mannans); 11028-71-0 (Concanavalin A); 15548-43-3 (mannobiose)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170920
[Lr] Data última revisão:
170920
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170829
[St] Status:MEDLINE
[do] DOI:10.1021/acs.biochem.7b00654


  5 / 17480 MEDLINE  
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[PMID]:28774703
[Au] Autor:Xu S; Wu L; Zhang Q; Feng J; Li S; Li J; Liu T; Mo W; Wang W; Lu X; Yu Q; Chen K; Xia Y; Lu J; Xu L; Zhou Y; Fan X; Guo C
[Ad] Endereço:Department of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai 200072, China; Department of Gastroenterology, Shanghai Tenth Hospital, School of Clinical Medicine of Nanjing Medical University, Shanghai 200072, China.
[Ti] Título:Pretreatment with propylene glycol alginate sodium sulfate ameliorated concanavalin A-induced liver injury by regulating the PI3K/Akt pathway in mice.
[So] Source:Life Sci;185:103-113, 2017 Sep 15.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: Propylene glycol alginate sodium sulfate (PSS), a sulfated polysaccharide possesses anti-inflammatory effects. Here, we investigated the effect of PSS on concanavalin A (Con A)-induced liver injury in mice and examined the underlying mechanisms. MAIN METHODS: Balb/C mice were injected intravenously with Con A (25mg/kg) to generate a model of acute liver injury. PSS (25 or 50mg/kg) was injected intraperitoneally 1h before the Con A administration. The levels of serum liver enzymes, inflammatory cytokines, and other marker proteins were determined, and liver injury was assessed histopathologically 2, 8, and 24h after Con A injection. KEY FINDINGS: Pretreatment with PSS reduced the levels of serum liver enzymes, inflammatory cytokines such as tumor necrosis factor (TNF)-α and interleukin (IL)-1ß, and attenuated histopathological damage in Con A-induced liver injury in mice. The effects of Con A were mediated by apoptosis and autophagy, as indicated by changes in protein and gene expression of related factors after Con A injection. PSS activated the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) pathway and showed a protective function against apoptosis and autophagy. SIGNIFICANCE: PSS ameliorated Con A-induced liver injury by downregulating inflammatory cytokines including TNF-α and IL-1ß and regulating apoptosis and autophagy via the PI3K/Akt pathway.
[Mh] Termos MeSH primário: Alginatos/farmacologia
Citocinas/metabolismo
Hepatite Autoimune/prevenção & controle
Fosfatidilinositol 3-Quinase/metabolismo
Proteínas Proto-Oncogênicas c-akt/metabolismo
[Mh] Termos MeSH secundário: Alginatos/administração & dosagem
Animais
Apoptose/efeitos dos fármacos
Autofagia/efeitos dos fármacos
Concanavalina A/toxicidade
Modelos Animais de Doenças
Relação Dose-Resposta a Droga
Hepatite Autoimune/patologia
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Transdução de Sinais/efeitos dos fármacos
Fatores de Tempo
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Alginates); 0 (Cytokines); 0 (Tumor Necrosis Factor-alpha); 0 (propylene glycol alginate sodium sulfate); 11028-71-0 (Concanavalin A); EC 2.7.1.137 (Phosphatidylinositol 3-Kinase); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170908
[Lr] Data última revisão:
170908
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170805
[St] Status:MEDLINE


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[PMID]:28715128
[Au] Autor:Le Cann F; Delehouzé C; Leverrier-Penna S; Filliol A; Comte A; Delalande O; Desban N; Baratte B; Gallais I; Piquet-Pellorce C; Faurez F; Bonnet M; Mettey Y; Goekjian P; Samson M; Vandenabeele P; Bach S; Dimanche-Boitrel MT
[Ad] Endereço:INSERM UMR 1085, l'Environnement et le Travail, Institut de Recherche sur la Santé, Rennes, France.
[Ti] Título:Sibiriline, a new small chemical inhibitor of receptor-interacting protein kinase 1, prevents immune-dependent hepatitis.
[So] Source:FEBS J;284(18):3050-3068, 2017 Sep.
[Is] ISSN:1742-4658
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Necroptosis is a regulated form of cell death involved in several disease models including in particular liver diseases. Receptor-interacting protein kinases, RIPK1 and RIPK3, are the main serine/threonine kinases driving this cell death pathway. We screened a noncommercial, kinase-focused chemical library which allowed us to identify Sibiriline as a new inhibitor of necroptosis induced by tumor necrosis factor (TNF) in Fas-associated protein with death domain (FADD)-deficient Jurkat cells. Moreover, Sib inhibits necroptotic cell death induced by various death ligands in human or mouse cells while not protecting from caspase-dependent apoptosis. By using competition binding assay and recombinant kinase assays, we demonstrated that Sib is a rather specific competitive RIPK1 inhibitor. Molecular docking analysis shows that Sib is trapped closed to human RIPK1 adenosine triphosphate-binding site in a relatively hydrophobic pocket locking RIPK1 in an inactive conformation. In agreement with its RIPK1 inhibitory property, Sib inhibits both TNF-induced RIPK1-dependent necroptosis and RIPK1-dependent apoptosis. Finally, Sib protects mice from concanavalin A-induced hepatitis. These results reveal the small-molecule Sib as a new RIPK1 inhibitor potentially of interest for the treatment of immune-dependent hepatitis.
[Mh] Termos MeSH primário: Alcaloides/farmacologia
Hepatite Animal/prevenção & controle
Fatores Imunológicos/farmacologia
Inibidores de Proteínas Quinases/farmacologia
Proteína Serina-Treonina Quinases de Interação com Receptores/genética
Compostos de Espiro/farmacologia
[Mh] Termos MeSH secundário: Alcaloides/química
Animais
Apoptose/efeitos dos fármacos
Apoptose/genética
Caspase 3/genética
Caspase 3/imunologia
Linhagem Celular Transformada
Concanavalina A
Cicloeximida/farmacologia
Fibroblastos/citologia
Fibroblastos/efeitos dos fármacos
Fibroblastos/metabolismo
Regulação da Expressão Gênica
Células HT29
Hepatite Animal/induzido quimicamente
Hepatite Animal/genética
Hepatite Animal/imunologia
Seres Humanos
Imidazóis/farmacologia
Fatores Imunológicos/química
Indóis/farmacologia
Células Jurkat
Masculino
Camundongos
Simulação de Acoplamento Molecular
Necrose/induzido quimicamente
Necrose/genética
Necrose/imunologia
Inibidores de Proteínas Quinases/química
Proteína Serina-Treonina Quinases de Interação com Receptores/antagonistas & inibidores
Proteína Serina-Treonina Quinases de Interação com Receptores/imunologia
Transdução de Sinais
Compostos de Espiro/química
Ligante Indutor de Apoptose Relacionado a TNF/farmacologia
Fator de Necrose Tumoral alfa/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Alkaloids); 0 (Imidazoles); 0 (Immunologic Factors); 0 (Indoles); 0 (Protein Kinase Inhibitors); 0 (Spiro Compounds); 0 (TNF-Related Apoptosis-Inducing Ligand); 0 (TNFSF10 protein, human); 0 (Tumor Necrosis Factor-alpha); 0 (necrostatin-1); 0 (sibirine); 11028-71-0 (Concanavalin A); 98600C0908 (Cycloheximide); EC 2.7.11.1 (RIPK1 protein, human); EC 2.7.11.1 (RIPK3 protein, human); EC 2.7.11.1 (Receptor-Interacting Protein Serine-Threonine Kinases); EC 3.4.22.- (CASP3 protein, human); EC 3.4.22.- (Caspase 3)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171004
[Lr] Data última revisão:
171004
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170718
[St] Status:MEDLINE
[do] DOI:10.1111/febs.14176


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[PMID]:28712788
[Au] Autor:Zhao X; Liu M; Li J; Yin S; Wu Y; Wang A
[Ad] Endereço:School of Veterinary Medicine, Yangzhou University, Yangzhou 225009, PR China; Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou 225009, PR China.
[Ti] Título:Antimalarial agent artesunate protects Concanavalin A-induced autoimmune hepatitis in mice by inhibiting inflammatory responses.
[So] Source:Chem Biol Interact;274:116-123, 2017 Aug 25.
[Is] ISSN:1872-7786
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:The anti-malarial drug artesunate (ARS) has been shown to possess anti-inflammatory activity. Its effect on autoimmune hepatitis remains unclear. Concanavalin A (Con A)-induced hepatitis was used in this study to reveal the potential action of ARS and the related mechanism. Mice were pretreated with ARS followed by Con A challenge. Con A caused obvious hepatic injury with higher levels of liver enzymes, elevated pro-inflammatory cytokines and activation of nuclear factor-κB (NF-κB) and mitogen activated protein kinase (MAPK) signaling pathways. However, ARS pretreatment notably inhibited Con A-induced liver injury with remarkable reduction of liver enzymes, and dramatically suppressed the expression of inflammatory cytokines including interferon (IFN)-γ, tumor necrosis factor (TNF)-α, interleukin (IL)-1ß, IL-6 and IL-17, and increased anti-inflammatory cytokines IL-10. In line with cytokines, the phosphorylation of extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), p38 mitogen-activated protein kinases (p38), nuclear factor-κBα (IκBα) and NF-κB p65 was also significantly inhibited by ARS pretreatment. As a contrast, the specific inhibitor of NF-κB pyrrolidine dithiocarbamate (PDTC) achieved similar repressive effects as ARS on phosphorylation of p65 and IκBα, and serum levels of aminotransferases. Taken together, these data highlight that ARS has facilitating to make a better understanding of ARS against acute autoimmune hepatitis, and indicating a promising therapy candidate for autoimmune hepatitis.
[Mh] Termos MeSH primário: Antimaláricos/farmacologia
Artemisininas/farmacologia
Hepatite Autoimune/prevenção & controle
Substâncias Protetoras/farmacologia
[Mh] Termos MeSH secundário: Animais
Concanavalina A/toxicidade
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Hepatite Autoimune/etiologia
Interleucina-17/análise
Interleucina-6/análise
Proteínas Quinases JNK Ativadas por Mitógeno/metabolismo
Fígado/efeitos dos fármacos
Fígado/metabolismo
Fígado/patologia
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Inibidor de NF-kappaB alfa/metabolismo
NF-kappa B/antagonistas & inibidores
NF-kappa B/metabolismo
Fosforilação/efeitos dos fármacos
Pirrolidinas/farmacologia
Transdução de Sinais/efeitos dos fármacos
Tiocarbamatos/farmacologia
Fator de Necrose Tumoral alfa/análise
Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antimalarials); 0 (Artemisinins); 0 (Interleukin-17); 0 (Interleukin-6); 0 (NF-kappa B); 0 (Protective Agents); 0 (Pyrrolidines); 0 (Thiocarbamates); 0 (Tumor Necrosis Factor-alpha); 11028-71-0 (Concanavalin A); 139874-52-5 (NF-KappaB Inhibitor alpha); 25769-03-3 (pyrrolidine dithiocarbamic acid); 60W3249T9M (artesunate); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases); EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170718
[St] Status:MEDLINE


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[PMID]:28710903
[Au] Autor:Rani R; Tandon A; Wang J; Kumar S; Gandhi CR
[Ad] Endereço:Department of Surgery, University of Cincinnati, Cincinnati, Ohio; Cincinnati Veterans Administration Medical Center, Cincinnati, Ohio; Department of Pediatrics, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio.
[Ti] Título:Stellate Cells Orchestrate Concanavalin A-Induced Acute Liver Damage.
[So] Source:Am J Pathol;187(9):2008-2019, 2017 Sep.
[Is] ISSN:1525-2191
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Concanavalin A (ConA) causes immune cell-mediated liver damage, but the contribution of resident nonparenchymal cells (NPCs) is also evident. Hepatic stellate cells (HSCs) induce hepatic inflammation and immunological reactions; we therefore investigated their role in ConA-induced liver injury. ConA was administered i.v. to control or HSC-depleted mice; hepatic histopathology and cytokines/chemokines were determined after 6 hours. In vitro, effects of ConA-conditioned HSC medium on hepatocytes were determined. ConA induced inflammation, sinusoidal congestion, and extensive midzonal hepatocyte death in control mice, which were strongly minimized in HSC-depleted mice. CD4 and natural killer T cells and neutrophils were markedly reduced in ConA-treated HSC-depleted mice compared with control mice. The increase in cytokines/chemokines of hepatic injury was much higher in ConA-treated control mice than in HSC-depleted mice. ConA-treated HSCs showed increased expression of interferon-ß, tumor necrosis factor-α, and CXCL1, induced oxidative stress in hepatocytes, and caused hepatocyte apoptosis. ConA induced nuclear translocation of interferon-regulatory factor-1 (IRF1) in hepatocytes in vivo, and ConA/HSC induced a similar effect in cultured hepatocytes. IRF1-knockout mice were resistant to ConA-induced liver damage, and anti-interferon ß antibody mitigated ConA/HSC-induced injury. In HSC-NPC co-culture, ConA-induced expression of inflammatory cytokines/chemokines was significantly augmented compared with NPCs alone. HSCs play an essential role in ConA-induced liver injury directly via the interferon-ß/IRF1 axis, and by modulating properties of NPCs.
[Mh] Termos MeSH primário: Doença Hepática Induzida por Substâncias e Drogas/patologia
Concanavalina A/toxicidade
Células Estreladas do Fígado/patologia
Fígado/patologia
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Doença Hepática Induzida por Substâncias e Drogas/metabolismo
Quimiocinas/metabolismo
Citocinas/metabolismo
Células Estreladas do Fígado/metabolismo
Hepatócitos/efeitos dos fármacos
Hepatócitos/metabolismo
Hepatócitos/patologia
Fígado/efeitos dos fármacos
Fígado/metabolismo
Masculino
Camundongos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chemokines); 0 (Cytokines); 11028-71-0 (Concanavalin A)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171114
[Lr] Data última revisão:
171114
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170716
[St] Status:MEDLINE


  9 / 17480 MEDLINE  
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[PMID]:28602504
[Au] Autor:Rathnasekara R; El Rassi Z
[Ad] Endereço:Department of Chemistry, Oklahoma State University, Stillwater, OK, 74078-3071, USA.
[Ti] Título:Polar silica-based stationary phases. Part III- Neutral silica stationary phase with surface bound maltose for affinity chromatography at reduced non-specific interactions.
[So] Source:J Chromatogr A;1508:33-41, 2017 Jul 28.
[Is] ISSN:1873-3778
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:This research article reports the coating of large pore silica microparticles with a maltose layer to which bioaffinity ligands were attached via reductive amination reaction between the aldehyde activated maltose and the amino groups of the bioaffinity ligands. This was achieved first by the periodate oxidation of the maltose-silica (MALT-silica) yielding pairs of aldehyde groups at each monosaccharide ring. These di-aldehyde functionalities were then reacted with the primary amino groups of protein bio-affinity ligands and eventually formed Schiff bases (i.e., aldimines) which were reduced using the mild reducing agent sodium cyanoborohydride to form stable amine linkages between the immobilized protein ligands and the maltose layer. Anti-human serum albumin antibody (aHSA), anti-human serum transferrin antibody (aTf) and concanavalin A (Con A) were the bio-affinity ligands immobilized onto the MALT-silica and were evaluated in high performance affinity chromatography (HPAC), namely immunoaffinity chromatography (IAC) and lectin affinity chromatography (LAC). Our initial studies reported here revealed zero or reduced nonspecific interactions with the two immunoaffinity sorbents (i.e., aHSA-MALT-silica and aTf-MALT-silica) and the lectin affinity sorbent (i.e., Con A-MALT-silica). The absence of nonspecific interactions is attributed to the hydrophilicity of the maltose layer and its shielding effect of the residual silanols (i.e., unreacted silanols) on the silica surface. Conversely, the IAC and LAC sorbents exhibited specific interactions with the target biomolecules, namely human serum albumin (HSA) and transferrin (Tf) in the case of aHSA-MALT-silica and aTf-MALT-silica columns, respectively, and glycoproteins known for their affinity to Con A in the case of Con A-MALT-silica column.
[Mh] Termos MeSH primário: Cromatografia de Afinidade/instrumentação
Maltose/química
Dióxido de Silício/química
[Mh] Termos MeSH secundário: Albuminas/química
Anticorpos/química
Anticorpos/isolamento & purificação
Cromatografia de Afinidade/métodos
Concanavalina A/química
Concanavalina A/isolamento & purificação
Seres Humanos
Interações Hidrofóbicas e Hidrofílicas
Ligantes
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Albumins); 0 (Antibodies); 0 (Ligands); 11028-71-0 (Concanavalin A); 69-79-4 (Maltose); 7631-86-9 (Silicon Dioxide)
[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:170613
[St] Status:MEDLINE


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[PMID]:28482408
[Au] Autor:Bi YZ; Fan Z; Chen DF; Li SS; Wang QY; Gao PF; Wang QQ; Duan ZP; Chen Y; Kong LB; Wang YB; Hong F
[Ad] Endereço:Shandong University School of Medicine, Jinan 250012, China.
[Ti] Título:[Protective effect of intraperitoneal transplantation of human liver-derived stem cells at different times against concanavalin A-induced acute liver injury in mice].
[So] Source:Zhonghua Gan Zang Bing Za Zhi;25(3):205-210, 2017 Mar 20.
[Is] ISSN:1007-3418
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:To investigate the protective effect of intraperitoneal transplantation of human liver-derived stem cells at different times against concanavalin A (ConA)-induced acute liver injury in mice. A total of 88 male C57BL/6 mice were randomly divided into normal control group (group C), ConA model group (group M), and human liver-derived stem cells (HYX1)+ConA group (group E); according to the interval between phosphate buffer/HYX1 injection and ConA injection, Groups M and E were further divided into 3-hour groups (M1 and E1 groups), 6-hour groups (M2 and E2 groups), 12-hour groups (M3 and E3 groups), 24-hour groups (M4 and E4 groups), and 48-hour groups (M5 and E5 groups). The levels of alanine aminotransferase (ALT), aspartate transaminase (AST), and total bilirubin (TBil) in peripheral blood were measured, liver tissue sections were used to observe pathological changes, and the Ishak score for liver inflammation was determined. The independent samples t-test was used for comparison between groups, and < 0.05 was considered statistically significant. The levels of ALT, AST, and TBil in group C were (36.25±1.16) U/L, (120.20±5.77) U/L, and (2.20±0.23) µmol/L, respectively; the levels of ALT, AST, and TBil and Ishak score were (8 721.23±837.39) U/L, (8 110.31±290.10) U/L, (8.41±0.10) µmol/L, and (13.32±1.30), respectively, in group M1, (8 334.31±666.50) U/L, (7 560.20±760.34) U/L, (10.40±0.80) µmol/L, and (12.67±0.81), respectively, in group M2, (8 960.75±551.93) U/L, (8 535.62±675.14) U/L, (10.95±1.43) µmol/L, and (14.57±0.65), respectively, in group M3, (8 618.57±886.40) U/L, (11 440.54 ± 1 327.86) U/L, (13.30±1.86) µmol/L, and (13.21±1.06), respectively, in group M4, and (10 170.13±1 112.37) U/L, (11 470.56±1 108.40) U/L, (12.75±1.55) µmol/L, and (15.07±1.58), respectively, in group M5. The levels of ALT, AST, and TBil and Ishak score were (1 016.35±163.47) U/L, (952.30±103.91) U/L, (7.77±0.62) µmol/L, and (3.50±0.21), respectively, in group E1, (42.10±6.20) U/L, (126.72±13.33) U/L, (3.41±0.53) µmol/L, and (2.01±0.40), respectively, in group E2, (44.21±4.30) U/L, (216.71±35.88) U/L, (3.47±0.44) µmol/L, and (2.13±0.25), respectively, in group E3, (2 909.69±212.14) U/L, (2 988.43±333.70) U/L, (7.03±0.93) µmol/L, and (4.70±0.50), respectively, in group E4, and (7 874.26±799.60) U/L, (10 940.54±947.35) U/L, (10.53±1.09) µmol/L, and (8.60±0.83), respectively, in group E5. Groups M1-M5 had significantly higher levels of ALT, AST, and TBil than group C (all < 0.01), and groups M1-M4 had significantly higher levels of AST and ALT than groups E1-E4 (all < 0.01), while there were no significant differences in the levels of AST and ALT between groups M5 and E5 (both > 0.05). The pathological sections of liver tissue showed that compared with group M, group E had significant reductions in the degree of necrosis and Ishak score (both < 0.05). Intraperitoneal transplantation of human liver-derived stem cells has a protective effect against ConA-induced acute liver injury in mice, and the injection at 6 and 12 hours in advance has the best protective effect.
[Mh] Termos MeSH primário: Doença Hepática Induzida por Substâncias e Drogas
Concanavalina A
Transplante de Células-Tronco Mesenquimais
Mitógenos
[Mh] Termos MeSH secundário: Alanina Transaminase/sangue
Animais
Aspartato Aminotransferases/sangue
Bilirrubina/sangue
Doença Hepática Induzida por Substâncias e Drogas/cirurgia
Concanavalina A/efeitos adversos
Seres Humanos
Fígado
Transplante de Fígado
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Mitógenos/efeitos adversos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Mitogens); 11028-71-0 (Concanavalin A); EC 2.6.1.1 (Aspartate Aminotransferases); EC 2.6.1.2 (Alanine Transaminase); RFM9X3LJ49 (Bilirubin)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171109
[Lr] Data última revisão:
171109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170509
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.1007-3418.2017.03.009



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