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[PMID]:28322751
[Au] Autor:Lee Y; Heo G; Lee KM; Kim AH; Chung KW; Im E; Chung HY; Lee J
[Ad] Endereço:Department of Pharmacy, College of Pharmacy, Molecular Inflammation Research Center for Aging Intervention, Pusan National University, Busan 609-735, Republic of Korea.
[Ti] Título:Neuroprotective effects of 2,4-dinitrophenol in an acute model of Parkinson's disease.
[So] Source:Brain Res;1663:184-193, 2017 May 15.
[Is] ISSN:1872-6240
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Neurons depend on mitochondria for homeostasis and survival, and thus, mitochondrial dysfunction has been implicated in neurodegenerative diseases, including Parkinson's disease (PD). Increasing evidence indicates the mitochondrial uncoupler, 2,4-dinitrophenol (DNP), protects neurons against neurodegeneration and enhances neural plasticity. Here, the authors evaluated the protective effects of intraperitoneally (i.p.) administered low dose DNP in an acute mouse model of PD. Mice were administered DNP (1 or 5mg/kg) for 12 consecutive days, and then on day 13, MPTP (20mg/kg, i.p.) was administered four times (with 2h intervals between injections) to induce PD. It was found that MPTP-induced motor dysfunction was ameliorated in the DNP-treated mice versus vehicle-treated controls. Additionally, DNP effectively attenuated dopaminergic neuronal loss observed in MPTP treated mice. Moreover, in primary cultured neurons, DNP at 10µM, but not at 100µM, prevented MPP -induced cell death and mitochondrial membrane potential (MMP) reduction. In addition, DNP was observed to cause the nuclear translocation of Nrf2 in primary neurons. Taken together, these findings of the present study suggest that DNP protects dopaminergic neurons against neurodegeneration and maintains MMP integrity in PD by activating adaptive stress responses.
[Mh] Termos MeSH primário: 2,4-Dinitrofenol/uso terapêutico
Doença de Parkinson/metabolismo
[Mh] Termos MeSH secundário: 1-Metil-4-Fenil-1,2,3,6-Tetra-Hidropiridina/farmacologia
2,4-Dinitrofenol/metabolismo
2,4-Dinitrofenol/farmacocinética
Animais
Morte Celular/efeitos dos fármacos
Dinitrofenóis/metabolismo
Modelos Animais de Doenças
Dopamina/metabolismo
Neurônios Dopaminérgicos/efeitos dos fármacos
Intoxicação por MPTP/fisiopatologia
Masculino
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Camundongos
Camundongos Endogâmicos C57BL
Mitocôndrias/efeitos dos fármacos
Fármacos Neuroprotetores/farmacologia
Substância Negra/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Dinitrophenols); 0 (Neuroprotective Agents); 9P21XSP91P (1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine); Q13SKS21MN (2,4-Dinitrophenol); VTD58H1Z2X (Dopamine)
[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:170322
[St] Status:MEDLINE


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[PMID]:27890918
[Au] Autor:Kim YY; Je IG; Kim MJ; Kang BC; Choi YA; Baek MC; Lee B; Choi JK; Park HR; Shin TY; Lee S; Yoon SB; Lee SR; Khang D; Kim SH
[Ad] Endereço:CMRI, Department of Pharmacology, Daegu 700-422, Republic of Korea.
[Ti] Título:2-Hydroxy-3-methoxybenzoic acid attenuates mast cell-mediated allergic reaction in mice via modulation of the FcεRI signaling pathway.
[So] Source:Acta Pharmacol Sin;38(1):90-99, 2017 Jan.
[Is] ISSN:1745-7254
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mast cells are important effector cells in immunoglobulin (Ig) E-mediated allergic reactions such as asthma, atopic dermatitis and rhinitis. Vanillic acid, a natural product, has shown anti-oxidant and anti-inflammatory activities. In the present study, we investigated the anti-allergic inflammatory effects of ortho-vanillic acid (2-hydroxy-3-methoxybenzoic acid, o-VA) that was a derivative of vanillic acid isolated from Amomum xanthioides. In mouse anaphylaxis models, oral administration of o-VA (2, 10, 50 mg/kg) dose-dependently attenuated ovalbumin-induced active systemic anaphylaxis and IgE-mediated cutaneous allergic reactions such as hypothermia, histamine release, IgE production and vasodilation; administration of o-VA also suppressed the mast cell degranulator compound 48/80-induced anaphylaxis. In cultured mast cell line RBL-2H3 and isolated rat peritoneal mast cells in vitro, pretreatment with o-VA (1-100 µmol/L) dose-dependently inhibited DNP-HSA-induced degranulation of mast cells by decreasing the intracellular free calcium level, and suppressed the expression of pro-inflammatory cytokines TNF-α and IL-4. Pretreatment of RBL-2H3 cells with o-VA suppressed DNP-HSA-induced phosphorylation of Lyn, Syk, Akt, and the nuclear translocation of nuclear factor-κB. In conclusion, o-VA suppresses the mast cell-mediated allergic inflammatory response by blocking the signaling pathways downstream of high affinity IgE receptor (FcεRI) on the surface of mast cells.
[Mh] Termos MeSH primário: Anafilaxia/tratamento farmacológico
Anafilaxia/imunologia
Benzoatos/farmacologia
Benzoatos/uso terapêutico
Hipersensibilidade/tratamento farmacológico
Mastócitos/efeitos dos fármacos
Receptores de IgE/imunologia
Ácido Vanílico/análogos & derivados
[Mh] Termos MeSH secundário: Anafilaxia/induzido quimicamente
Animais
Cálcio/metabolismo
Degranulação Celular/efeitos dos fármacos
Células Cultivadas
Dinitrofenóis/antagonistas & inibidores
Relação Dose-Resposta a Droga
Hipersensibilidade/imunologia
Imunoglobulina E/efeitos dos fármacos
Mediadores da Inflamação/metabolismo
Masculino
Mastócitos/imunologia
Camundongos
NF-kappa B/metabolismo
Ovalbumina/antagonistas & inibidores
Fosforilação/efeitos dos fármacos
Ratos
Receptores de IgE/antagonistas & inibidores
Albumina Sérica/antagonistas & inibidores
Transdução de Sinais/efeitos dos fármacos
p-Metoxi-N-metilfenetilamina/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (2-hydroxy-3-methoxybenzoic acid); 0 (Benzoates); 0 (Dinitrophenols); 0 (FcepsilonRI protein, rat); 0 (Inflammation Mediators); 0 (NF-kappa B); 0 (Receptors, IgE); 0 (Serum Albumin); 0 (dinitrophenyl-human serum albumin conjugate); 37341-29-0 (Immunoglobulin E); 4091-50-3 (p-Methoxy-N-methylphenethylamine); 9006-59-1 (Ovalbumin); GM8Q3JM2Y8 (Vanillic Acid); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170912
[Lr] Data última revisão:
170912
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161129
[St] Status:MEDLINE
[do] DOI:10.1038/aps.2016.112


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[PMID]:27193167
[Au] Autor:Lou S; Lepak VC; Eberly LE; Roth B; Cui W; Zhu XH; Öz G; Dubinsky JM
[Ad] Endereço:Department of Neuroscience.
[Ti] Título:Oxygen consumption deficit in Huntington disease mouse brain under metabolic stress.
[So] Source:Hum Mol Genet;25(13):2813-2826, 2016 Jul 01.
[Is] ISSN:1460-2083
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:In vivo evidence for brain mitochondrial dysfunction in animal models of Huntington disease (HD) is scarce. We applied the novel O magnetic resonance spectroscopy (MRS) technique on R6/2 mice to directly determine rates of oxygen consumption (CMRO ) and assess mitochondrial function in vivo Basal respiration and maximal CMRO in the presence of the mitochondrial uncoupler dinitrophenol (DNP) were compared using 16.4 T in isoflurane anesthetized wild type (WT) and HD mice at 9 weeks. At rest, striatal CMRO of R6/2 mice was equivalent to that of WT, indicating comparable mitochondrial output despite onset of motor symptoms in R6/2. After DNP injection, the maximal CMRO in both striatum and cortex of R6/2 mice was significantly lower than that of WT, indicating less spare energy generating capacity. In a separate set of mice, oligomycin injection to block ATP generation decreased CMRO equally in brains of R6/2 and WT mice, suggesting oxidative phosphorylation capacity and respiratory coupling were equivalent at rest. Expression levels of representative mitochondrial proteins were compared from harvested tissue samples. Significant differences between R6/2 and WT included: in striatum, lower VDAC and the mitochondrially encoded cytochrome oxidase subunit I relative to actin; in cortex, lower tricarboxylic acid cycle enzyme aconitase and higher protein carbonyls; in both, lower glycolytic enzyme enolase. Therefore in R6/2 striatum, lowered CMRO may be attributed to a decrease in mitochondria while the cortical CMRO decrease may result from constraints upstream in energetic pathways, suggesting regionally specific changes and possibly rates of metabolic impairment.
[Mh] Termos MeSH primário: Doença de Huntington/metabolismo
Consumo de Oxigênio/fisiologia
[Mh] Termos MeSH secundário: Animais
Encéfalo/metabolismo
Corpo Estriado/metabolismo
Dinitrofenóis
Modelos Animais de Doenças
Imagem por Ressonância Magnética/métodos
Masculino
Camundongos
Camundongos Transgênicos
Mitocôndrias/metabolismo
Neostriado/metabolismo
Fosforilação Oxidativa
Consumo de Oxigênio/genética
Estresse Fisiológico/genética
Estresse Fisiológico/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Dinitrophenols)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170921
[Lr] Data última revisão:
170921
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160520
[St] Status:MEDLINE


  4 / 7055 MEDLINE  
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[PMID]:26984528
[Au] Autor:Malik M; Mustaev A; Schwanz HA; Luan G; Shah N; Oppegard LM; de Souza EC; Hiasa H; Zhao X; Kerns RJ; Drlica K
[Ad] Endereço:Public Heath Research Institute, New Jersey Medical School, Rutgers Biomedical and Health Science, 225 Warren Street, Newark, NJ 07103, USA.
[Ti] Título:Suppression of gyrase-mediated resistance by C7 aryl fluoroquinolones.
[So] Source:Nucleic Acids Res;44(7):3304-16, 2016 Apr 20.
[Is] ISSN:1362-4962
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Fluoroquinolones form drug-topoisomerase-DNA complexes that rapidly block transcription and replication. Crystallographic and biochemical studies show that quinolone binding involves a water/metal-ion bridge between the quinolone C3-C4 keto-acid and amino acids in helix-4 of the target proteins, GyrA (gyrase) and ParC (topoisomerase IV). A recent cross-linking study revealed a second drug-binding mode in which the other end of the quinolone, the C7 ring system, interacts with GyrA. We report that addition of a dinitrophenyl (DNP) moiety to the C7 end of ciprofloxacin (Cip-DNP) reduced protection due to resistance substitutions in Escherichia coli GyrA helix-4, consistent with the existence of a second drug-binding mode not evident in X-ray structures of drug-topoisomerase-DNA complexes. Several other C7 aryl fluoroquinolones behaved in a similar manner with particular GyrA mutants. Treatment of E. coli cultures with Cip-DNP selectively enriched an uncommon variant, GyrA-A119E, a change that may impede binding of the dinitrophenyl group at or near the GyrA-GyrA interface. Collectively the data support the existence of a secondary quinolone-binding mode in which the quinolone C7 ring system interacts with GyrA; the data also identify C7 aryl derivatives as a new way to obtain fluoroquinolones that overcome existing GyrA-mediated quinolone resistance.
[Mh] Termos MeSH primário: Antibacterianos/química
DNA Girase/genética
Fluoroquinolonas/química
Inibidores da Topoisomerase II/química
[Mh] Termos MeSH secundário: Antibacterianos/farmacologia
DNA Girase/química
Dinitrofenóis/química
Farmacorresistência Bacteriana/genética
Escherichia coli/efeitos dos fármacos
Escherichia coli/enzimologia
Fluoroquinolonas/farmacologia
Mutação
Inibidores da Topoisomerase II/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (Dinitrophenols); 0 (Fluoroquinolones); 0 (Topoisomerase II Inhibitors); EC 5.99.1.3 (DNA Gyrase)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160318
[St] Status:MEDLINE
[do] DOI:10.1093/nar/gkw161


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[PMID]:26936360
[Au] Autor:Zotz JS; Wölbing F; Lassnig C; Kauffmann M; Schulte U; Kolb A; Whitelaw B; Müller M; Biedermann T; Huber M
[Ad] Endereço:Institute of Biochemistry and Molecular Immunology, University Hospital, Rheinisch-Westfälische Technische Hochschule (RWTH) Aachen University, Aachen, Germany;
[Ti] Título:CD13/aminopeptidase N is a negative regulator of mast cell activation.
[So] Source:FASEB J;30(6):2225-35, 2016 06.
[Is] ISSN:1530-6860
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Antigen-induced mast cell (MC) activation via cross-linking of IgE-bound high-affinity receptors for IgE (FcεRI) underlies type I allergy and anaphylactic shock. Comprehensive knowledge of FcεRI regulation is thus required. We have identified a functional interaction between FcεRI and CD13 in murine MCs. Antigen-triggered activation of IgE-loaded FcεRI results in cocapping and cointernalization of CD13 and equivalent internalization rates of up to 40%. Cointernalization is not unspecific, because ligand-driven KIT internalization is not accompanied by CD13 internalization. Moreover, antibody-mediated cross-linking of CD13 causes IL-6 production in an FcεRI-dependent manner. These data are indicative of a functional interaction between FcεRI and CD13 on MCs. To determine the role of this interaction, CD13-deficient bone marrow-derived MCs (BMMCs) were analyzed. Intriguingly, antigen stimulation of CD13-deficient BMMCs results in significantly increased degranulation and proinflammatory cytokine production compared to wild-type cells. Furthermore, in a low-dose model of passive systemic anaphylaxis, antigen-dependent decrease in body temperature, reflecting the anaphylactic reaction, is substantially enhanced by the CD13 inhibitor bestatin (-5.9 ± 0.6°C) and by CD13 deficiency (-8.8 ± 0.6°C) in contrast to controls (-1.2 ± 1.97°C). Importantly, bestatin does not aggravate anaphylaxis in CD13-deficient mice. Thus, we have identified CD13 as a novel negative regulator of MC activation in vitro and in vivo-Zotz, J. S., Wölbing, F., Lassnig, C., Kauffmann, M., Schulte, U., Kolb, A., Whitelaw, B., Müller, M., Biedermann, T., Huber, M. CD13/aminopeptidase N is a negative regulator of mast cell activation.
[Mh] Termos MeSH primário: Antígenos CD13/metabolismo
Mastócitos/fisiologia
[Mh] Termos MeSH secundário: Anafilaxia
Animais
Antígenos CD13/antagonistas & inibidores
Antígenos CD13/genética
Proliferação Celular
Dinitrofenóis/imunologia
Regulação da Expressão Gênica/fisiologia
Leucina/análogos & derivados
Leucina/farmacologia
Macrófagos
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Receptores de IgE/genética
Receptores de IgE/metabolismo
Albumina Sérica/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Dinitrophenols); 0 (Receptors, IgE); 0 (Serum Albumin); 0 (dinitrophenyl-human serum albumin conjugate); EC 3.4.11.2 (CD13 Antigens); GMW67QNF9C (Leucine); I0J33N5627 (ubenimex)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171118
[Lr] Data última revisão:
171118
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160304
[St] Status:MEDLINE
[do] DOI:10.1096/fj.201600278


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[PMID]:26894427
[Au] Autor:Genady AR; Janzen N; Banevicius L; El-Gamal M; El-Zaria ME; Valliant JF
[Ad] Endereço:Department of Chemistry and Chemical Biology, McMaster University , 1280 Main Street West, Hamilton, Ontario L8S 4M1, Canada.
[Ti] Título:Preparation and Evaluation of Radiolabeled Antibody Recruiting Small Molecules That Target Prostate-Specific Membrane Antigen for Combined Radiotherapy and Immunotherapy.
[So] Source:J Med Chem;59(6):2660-73, 2016 Mar 24.
[Is] ISSN:1520-4804
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The feasibility of developing a single agent that can deliver radioactive iodine and also direct cellular immune function by engaging endogenous antibodies as an antibody-recruiting small molecule (ARM) was determined. A library of new prostate-specific membrane antigen (PSMA)-binding ligands that contained antibody-recruiting 2,4-dinitrophenyl (DNP) groups and iodine were synthesized and screened in vitro and in vivo. A lead compound (9b) showed high affinity for PSMA and the ability to bind anti-DNP antibodies. Biodistribution studies of the iodine-125 analogue showed 3% ID/g in LNCaP xenograft tumors at 1 h postinjection with tumor-to-blood and tumor-to-muscle ratios of 10:1 and 44:1, respectively. The radiolabeled analogue was bound and internalized by LNCaP cells, with both functions blocked using a known PSMA inhibitor. A second candidate showed high tumor uptake (>10% ID/g) but had minimal binding to anti-DNP antibodies. The compounds reported represent the first examples of small molecules developed specifically for combination immunotherapy and radiotherapy for prostate cancer.
[Mh] Termos MeSH primário: Antígenos de Neoplasias/efeitos dos fármacos
Antígeno Prostático Específico/imunologia
Neoplasias da Próstata/terapia
Radioimunoterapia/métodos
Compostos Radiofarmacêuticos/síntese química
Compostos Radiofarmacêuticos/farmacologia
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Dinitrofenóis/síntese química
Dinitrofenóis/farmacologia
Feminino
Seres Humanos
Ligantes
Masculino
Camundongos
Camundongos Nus
Neoplasias da Próstata/metabolismo
Compostos Radiofarmacêuticos/farmacocinética
Bibliotecas de Moléculas Pequenas
Distribuição Tecidual
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens, Neoplasm); 0 (Dinitrophenols); 0 (Ligands); 0 (Radiopharmaceuticals); 0 (Small Molecule Libraries); EC 3.4.21.77 (Prostate-Specific Antigen)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:160324
[Lr] Data última revisão:
160324
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160220
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jmedchem.5b01881


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[PMID]:26686301
[Au] Autor:Jayant K; Singhai A; Cao Y; Phelps JB; Lindau M; Holowka DA; Baird BA; Kan EC
[Ad] Endereço:Electrical and Computer Engineering, Cornell University, Ithaca, NY 14853, USA.
[Ti] Título:Non-Faradaic Electrochemical Detection of Exocytosis from Mast and Chromaffin Cells Using Floating-Gate MOS Transistors.
[So] Source:Sci Rep;5:18477, 2015 Dec 21.
[Is] ISSN:2045-2322
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:We present non-faradaic electrochemical recordings of exocytosis from populations of mast and chromaffin cells using chemoreceptive neuron MOS (CνMOS) transistors. In comparison to previous cell-FET-biosensors, the CνMOS features control (CG), sensing (SG) and floating gates (FG), allows the quiescent point to be independently controlled, is CMOS compatible and physically isolates the transistor channel from the electrolyte for stable long-term recordings. We measured exocytosis from RBL-2H3 mast cells sensitized by IgE (bound to high-affinity surface receptors FcεRI) and stimulated using the antigen DNP-BSA. Quasi-static I-V measurements reflected a slow shift in surface potential () which was dependent on extracellular calcium ([Ca]o) and buffer strength, which suggests sensitivity to protons released during exocytosis. Fluorescent imaging of dextran-labeled vesicle release showed evidence of a similar time course, while un-sensitized cells showed no response to stimulation. Transient recordings revealed fluctuations with a rapid rise and slow decay. Chromaffin cells stimulated with high KCl showed both slow shifts and extracellular action potentials exhibiting biphasic and inverted capacitive waveforms, indicative of varying ion-channel distributions across the cell-transistor junction. Our approach presents a facile method to simultaneously monitor exocytosis and ion channel activity with high temporal sensitivity without the need for redox chemistry.
[Mh] Termos MeSH primário: Técnicas Biossensoriais/métodos
Células Cromafins/química
Exocitose
Mastócitos/química
[Mh] Termos MeSH secundário: Animais
Dinitrofenóis/química
Técnicas Eletroquímicas
Imunoglobulina E/química
Ratos
Soroalbumina Bovina/química
Transistores Eletrônicos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (Dinitrophenols); 0 (dinitrophenyl-bovine serum albumin); 27432CM55Q (Serum Albumin, Bovine); 37341-29-0 (Immunoglobulin E)
[Em] Mês de entrada:1610
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151222
[St] Status:MEDLINE
[do] DOI:10.1038/srep18477


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[PMID]:26621445
[Au] Autor:Han SY; Choi YJ; Kang MK; Park JH; Kang YH
[Ti] Título:Resveratrol Suppresses Cytokine Production Linked to FcεRI-MAPK Activation in IgE-Antigen Complex-Exposed Basophilic Mast Cells and Mice.
[So] Source:Am J Chin Med;43(8):1605-23, 2015.
[Is] ISSN:0192-415X
[Cp] País de publicação:Singapore
[La] Idioma:eng
[Ab] Resumo:A complicated interplay between resident mast cells and other recruited inflammatory cells contributes to the development and progression of allergic inflammation entailing the promotion of T helper 2 (Th2) cytokine responses. The current study examined whether resveratrol suppressed the production of inflammatory Th2 cytokines in cultured rat basophilic leukemia RBL-2H3 cells. Cells pre-treated with resveratrol nontoxic at 1­25 µM were sensitized with anti-dinitrophenyl (anti-DNP), and subsequently stimulated by dinitrophenyl-human serum albumin (DNP­HSA) antigen. Resveratrol dose-dependently diminished the secretion of interleukin (IL)-3, IL-4, IL-13 as well as tumor necrosis factor (TNF)-α by the antigen stimulation from sensitized cells. It was found that resveratrol mitigated the phosphorylation of p38 MAPK, ERK, and JNK elevated in mast cells exposed to Fc epsilon receptor I (FcεRI)-mediated immunoglobulin E (IgE)-antigen complex. The FcεRI aggregation was highly enhanced on the surface of mast cells following the HSA stimulation, which was retarded by treatment with 1­25 µM resveratrol. The IgE-receptor engagement rapidly induced tyrosine phosphorylation of c-Src-related focal adhesion protein paxillin involved in the cytoskeleton rearrangement. The FcεRI-mediated rapid activation of c-Src and paxillin was attenuated in a dose-dependent manner. In addition, the paxillin activation entailed p38 MAPK and ERK-responsive signaling, but the JNK activation was less involved. Consistently, oral administration of resveratrol reduced the tissue level of phosphorylated paxillin in the dorsal skin of DNP­HSA-challenged mice. The other tyrosine kinase Tyk2-STAT1 signaling was activated in the dorsal epidermis of antigen-exposed mice, which was associated with allergic inflammation. These results showed that resveratrol inhibited Th2 cytokines- and paxillin-linked allergic responses dependent upon MAPK signaling. Therefore, resveratrol may possess the therapeutic potential of targeting mast cells in preventing the development of allergic inflammation.
[Mh] Termos MeSH primário: Citocinas/secreção
Dinitrofenóis/imunologia
Hipersensibilidade/tratamento farmacológico
Hipersensibilidade/imunologia
Imunoglobulina E/imunologia
Inflamação/tratamento farmacológico
Inflamação/imunologia
Mastócitos/imunologia
Fitoterapia
Receptores de IgE/imunologia
Albumina Sérica/imunologia
Estilbenos/farmacologia
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Modelos Animais de Doenças
Relação Dose-Resposta a Droga
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Sistema de Sinalização das MAP Quinases/imunologia
Masculino
Mastócitos/secreção
Camundongos
Camundongos Endogâmicos BALB C
Terapia de Alvo Molecular
Fosforilação/efeitos dos fármacos
Estilbenos/uso terapêutico
Células Th2/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cytokines); 0 (Dinitrophenols); 0 (Receptors, IgE); 0 (Serum Albumin); 0 (Stilbenes); 0 (dinitrophenyl-human serum albumin conjugate); 37341-29-0 (Immunoglobulin E); Q369O8926L (resveratrol)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:160426
[Lr] Data última revisão:
160426
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151202
[St] Status:MEDLINE


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[PMID]:26376734
[Au] Autor:Matsui T; Ito C; Masubuchi S; Itoigawa M
[Ad] Endereço:Department of Physiology, Aichi Medical University, Aichi, Japan.
[Ti] Título:Licarin A is a candidate compound for the treatment of immediate hypersensitivity via inhibition of rat mast cell line RBL-2H3 cells.
[So] Source:J Pharm Pharmacol;67(12):1723-32, 2015 Dec.
[Is] ISSN:2042-7158
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: We previously demonstrated that some phenylpropanoids are capable of inhibiting activated mast cells. This study evaluated the anti-allergic effects of licarin A, a neolignan isolated from various plants, on antigen-stimulated rat mast cell line. METHODS: The inhibitory effects of licarin A on histamine release, tumour necrosis factor-α (TNF-α) and prostaglandin D2 (PGD2) production, and cyclooxygenase-2 (COX-2) expression in dinitrophenyl-human serum albumin (DNP-HSA) rat basophilic leukemia cells (DNP-HSA-stimulated RBL-2H3 cells), were investigated by spectrofluorometry, ELISA and immunoblotting. KEY FINDINGS: Licarin A significantly and dose-dependently reduced TNF-α production (IC50 12.6 ± 0.3 µm) in DNP-HSA-stimulated RBL-2H3 cells. Furthermore, the levels of PGD2 secretion in DNP-HSA-stimulated cells pretreated with licarin A were lower than those stimulated with DNP-HSA alone (positive control). Treatment with licarin A at 20 µm produced slight suppression of DNP-HSA-induced increases in COX-2 mRNA and protein levels. We identified several signalling pathways that mediated these pharmacological effects. Licarin A treatment tended to reduce phosphorylated protein kinase C alpha/beta II (PKCα/ßII) and p38 mitogen-activated protein kinase (MAPK) protein levels. CONCLUSIONS: Our results demonstrate that licarin A reduces TNF-α and PGD2 secretion via the inhibition of PKCα/ßII and p38 MAPK pathways; this compound may be useful for attenuating immediate hypersensitivity.
[Mh] Termos MeSH primário: Antialérgicos/farmacologia
Hipersensibilidade Imediata/tratamento farmacológico
Lignanas/farmacologia
Mastócitos/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Ciclo-Oxigenase 2/genética
Ciclo-Oxigenase 2/metabolismo
Dinitrofenóis/imunologia
Relação Dose-Resposta a Droga
Ativação Enzimática
Liberação de Histamina/efeitos dos fármacos
Hipersensibilidade Imediata/genética
Hipersensibilidade Imediata/imunologia
Hipersensibilidade Imediata/metabolismo
Mastócitos/imunologia
Mastócitos/metabolismo
Fosforilação
Prostaglandina D2/metabolismo
Proteína Quinase C beta/metabolismo
Proteína Quinase C-alfa/metabolismo
Ratos
Albumina Sérica/imunologia
Transdução de Sinais/efeitos dos fármacos
Fatores de Tempo
Fator de Necrose Tumoral alfa/metabolismo
Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Allergic Agents); 0 (Dinitrophenols); 0 (Lignans); 0 (Serum Albumin); 0 (Tumor Necrosis Factor-alpha); 0 (dinitrophenyl-human serum albumin conjugate); 0 (licarin A); EC 1.14.99.1 (Cyclooxygenase 2); EC 1.14.99.1 (Ptgs2 protein, rat); EC 2.7.11.13 (Protein Kinase C beta); EC 2.7.11.13 (Protein Kinase C-alpha); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases); RXY07S6CZ2 (Prostaglandin D2)
[Em] Mês de entrada:1611
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150918
[St] Status:MEDLINE
[do] DOI:10.1111/jphp.12475


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[PMID]:26350567
[Au] Autor:Furuno T; Shinkai N; Inoh Y; Nakanishi M
[Ad] Endereço:School of Pharmacy, Aichi Gakuin University, 1-100 Kusumoto-cho, Chikusa-ku, Nagoya, 464-8650, Japan. furuno@dpc.agu.ac.jp.
[Ti] Título:Impaired expression of the mitochondrial calcium uniporter suppresses mast cell degranulation.
[So] Source:Mol Cell Biochem;410(1-2):215-21, 2015 Dec.
[Is] ISSN:1573-4919
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Calcium ion (Ca(2+)) uptake into the mitochondrial matrix influences ATP production, Ca(2+) homeostasis, and apoptosis regulation. Ca(2+) uptake across the ion-impermeable inner mitochondrial membrane is mediated by the mitochondrial Ca(2+) uniporter (MCU) complex. The MCU complex forms a pore structure composed of several proteins. MCU is a Ca(2+)-selective channel in the inner-mitochondrial membrane that allows electrophoretic Ca(2+) entry into the matrix. Mitochondrial Ca(2+) uptake 1 (MICU1) functions as a Ca(2+)-sensing regulator of the MCU complex. Previously, by microscopic analysis at the single-cell level, we found that during mast cell activation, mitochondria capture cytosolic Ca(2+) in two steps. Consequently, mitochondrial Ca(2+) uptake likely plays a role in cellular function through cytosolic Ca(2+) buffering. Here, we investigate the role of MCU and MICU1 in mitochondrial Ca(2+) uptake and mast cell degranulation using MCU- and MICU1-knockdown (KD) mast cells. Whereas MCU- and MICU1-KD mast cells show normal proliferation rates and mitochondrial membrane potential, they exhibit slow and reduced cytosolic and mitochondrial Ca(2+) elevation after antigen stimulation. Moreover, ß-hexosaminidase release induced by antigen was significantly suppressed in MCU-KD cells but not MICU1-KD cells. This suggests that both MCU and MICU1 are involved in mitochondrial Ca(2+) uptake in mast cells, while MCU plays a role in mast cell degranulation.
[Mh] Termos MeSH primário: Canais de Cálcio/metabolismo
Cálcio/metabolismo
Degranulação Celular
Mastócitos/metabolismo
Mitocôndrias/metabolismo
[Mh] Termos MeSH secundário: Animais
Antígenos/imunologia
Canais de Cálcio/genética
Linhagem Celular
Proliferação Celular
Dinitrofenóis/imunologia
Regulação da Expressão Gênica
Mastócitos/imunologia
Potencial da Membrana Mitocondrial
Mitocôndrias/imunologia
Proteínas de Transporte da Membrana Mitocondrial/genética
Proteínas de Transporte da Membrana Mitocondrial/metabolismo
Interferência de RNA
Ratos
Soroalbumina Bovina/imunologia
Transdução de Sinais
Fatores de Tempo
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens); 0 (Calcium Channels); 0 (Dinitrophenols); 0 (Mitochondrial Membrane Transport Proteins); 0 (dinitrophenyl-bovine serum albumin); 0 (mitochondrial calcium uniporter); 27432CM55Q (Serum Albumin, Bovine); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150910
[St] Status:MEDLINE
[do] DOI:10.1007/s11010-015-2554-4



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