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  1 / 1523 MEDLINE  
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[PMID]:28130148
[Au] Autor:Strzepa A; Majewska-Szczepanik M; Lobo FM; Wen L; Szczepanik M
[Ad] Endereço:Department of Medical Biology, Faculty of Health Sciences, Jagiellonian University Medical College, Krakow, Poland.
[Ti] Título:Broad spectrum antibiotic enrofloxacin modulates contact sensitivity through gut microbiota in a murine model.
[So] Source:J Allergy Clin Immunol;140(1):121-133.e3, 2017 Jul.
[Is] ISSN:1097-6825
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Medical advances in the field of infection therapy have led to an increasing use of antibiotics, which, apart from eliminating pathogens, also partially eliminate naturally existing commensal bacteria. It has become increasingly clear that less exposure to microbiota early in life may contribute to the observed rise in "immune-mediated" diseases, including autoimmunity and allergy. OBJECTIVE: We sought to test whether the change of gut microbiota with the broad spectrum antibiotic enrofloxacin will modulate contact sensitivity (CS) in mice. METHODS: Natural gut microbiota were modified by oral treatment with enrofloxacin prior to sensitization with trinitrophenyl chloride followed by CS testing. Finally, adoptive cell transfers were performed to characterize the regulatory cells that are induced by microbiota modification. RESULTS: Oral treatment with enrofloxacin suppresses CS and production of anti-trinitrophenyl chloride IgG1 antibodies. Adoptive transfer experiments show that antibiotic administration favors induction of regulatory cells that suppress CS. Flow cytometry and adoptive transfer of purified cells show that antibiotic-induced suppression of CS is mediated by TCR αß CD4 CD25 FoxP3 Treg, CD19 B220 CD5 IL-10 , IL-10 Tr1, and IL-10 TCR γδ cells. Treatment with the antibiotic induces dysbiosis characterized by increased proportion of Clostridium coccoides (cluster XIVa), C coccoides-Eubacterium rectale (cluster XIVab), Bacteroidetes, and Bifidobacterium spp, but decreased segmented filamentous bacteria. Transfer of antibiotic-modified gut microbiota inhibits CS, but this response can be restored through oral transfer of control gut bacteria to antibiotic-treated animals. CONCLUSIONS: Oral treatment with a broad spectrum antibiotic modifies gut microbiota composition and promotes anti-inflammatory response, suggesting that manipulation of gut microbiota can be a powerful tool to modulate the course of CS.
[Mh] Termos MeSH primário: Antibacterianos/farmacologia
Dermatite de Contato/imunologia
Fluoroquinolonas/farmacologia
Microbioma Gastrointestinal/efeitos dos fármacos
[Mh] Termos MeSH secundário: Transferência Adotiva
Animais
Linfonodos/citologia
Camundongos Endogâmicos C57BL
Baço/citologia
Trinitrobenzenos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (Fluoroquinolones); 0 (Trinitrobenzenes); 3DX3XEK1BN (enrofloxacin)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170829
[Lr] Data última revisão:
170829
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170129
[St] Status:MEDLINE


  2 / 1523 MEDLINE  
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[PMID]:27871626
[Au] Autor:Luning Prak DJ; Breuer JE; Rios EA; Jedlicka EE; O'Sullivan DW
[Ad] Endereço:Chemistry Department, U.S. Naval Academy, 572 M Holloway Road, Annapolis, MD 21402, United States. Electronic address: prak@usna.edu.
[Ti] Título:Photolysis of 2,4,6-trinitrotoluene in seawater and estuary water: Impact of pH, temperature, salinity, and dissolved organic matter.
[So] Source:Mar Pollut Bull;114(2):977-986, 2017 Jan 30.
[Is] ISSN:1879-3363
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The influence of salinity, pH, temperature, and dissolved organic matter on the photolysis rate of 2,4,6-trinitrotoluene (TNT) in marine, estuary, and laboratory-prepared waters was studied using a Suntest CPS+® solar simulator equipped with optical filters. TNT degradation rates were determined using HPLC analysis, and products were identified using LC/MS. Minimal or no TNT photolysis occurred under a 395-nm long pass filter, but under a 295-nm filter, first-order TNT degradation rate constants and apparent quantum yields increased with increasing salinity in both natural and artificial seawater. TNT rate constants increased slightly with increasing temperature (10 to 32°C) but did not change significantly with pH (6.4 to 8.1). The addition of dissolved organic matter (up to 5mg/L) to ultrapure water, artificial seawater, and natural seawater increased the TNT photolysis rate constant. Products formed by TNT photolysis in natural seawater were determined to be 2,4,6-trinitrobenzaldehyde, 1,3,5-trinitrobenzene, 2,4,6-trinitrobenzoic acid, and 2-amino-4,6-dinitrobenzoic acid.
[Mh] Termos MeSH primário: Estuários
Fotólise
Água do Mar/química
Trinitrotolueno/química
Poluentes Químicos da Água/química
[Mh] Termos MeSH secundário: Substâncias Húmicas
Concentração de Íons de Hidrogênio
Nitrobenzoatos
Salinidade
Luz Solar
Temperatura Ambiente
Trinitrobenzenos
Trinitrotolueno/análise
Água
Poluentes Químicos da Água/análise
ortoaminobenzoatos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (2-amino-4,6-dinitrobenzoic acid); 0 (Humic Substances); 0 (Nitrobenzoates); 0 (Trinitrobenzenes); 0 (Water Pollutants, Chemical); 0 (ortho-Aminobenzoates); 059QF0KO0R (Water); 118-96-7 (Trinitrotoluene); 2H75703R1X (sym-trinitrobenzene)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161123
[St] Status:MEDLINE


  3 / 1523 MEDLINE  
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[PMID]:27806407
[Au] Autor:Eun SH; Woo JT; Kim DH
[Ad] Endereço:Department of Life and Nanopharmaceutical Sciences and Department of Pharmacy, Kyung Hee University, Seoul, Korea.
[Ti] Título:Tangeretin Inhibits IL-12 Expression and NF-κB Activation in Dendritic Cells and Attenuates Colitis in Mice.
[So] Source:Planta Med;83(6):527-533, 2017 Apr.
[Is] ISSN:1439-0221
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:In the preliminary study, tangeretin (5,6,7,8,4'-pentamethoxy flavone), a major constituent of the pericarp of sp., inhibited TNF- , IL-12, and IL-23 expression and nuclear factor kappa-B activation in lipopolysaccharide-stimulated dendritic cells; however, it did not affect IL-10 expression. Furthermore, tangeretin (5, 10, and 20 µM) suppressed the activation and translocation of nuclear factor kappa-B (p65) into the nuclei by inhibiting the binding of lipopolysaccharide on dendritic cells. Oral administration of tangeretin (10 and 20 mg/kg) suppressed the inflammatory responses, such as nuclear factor kappa-B and mitogen-activated protein kinase activation and myeloperoxidase activity, in the colon of mice with 2,4,6-trinitrobenzene sulfonic acid-induced colitis. Tangeretin increased 2,4,6-trinitrobenzene sulfonic acid-suppressed expression of tight junction proteins occludin, claudin-1, and ZO-1. Tangeretin also inhibited 2,4,6-trinitrobenzene sulfonic acid-induced differentiation of Th1 and Th17 cells as well as the expression of T-bet, ROR t, interferon- , IL-12, IL-17, and TNF- . However, tangeretin increased 2,4,6-trinitrobenzene sulfonic acid-suppressed differentiation of regulatory T cells as well as the expression of Foxp3 and IL-10. These results suggest that oral administration of tangeretin may attenuate colitis by suppressing IL-12 and TNF- expression and nuclear factor kappa-B activation through the inhibition of lipopolysaccharide binding on immune cells such as dendritic cells.
[Mh] Termos MeSH primário: Anti-Inflamatórios/farmacologia
Citrus/química
Colite/tratamento farmacológico
Citocinas/efeitos dos fármacos
Flavonas/farmacologia
NF-kappa B/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Anti-Inflamatórios/química
Colite/induzido quimicamente
Colo/efeitos dos fármacos
Colo/metabolismo
Citocinas/metabolismo
Células Dendríticas/efeitos dos fármacos
Células Dendríticas/metabolismo
Flavonas/química
Lipopolissacarídeos/efeitos adversos
Camundongos
Camundongos Endogâmicos C57BL
Proteínas Quinases Ativadas por Mitógeno/efeitos dos fármacos
Proteínas Quinases Ativadas por Mitógeno/metabolismo
NF-kappa B/metabolismo
Transdução de Sinais/efeitos dos fármacos
Linfócitos T Reguladores/efeitos dos fármacos
Linfócitos T Reguladores/metabolismo
Trinitrobenzenos/metabolismo
Ácido Trinitrobenzenossulfônico/efeitos adversos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Cytokines); 0 (Flavones); 0 (Lipopolysaccharides); 0 (NF-kappa B); 0 (Trinitrobenzenes); 2H75703R1X (sym-trinitrobenzene); 8T3HQG2ZC4 (Trinitrobenzenesulfonic Acid); EC 2.7.11.24 (Mitogen-Activated Protein Kinases); I4TLA1DLX6 (tangeretin)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170605
[Lr] Data última revisão:
170605
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161103
[St] Status:MEDLINE
[do] DOI:10.1055/s-0042-119074


  4 / 1523 MEDLINE  
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[PMID]:27967303
[Au] Autor:Kwast L; Aida T; Fiechter D; Kruijssen L; Bleumink R; Boon L; Ludwig I; Pieters R
[Ad] Endereço:a Division of Toxicology , Institute for Risk Assessment Sciences (IRAS), Utrecht University , Utrecht , The Netherlands.
[Ti] Título:Immune responses induced by diclofenac or carbamazepine in an oral exposure model using TNP-Ficoll as reporter antigen.
[So] Source:J Immunotoxicol;13(6):918-926, 2016 Nov.
[Is] ISSN:1547-6901
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Immune-mediated drug hypersensitivity reactions (IDHR) may result from immuno-sensitization to a drug-induced neo-antigen. They rarely occur in patients and are usually not predicted preclinically using standard toxicity studies. To assess the potential of a drug to induce T-cell sensitization, trinitrophenyl (TNP)-Ficoll was used here as a bystander antigen in animal experiments. TNP-Ficoll will only elicit TNP-specific IgG antibodies in the presence of non-cognate T-cell help. Therefore, the presence of TNP-specific IgG antibodies after co-injection of drug and TNP-Ficoll was indicative of T-cell sensitization potential. This TNP-Ficoll-approach was used here to characterize T-cell help induced by oral exposure to diclofenac (DF) or carbamazepine (CMZ). DF or CMZ was administered orally to BALB/c mice and after 3 w, the mice were challenged in a hind paw with TNP-Ficoll and a dose of the drug that by itself does only elicit a sub-optimal popliteal lymph node assay (PLNA) response. T-cell-dependent responses were then evaluated in paw-draining popliteal lymph nodes (PLN). Also, shortly after oral exposure, mesenteric lymph nodes (MLN) were excised for evaluation of local responses. Both drugs were able to increase PLN cellularity and TNP-specific IgG production after challenge. Both DF and CMZ stimulated CD4 and CD8 T-cells and caused shifts of the subsets toward an effector phenotype. DF, but not CMZ, appeared to stimulate interferon (IFN)-γ production. Remarkably, depletion of CD8 , but not CD4 , T-cells reduced TNP-specific IgG production, and was more pronounced in CMZ- than in DF-exposed animals. Local responses in the MLN caused by DF or CMZ also showed shifts of CD4 and CD8 -cells toward a memory phenotype. Together, the data indicate that oral exposure to CMZ and DF differentially induced neo-antigen-specific T-cell reactions in the PLNA.
[Mh] Termos MeSH primário: Anti-Inflamatórios não Esteroides/efeitos adversos
Carbamazepina/efeitos adversos
Diclofenaco/efeitos adversos
Hipersensibilidade a Drogas/imunologia
Linfócitos T/imunologia
[Mh] Termos MeSH secundário: Administração Oral
Animais
Anti-Inflamatórios não Esteroides/uso terapêutico
Antígenos/imunologia
Carbamazepina/uso terapêutico
Diclofenaco/uso terapêutico
Ficoll/análogos & derivados
Ficoll/imunologia
Imunoglobulina G/metabolismo
Interferon gama/metabolismo
Linfonodos/patologia
Ativação Linfocitária
Camundongos
Camundongos Endogâmicos BALB C
Trinitrobenzenos/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Antigens); 0 (Immunoglobulin G); 0 (TNP-ficoll); 0 (Trinitrobenzenes); 144O8QL0L1 (Diclofenac); 25702-74-3 (Ficoll); 33CM23913M (Carbamazepine); 82115-62-6 (Interferon-gamma)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161215
[St] Status:MEDLINE


  5 / 1523 MEDLINE  
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[PMID]:27448756
[Au] Autor:Liang Y; Kuo DTF; Allen HE; Di Toro DM
[Ad] Endereço:Department of Civil and Environmental Engineering, University of Delaware, Newark, 19716, DE, USA. Electronic address: yzliang@udel.edu.
[Ti] Título:Experimental determination of solvent-water partition coefficients and Abraham parameters for munition constituents.
[So] Source:Chemosphere;161:429-437, 2016 Oct.
[Is] ISSN:1879-1298
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:There is concern about the environmental fate and effects of munition constituents (MCs). Polyparameter linear free energy relationships (pp-LFERs) that employ Abraham solute parameters can aid in evaluating the risk of MCs to the environment. However, poor predictions using pp-LFERs and ABSOLV estimated Abraham solute parameters are found for some key physico-chemical properties. In this work, the Abraham solute parameters are determined using experimental partition coefficients in various solvent-water systems. The compounds investigated include hexahydro-1,3,5-trinitro-1,3,5-triazacyclohexane (RDX), octahydro-1,3,5,7-tetranitro-1,3,5,7-tetraazacyclooctane (HMX), hexahydro-1-nitroso-3,5-dinitro-1,3,5-triazine (MNX), hexahydro-1,3,5-trinitroso-1,3,5-triazine (TNX), hexahydro-1,3-dinitroso-5- nitro-1,3,5-triazine (DNX), 2,4,6-trinitrotoluene (TNT), 1,3,5-trinitrobenzene (TNB), and 4-nitroanisole. The solvents in the solvent-water systems are hexane, dichloromethane, trichloromethane, octanol, and toluene. The only available reported solvent-water partition coefficients are for octanol-water for some of the investigated compounds and they are in good agreement with the experimental measurements from this study. Solvent-water partition coefficients fitted using experimentally derived solute parameters from this study have significantly smaller root mean square errors (RMSE = 0.38) than predictions using ABSOLV estimated solute parameters (RMSE = 3.56) for the investigated compounds. Additionally, the predictions for various physico-chemical properties using the experimentally derived solute parameters agree with available literature reported values with prediction errors within 0.79 log units except for water solubility of RDX and HMX with errors of 1.48 and 2.16 log units respectively. However, predictions using ABSOLV estimated solute parameters have larger prediction errors of up to 7.68 log units. This large discrepancy is probably due to the missing R2NNO2 and R2NNO2 functional groups in the ABSOLV fragment database.
[Mh] Termos MeSH primário: Modelos Químicos
Solventes/química
Termodinâmica
Água/química
[Mh] Termos MeSH secundário: Anisóis/química
Octanóis/química
Triazinas/química
Trinitrobenzenos/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anisoles); 0 (Octanols); 0 (Solvents); 0 (Triazines); 0 (Trinitrobenzenes); 0 (hexahydro-1-nitroso-3,5-dinitro-1,3,5-triazine); 059QF0KO0R (Water); 2H75703R1X (sym-trinitrobenzene); G989Z7WOLH (4-nitroanisole); W91SSV5831 (cyclonite)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160725
[St] Status:MEDLINE


  6 / 1523 MEDLINE  
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[PMID]:26995548
[Au] Autor:Bang B; Lichtenberger LM
[Ad] Endereço:Department of Internal Medicine, Inha University School of Medicine, Incheon, Korea.
[Ti] Título:Methods of Inducing Inflammatory Bowel Disease in Mice.
[So] Source:Curr Protoc Pharmacol;72:5.58.1-42, 2016 Mar 18.
[Is] ISSN:1934-8290
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Animal models of experimentally induced inflammatory bowel disease (IBD) are useful for understanding more about the mechanistic basis of the disease, identifying new targets for therapeutic intervention, and testing novel therapeutics. This unit provides detailed protocols for five widely used mouse models of experimentally induced intestinal inflammation: chemical induction of colitis by dextran sodium sulfate (DSS), hapten-induced colitis via 2,4,6-trinitrobenzene sulfonic acid (TNBS), Helicobacter-induced colitis in mdr1a(-/-) mice, the CD4(+) CD45RB(hi) SCID transfer colitis model, and the IL-10(-/-) colitis model. © 2016 by John Wiley & Sons, Inc.
[Mh] Termos MeSH primário: Modelos Animais de Doenças
Inflamação/induzido quimicamente
Doenças Inflamatórias Intestinais/induzido quimicamente
[Mh] Termos MeSH secundário: Animais
Colite/induzido quimicamente
Colite/metabolismo
Sulfato de Dextrana/farmacologia
Feminino
Inflamação/metabolismo
Doenças Inflamatórias Intestinais/metabolismo
Interleucina-10/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C57BL
Camundongos SCID
Trinitrobenzenos/farmacologia
Ácido Trinitrobenzenossulfônico/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Trinitrobenzenes); 130068-27-8 (Interleukin-10); 2H75703R1X (sym-trinitrobenzene); 8T3HQG2ZC4 (Trinitrobenzenesulfonic Acid); 9042-14-2 (Dextran Sulfate)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160321
[St] Status:MEDLINE
[do] DOI:10.1002/0471141755.ph0558s72


  7 / 1523 MEDLINE  
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[PMID]:26943952
[Au] Autor:Kubo M; Nagashima R; Ohta E; Maekawa T; Isobe Y; Kurihara M; Eshima K; Iwabuchi K; Sasaoka T; Azuma S; Melrose HL; Farrer MJ; Obata F
[Ad] Endereço:Division of Immunology, Kitasato University School of Allied Health Sciences, 1-15-1 Kitasato, Minami-ku, Sagamihara, Kanagawa 252-0373, Japan; Division of Clinical Immunology, Graduate School of Medical Sciences, Kitasato University, 1-15-1 Kitasato, Minami-ku, Sagamihara, Kanagawa 252-0373, Japan;
[Ti] Título:Leucine-rich repeat kinase 2 is a regulator of B cell function, affecting homeostasis, BCR signaling, IgA production, and TI antigen responses.
[So] Source:J Neuroimmunol;292:1-8, 2016 Mar 15.
[Is] ISSN:1872-8421
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:LRRK2 is the causal molecule of autosomal dominant familial Parkinson's disease. B2 cells express a much higher LRRK2 mRNA level than B1 cells. To reveal the function of LRRK2 in B cells, we analyzed B cell functions in LRRK2-knockout (LRRK2(-/-)) mice. LRRK2(-/-) mice had significantly higher counts of peritoneal B1 cells than wild-type mice. After BCR stimulation, phosphor-Erk1/2 of splenic B2 cells was enhanced to a higher degree in LRRK2(-/-) mice. LRRK2(-/-) mice had a significantly higher serum IgA level, and TNP-Ficoll immunization increased the titer of serum anti-TNP IgM antibody. LRRK2 may play important roles in B cells.
[Mh] Termos MeSH primário: Linfócitos B/metabolismo
Homeostase/genética
Imunoglobulina A/sangue
Proteínas Serina-Treonina Quinases/metabolismo
Transdução de Sinais/fisiologia
[Mh] Termos MeSH secundário: Fatores Etários
Animais
Antígenos CD/metabolismo
Linfócitos B/classificação
Ensaio de Imunoadsorção Enzimática
Ficoll/análogos & derivados
Ficoll/imunologia
Citometria de Fluxo
Serina-Treonina Proteína Quinase-2 com Repetições Ricas em Leucina
Sistema de Sinalização das MAP Quinases/imunologia
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Cavidade Peritoneal/citologia
Proteínas Serina-Treonina Quinases/genética
Proteínas Proto-Oncogênicas c-akt/metabolismo
RNA Mensageiro/metabolismo
Transdução de Sinais/genética
Baço/citologia
Fator de Crescimento Transformador beta1/sangue
Trinitrobenzenos/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Immunoglobulin A); 0 (RNA, Messenger); 0 (TNP-ficoll); 0 (Transforming Growth Factor beta1); 0 (Trinitrobenzenes); 25702-74-3 (Ficoll); EC 2.7.11.1 (Akt1 protein, mouse); EC 2.7.11.1 (Leucine-Rich Repeat Serine-Threonine Protein Kinase-2); EC 2.7.11.1 (Lrrk2 protein, mouse); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:161126
[Lr] Data última revisão:
161126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160306
[St] Status:MEDLINE


  8 / 1523 MEDLINE  
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[PMID]:26695037
[Au] Autor:Clausen JD; McIntosh DB; Woolley DG; Andersen JP
[Ad] Endereço:Department of Biomedicine, Aarhus University, Ole Worms Allé 4, Building 1160, 8000, Aarhus C, Denmark. jdc@fi.au.dk.
[Ti] Título:Determination of the ATP Affinity of the Sarcoplasmic Reticulum Ca(2+)-ATPase by Competitive Inhibition of [γ-(32)P]TNP-8N3-ATP Photolabeling.
[So] Source:Methods Mol Biol;1377:233-59, 2016.
[Is] ISSN:1940-6029
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The photoactivation of aryl azides is commonly employed as a means to covalently attach cross-linking and labeling reagents to proteins, facilitated by the high reactivity of the resultant aryl nitrenes with amino groups present in the protein side chains. We have developed a simple and reliable assay for the determination of the ATP binding affinity of native or recombinant sarcoplasmic reticulum Ca(2+)-ATPase, taking advantage of the specific photolabeling of Lys(492) in the Ca(2+)-ATPase by [γ-(32)P]2',3'-O-(2,4,6-trinitrophenyl)-8-azido-adenosine 5'-triphosphate ([γ-(32)P]TNP-8N3-ATP) and the competitive inhibition by ATP of the photolabeling reaction. The method allows determination of the ATP affinity of Ca(2+)-ATPase mutants expressed in mammalian cell culture in amounts too minute for conventional equilibrium binding studies. Here, we describe the synthesis and purification of the [γ-(32)P]TNP-8N3-ATP photolabel, as well as its application in ATP affinity measurements.
[Mh] Termos MeSH primário: Trifosfato de Adenosina/análogos & derivados
Trifosfato de Adenosina/metabolismo
Ligação Competitiva
Fotólise
ATPases Transportadoras de Cálcio do Retículo Sarcoplasmático/química
ATPases Transportadoras de Cálcio do Retículo Sarcoplasmático/metabolismo
Coloração e Rotulagem
[Mh] Termos MeSH secundário: Trifosfato de Adenosina/química
Animais
Eletroforese em Gel de Poliacrilamida
Modelos Moleculares
Radioisótopos de Fósforo
Ligação Proteica
Conformação Proteica
Coelhos
Trinitrobenzenos/química
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Phosphorus Radioisotopes); 0 (Trinitrobenzenes); 61368-63-6 (2',3'-O-(2,4,6-trinitro-cyclohexadienylidine)adenosine 5'-triphosphate); 8L70Q75FXE (Adenosine Triphosphate); EC 3.6.3.8 (Sarcoplasmic Reticulum Calcium-Transporting ATPases)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:151223
[Lr] Data última revisão:
151223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151224
[St] Status:MEDLINE
[do] DOI:10.1007/978-1-4939-3179-8_22


  9 / 1523 MEDLINE  
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[PMID]:26332307
[Au] Autor:Jin Y; Pridgen TA; Blikslager AT
[Ad] Endereço:Department of Clinical Sciences, Center for Comparative Medicine and Translational Research, College of Veterinary Medicine, North Carolina State University, Raleigh, North Carolina.
[Ti] Título:Pharmaceutical Activation or Genetic Absence of ClC-2 Alters Tight Junctions During Experimental Colitis.
[So] Source:Inflamm Bowel Dis;21(12):2747-57, 2015 Dec.
[Is] ISSN:1536-4844
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: We have previously reported that the ClC-2 chloride channel has an important role in regulation of tight junction barrier function during experimental colitis, and the pharmaceutical ClC-2 activator lubiprostone initiates intestinal barrier repair in ischemic-injured intestine. Thus, we hypothesized that pharmaceutical ClC-2 activation would have a protective and therapeutic effect in murine models of colitis, which would be absent in ClC-2 mice. METHODS: We administered lubiprostone to wild-type or ClC-2 mice with dextran sulfate sodium (DSS) or 2, 4, 5-trinitrobenzene sulfonic acid-induced colitis. We determined the severity of colitis and assessed intestinal permeability. Selected tight junction proteins were analyzed by Western blotting and immunofluorescence/confocal microscopy, whereas proliferative and differentiated cells were examined with special staining and immunohistochemistry. RESULTS: Oral preventive or therapeutic administration of lubiprostone significantly reduced the severity of colitis and reduced intestinal permeability in both DSS and trinitrobenzene sulfonic acid-induced colitis. Preventive treatment with lubiprostone induced significant recovery of the expression and distribution of selected sealing tight junction proteins in mice with DSS-induced colitis. In addition, lubiprostone reduced crypt proliferation and increased the number of differentiated epithelial cells. Alternatively, when lubiprostone was administered to ClC-2 mice, the protective effect against DSS colitis was limited. CONCLUSIONS: This study suggests a central role for ClC-2 in restoration of barrier function and tight junction architecture in experimental murine colitis, which can be therapeutically targeted with lubiprostone.
[Mh] Termos MeSH primário: Agonistas dos Canais de Cloreto/farmacologia
Canais de Cloreto/efeitos dos fármacos
Colite/tratamento farmacológico
Lubiprostona/farmacologia
Junções Íntimas/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Western Blotting
Canais de Cloreto/deficiência
Colite/induzido quimicamente
Colite/genética
Sulfato de Dextrana
Imunofluorescência
Intestinos/efeitos dos fármacos
Intestinos/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Microscopia Confocal
Permeabilidade/efeitos dos fármacos
Proteínas de Junções Íntimas/metabolismo
Junções Íntimas/metabolismo
Trinitrobenzenos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Chloride Channel Agonists); 0 (Chloride Channels); 0 (ClC-2 chloride channels); 0 (Tight Junction Proteins); 0 (Trinitrobenzenes); 7662KG2R6K (Lubiprostone); 9042-14-2 (Dextran Sulfate)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:151120
[Lr] Data última revisão:
151120
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150903
[St] Status:MEDLINE
[do] DOI:10.1097/MIB.0000000000000550


  10 / 1523 MEDLINE  
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[PMID]:26069953
[Au] Autor:Liu L; Liu Z; Zhang T; Shi L; Zhang W; Zhang Y
[Ad] Endereço:Department of Pharmaceutical, Tangdu Hospital, Fourth Military Medical University, Xi'an, China.
[Ti] Título:Combined Therapy with Rheum tanguticum Polysaccharide and Low-dose 5-ASA Ameliorates TNBS-Induced Colitis in Rats by Suppression of NF-κB.
[So] Source:Planta Med;81(9):705-12, 2015 Jun.
[Is] ISSN:1439-0221
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:The most common conventional therapy for inflammatory bowel disease in clinical practice involves the use of nonsteroidal anti-inflammatory drugs, such as 5-amino salicylic acid. However, a high dose of 5-amino salicylic acid may bring about severe side effects. Chinese people have used Rheum tanguticum as a folk remedy for gastrointestinal disease for two thousand years. Our group has isolated R. tanguticum polysaccharide 1 from R. tanguticum and verified that it can attenuate 2,4,6-trinitrobenzene sulfonic acid-induced colitis in murines/rats. The present study aims to evaluate whether the addition of R. tanguticum polysaccharide 1 can improve efficacy and limit subsequent side effects of conventional treatment (5-amino salicylic acid) in rats with 2,4,6-trinitrobenzene sulfonic acid-induced colitis. Sixty Sprague-Dawley male rats were randomized into five groups and treated with (1) saline (saline, 0.2 mL/day × 5, p. o.), (2) 2,4,6-trinitrobenzene sulfonic acid alone (saline, 0.2 mL/day × 5, p. o.), (3) 2,4,6-trinitrobenzene sulfonic acid + 5-amino salicylic acid (5-amino salicylic acid, 75 mg/kg/day × 5, p.o), (4) 2,4,6-trinitrobenzene sulfonic acid + R. tanguticum polysaccharide 1 (R. tanguticum polysaccharide 1, 200 mg/kg/day × 5, p. o.), and (5) 2,4,6-trinitrobenzene sulfonic acid + 5-amino salicylic acid + R. tanguticum polysaccharide 1 (5-amino salicylic acid, 25 mg/kg/day × 5, p.o; R. tanguticum polysaccharide 1, 200 mg/kg/day × 5, p. o.). All the rats were sacrificed on the 6th day after treatment using an overdose of anesthesia. A histological assessment was performed using semiquantitative scores; nuclear factor-kappa B and tumor necrosis factor-α were measured with Western blot, cyclooxygenase 1 and cyclooxygenase 2 protein expressions were investigated by RT-polymerase chain reaction, and prostoglandin E2 and inducible nitric oxide synthase productions were investigated by ELISA. The extent and severity of histological signs were attenuated significantly in the 2,4,6-trinitrobenzene sulfonic acid + 5-amino salicylic acid + R. tanguticum polysaccharide 1 group. Treatment with R. tanguticum polysaccharide 1 plus 5-amino salicylic acid markedly decreased nuclear factor-kappa Bp65 and tumor necrosis factor-α protein expressions. R. tanguticum polysaccharide 1 and 5-amino salicylic acid had no effect on cyclooxygenase 1 protein expression, but inhibited the overexpression of the cyclooxygenase 2 protein. After treatment with 5-amino salicylic acid and R. tanguticum polysaccharide 1, the prostoglandin E2 level increased significantly and the inducible nitric oxide synthase level decreased considerably in the 2,4,6-trinitrobenzene sulfonic acid + 5-amino salicylic acid + R. tanguticum polysaccharide 1 group compared with the 2,4,6-trinitrobenzene sulfonic acid alone group. These results demonstrate that combined therapy with R. tanguticum polysaccharide 1 and low-dose 5-amino salicylic acid had more favorable effects on 2,4,6-trinitrobenzene sulfonic acid-induced colitis in rats, and its effects may be associated with inhibiting nuclear factor-kappa Bp65 protein expression and tumor necrosis factor-α production, resulting in a decrease of cyclooxygenase 2 and inducible nitric oxide synthase protein expressions.
[Mh] Termos MeSH primário: Colite/tratamento farmacológico
NF-kappa B/efeitos dos fármacos
Polissacarídeos/farmacologia
Rheum/química
Fator de Necrose Tumoral alfa/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Peso Corporal/efeitos dos fármacos
Colite/induzido quimicamente
Ciclo-Oxigenase 1/efeitos dos fármacos
Ciclo-Oxigenase 1/genética
Ciclo-Oxigenase 2/efeitos dos fármacos
Ciclo-Oxigenase 2/genética
Modelos Animais de Doenças
Quimioterapia Combinada
Masculino
NF-kappa B/metabolismo
Óxido Nítrico Sintase Tipo II/efeitos dos fármacos
Óxido Nítrico Sintase Tipo II/metabolismo
Ratos
Ratos Sprague-Dawley
Trinitrobenzenos/efeitos adversos
Ácido Trinitrobenzenossulfônico/efeitos adversos
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (NF-kappa B); 0 (Polysaccharides); 0 (Trinitrobenzenes); 0 (Tumor Necrosis Factor-alpha); 2H75703R1X (sym-trinitrobenzene); 8T3HQG2ZC4 (Trinitrobenzenesulfonic Acid); EC 1.14.13.39 (Nitric Oxide Synthase Type II); EC 1.14.99.1 (Cyclooxygenase 1); EC 1.14.99.1 (Cyclooxygenase 2)
[Em] Mês de entrada:1601
[Cu] Atualização por classe:150703
[Lr] Data última revisão:
150703
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150613
[St] Status:MEDLINE
[do] DOI:10.1055/s-0035-1545945



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