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Pesquisa : D12.644.360.365.500 [Categoria DeCS]
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[PMID]:27775688
[Au] Autor:Nomura A; Majumder K; Giri B; Dauer P; Dudeja V; Roy S; Banerjee S; Saluja AK
[Ad] Endereço:Division of Surgical Oncology, Department of Surgery Sylvester Comprehensive Cancer Center, University of Miami, Miami, FL, USA.
[Ti] Título:Inhibition of NF-kappa B pathway leads to deregulation of epithelial-mesenchymal transition and neural invasion in pancreatic cancer.
[So] Source:Lab Invest;96(12):1268-1278, 2016 12.
[Is] ISSN:1530-0307
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:NF-κB has an essential role in the initiation and progression of pancreatic cancer and specifically mediates the induction of epithelial-mesenchymal transition and invasiveness. In this study, we demonstrate the importance of activated NF-κB signaling in EMT induction, lymphovascular metastasis, and neural invasion. Modulation of NF-κB activity was accomplished through the specific NF-κB inhibitor (BAY 11-7085), triptolide, and Minnelide treatment, as well as overexpression of IKBα repressor and IKK activator plasmids. In the classical lymphovascular metastatic cascade, inhibition of NF-κB decreased the expression of several EMT transcription factors (SNAI1, SNAI2, and ZEB1) and mesenchymal markers (VIM and CDH2) and decreased in vitro invasion, which was rescued by IKK activation. This was further demonstrated in vivo via BAY 11-7085 treatment in a orthotopic model of pancreatic cancer. In vivo NF-κB inhibition decreased tumor volume; decreased tumor EMT gene expression, while restoring cell-cell junctions; and decreasing overall metastasis. Furthermore, we demonstrate the importance of active NF-κB signaling in neural invasion. Triptolide treatment inhibits Nerve Growth Factor (NGF) mediated, neural-tumor co-culture in vitro invasion, and dorsal root ganglia (DRG) neural outgrowth through a disruption in tumor-neural cross talk. In vivo, Minnelide treatment decreased neurotrophin expression, nerve density, and sciatic nerve invasion. Taken together, this study demonstrates the importance of NF-κB signaling in the progression of pancreatic cancer through the modulation of EMT induction, lymphovascular invasion, and neural invasion.
[Mh] Termos MeSH primário: Transição Epitelial-Mesenquimal
NF-kappa B/metabolismo
Pâncreas/metabolismo
Neoplasias Pancreáticas/metabolismo
Nervos Periféricos/metabolismo
Neoplasias do Sistema Nervoso Periférico/secundário
Transdução de Sinais
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/farmacologia
Antineoplásicos/uso terapêutico
Linhagem Celular
Linhagem Celular Tumoral
Técnicas de Cocultura
Transição Epitelial-Mesenquimal/efeitos dos fármacos
Gânglios Espinais/citologia
Gânglios Espinais/efeitos dos fármacos
Gânglios Espinais/metabolismo
Gânglios Espinais/patologia
Seres Humanos
Metástase Linfática/patologia
Metástase Linfática/prevenção & controle
Camundongos
Camundongos Nus
Inibidor de NF-kappaB alfa/genética
Inibidor de NF-kappaB alfa/metabolismo
NF-kappa B/antagonistas & inibidores
Invasividade Neoplásica/patologia
Transplante de Neoplasias
Pâncreas/efeitos dos fármacos
Pâncreas/patologia
Neoplasias Pancreáticas/tratamento farmacológico
Neoplasias Pancreáticas/patologia
Nervos Periféricos/citologia
Nervos Periféricos/efeitos dos fármacos
Nervos Periféricos/patologia
Neoplasias do Sistema Nervoso Periférico/metabolismo
Neoplasias do Sistema Nervoso Periférico/patologia
Neoplasias do Sistema Nervoso Periférico/prevenção & controle
Proteínas Recombinantes/metabolismo
Nervo Isquiático/citologia
Nervo Isquiático/efeitos dos fármacos
Nervo Isquiático/metabolismo
Nervo Isquiático/patologia
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (NF-kappa B); 0 (Recombinant Proteins); 139874-52-5 (NF-KappaB Inhibitor alpha)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE
[do] DOI:10.1038/labinvest.2016.109


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[PMID]:29317652
[Au] Autor:Santos-Barriopedro I; Bosch-Presegué L; Marazuela-Duque A; de la Torre C; Colomer C; Vazquez BN; Fuhrmann T; Martínez-Pastor B; Lu W; Braun T; Bober E; Jenuwein T; Serrano L; Esteller M; Chen Z; Barceló-Batllori S; Mostoslavsky R; Espinosa L; Vaquero A
[Ad] Endereço:Chromatin Biology Laboratory, Cancer Epigenetics and Biology Program (PEBC), Bellvitge Biomedical Research Institute (IDIBELL), Av. Gran Via de l'Hospitalet 199-203, 08908, L'Hospitalet de Llobregat (Barcelona), Spain.
[Ti] Título:SIRT6-dependent cysteine monoubiquitination in the PRE-SET domain of Suv39h1 regulates the NF-κB pathway.
[So] Source:Nat Commun;9(1):101, 2018 01 09.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Sirtuins are NAD -dependent deacetylases that facilitate cellular stress response. They include SirT6, which protects genome stability and regulates metabolic homeostasis through gene silencing, and whose loss induces an accelerated aging phenotype directly linked to hyperactivation of the NF-κB pathway. Here we show that SirT6 binds to the H3K9me3-specific histone methyltransferase Suv39h1 and induces monoubiquitination of conserved cysteines in the PRE-SET domain of Suv39h1. Following activation of NF-κB signaling Suv39h1 is released from the IκBα locus, subsequently repressing the NF-κB pathway. We propose that SirT6 attenuates the NF-κB pathway through IκBα upregulation via cysteine monoubiquitination and chromatin eviction of Suv39h1. We suggest a mechanism based on SirT6-mediated enhancement of a negative feedback loop that restricts the NF-κB pathway.
[Mh] Termos MeSH primário: Cisteína/metabolismo
Metiltransferases/metabolismo
NF-kappa B/metabolismo
Domínios PR-SET
Proteínas Repressoras/metabolismo
Sirtuínas/metabolismo
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Células Cultivadas
Cromatina/metabolismo
Cisteína/genética
Células HCT116
Células HEK293
Células HeLa
Seres Humanos
Metiltransferases/genética
Camundongos
Inibidor de NF-kappaB alfa/metabolismo
Células NIH 3T3
Ligação Proteica
Proteínas Repressoras/genética
Transdução de Sinais
Sirtuínas/genética
Ubiquitinação
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Chromatin); 0 (NF-kappa B); 0 (Repressor Proteins); 139874-52-5 (NF-KappaB Inhibitor alpha); EC 2.1.1. (SUV39H1 protein, human); EC 2.1.1.- (Methyltransferases); EC 3.5.1.- (SIRT6 protein, human); EC 3.5.1.- (Sirtuins); K848JZ4886 (Cysteine)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180111
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02586-x


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[PMID]:28456771
[Au] Autor:Kim EK; Cho JH; Jeong AR; Kim EJ; Park DK; Kwon KA; Chung JW; Kim KO; Kim JH; Kim JH; Kim YJ
[Ad] Endereço:Division of Gastroenterology, Department of Internal Medicine, Gachon University Gil Medical Center, Incheon, Republic of Korea. yoonmed@gilhospital.com.
[Ti] Título:Anti-inflammatory effects of simvastatin in nonsteroidal anti-inflammatory drugs-induced small bowel injury.
[So] Source:J Physiol Pharmacol;68(1):69-77, 2017 Feb.
[Is] ISSN:1899-1505
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:Small bowel injury can occur as the result of a multifaceted process that includes increased acid secretion, generation of reactive oxygen species, and cyclooxygenase inhibition. However, no effective medication for small bowel ulceration is available. Simvastatin is an important lipid-lowering agent with anti-inflammatory activity. We aimed to validate the effects of simvastatin in vitro and in vivo. In presence or absence of simvastatin, IEC-6 small bowel cell line with 50 ng/ml of tumor nectosis factor α (TNF-α) was investigated by western blotting, qRT-PCR, and DCF-DA assay. In addition, an in vivo study of nonsteroidal anti-inflammatory drugs (NSAID)-induced small bowel inflammation was performed using 7-week-old specific-pathogen-free (SPF) male C57BL/6 mice. Simvastatin treatment reduced the mRNA levels of interleukin-6 and interleukin-8 by approximately 50% in TNF-α-stimulated IEC-6 cells. Treatment with a combination of 50 ng/ml TNF-α and µM simvastatin decreased activation of Akt, IκBα, and nuclear factor-κB p65 level in IEC-6 cells. By DCF-DA staining, intracellular reactive oxygen species (ROS) production was increased in TNF-α-stimulated cells, and treatment with simvastatin decreased the level of ROS. In addition, in vivo mouse model of NSAID-induced small bowel inflammation, the administration of simvastatin reduced the number of small bowel hemorrhagic lesions and the level of ROS production as determined by gross examination and 8-hydroxydeoxyguanosine immunohistochemistry of small bowel tissue, respectively. Simvastatin reduced NSAID-induced injuries by both suppression of ROS generation and modulation of inflammatory cytokines in vitro and in vivo. Therefore, simvastatin, an HMG-CoA reductase inhibitor, has potential as a prophylactic and therapeutic agent for NSAID-induced small bowel injury.
[Mh] Termos MeSH primário: Anti-Inflamatórios/efeitos adversos
Anti-Inflamatórios/uso terapêutico
Inibidores de Hidroximetilglutaril-CoA Redutases/uso terapêutico
Indometacina/efeitos adversos
Enteropatias/tratamento farmacológico
Intestino Delgado/lesões
Sinvastatina/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Ciclo-Oxigenase 1/genética
Ciclo-Oxigenase 2/genética
Desoxiguanosina/análogos & derivados
Desoxiguanosina/metabolismo
Inibidores de Hidroximetilglutaril-CoA Redutases/farmacologia
Interleucina-6/metabolismo
Interleucina-8/metabolismo
Enteropatias/induzido quimicamente
Enteropatias/metabolismo
Enteropatias/patologia
Intestino Delgado/metabolismo
Intestino Delgado/patologia
Masculino
Proteínas de Membrana/genética
Camundongos Endogâmicos C57BL
Inibidor de NF-kappaB alfa/metabolismo
Ratos
Espécies Reativas de Oxigênio/metabolismo
Sinvastatina/farmacologia
Fator de Necrose Tumoral alfa/metabolismo
Fator de Necrose Tumoral alfa/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors); 0 (Interleukin-6); 0 (Interleukin-8); 0 (Membrane Proteins); 0 (Reactive Oxygen Species); 0 (Tumor Necrosis Factor-alpha); 139874-52-5 (NF-KappaB Inhibitor alpha); 88847-89-6 (8-oxo-7-hydrodeoxyguanosine); AGG2FN16EV (Simvastatin); EC 1.14.99.1 (Cyclooxygenase 1); EC 1.14.99.1 (Cyclooxygenase 2); EC 1.14.99.1 (Ptgs1 protein, rat); EC 1.14.99.1 (Ptgs2 protein, rat); G9481N71RO (Deoxyguanosine); XXE1CET956 (Indomethacin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170501
[St] Status:MEDLINE


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[PMID]:29247640
[Au] Autor:Gilmore SP; Gonye ALK; Li EC; Espinosa de Los Reyes S; Gupton JT; Quintero OA; Fischer-Stenger K
[Ad] Endereço:Department of Biology, University of Richmond, VA 23173, USA. Electronic address: samuel.gilmore@richmond.edu.
[Ti] Título:Effects of a novel microtubule-depolymerizer on pro-inflammatory signaling in RAW264.7 macrophages.
[So] Source:Chem Biol Interact;280:109-116, 2018 Jan 25.
[Is] ISSN:1872-7786
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:The Nuclear Factor-kappa B (NF-κB) pathway is vital for immune system regulation and pro-inflammatory signaling. Many inflammatory disorders and diseases, including cancer, are linked to dysregulation of NF-κB signaling. When macrophages recognize the presence of a pathogen, the signaling pathway is activated, resulting in the nuclear translocation of the transcription factor, NF-κB, to turn on pro-inflammatory genes. Here, we demonstrate the effects of a novel microtubule depolymerizer, NT-07-16, a polysubstituted pyrrole compound, on this process. Treatment with NT-07-16 decreased the production of pro-inflammatory cytokines in RAW264.7 mouse macrophages. It appears that the reduction in pro-inflammatory mediators produced by the macrophages after exposure to NT-07-16 may be due to activities upstream of the translocation of NF-κB into the nucleus. NF-κB translocation occurs after its inhibitory protein, IκB-α is phosphorylated which signals for its degradation releasing NF-κB so it is free to move into the nucleus. Previous studies from other laboratories indicate that these processes are associated with the microtubule network. Our results show that exposure to the microtubule-depolymerizer, NT-07-16 reduces the phosphorylation of IκB-α and also decreases the association of NF-κB with tubulin which may affect the ability of NF-κB to translocate into the nucleus. Therefore, the anti-inflammatory activity of NT-07-16 may be explained, at least in part, by alterations in these steps in the NF-κB signaling pathway leading to less NF-κB entering the nucleus and reducing the production of pro-inflammatory mediators by the activated macrophages.
[Mh] Termos MeSH primário: Transdução de Sinais/efeitos dos fármacos
Moduladores de Tubulina/farmacologia
[Mh] Termos MeSH secundário: Animais
Sobrevivência Celular/efeitos dos fármacos
Citocinas/análise
Citocinas/genética
Citocinas/metabolismo
Regulação para Baixo/efeitos dos fármacos
Ensaio de Imunoadsorção Enzimática
Mediadores da Inflamação/metabolismo
Lipopolissacarídeos/toxicidade
Macrófagos/citologia
Macrófagos/efeitos dos fármacos
Macrófagos/metabolismo
Camundongos
Microscopia de Fluorescência
Inibidor de NF-kappaB alfa/metabolismo
NF-kappa B/metabolismo
Fosforilação/efeitos dos fármacos
Pirróis/química
Pirróis/farmacologia
Células RAW 264.7
Reação em Cadeia da Polimerase em Tempo Real
Moduladores de Tubulina/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Inflammation Mediators); 0 (Lipopolysaccharides); 0 (NF-kappa B); 0 (Pyrroles); 0 (Tubulin Modulators); 139874-52-5 (NF-KappaB Inhibitor alpha)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180210
[Lr] Data última revisão:
180210
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171217
[St] Status:MEDLINE


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[PMID]:28574596
[Au] Autor:Park JW; Yoon HJ; Kang WY; Cho S; Seong SJ; Lee HW; Yoon YR; Kim HJ
[Ad] Endereço:Department of Biomedical Science, Cell and Matrix Research Institute, BK21 Plus KNU Biomedical Convergence Program, Clinical Trial Center, School of Medicine, Kyungpook National University and Hospital, Daegu, Republic of Korea.
[Ti] Título:G protein-coupled receptor 84 controls osteoclastogenesis through inhibition of NF-κB and MAPK signaling pathways.
[So] Source:J Cell Physiol;233(2):1481-1489, 2018 Feb.
[Is] ISSN:1097-4652
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:GPR84, a member of the G protein-coupled receptor family, is found predominantly in immune cells, such as macrophages, and functions as a pivotal modulator of inflammatory responses. In this study, we investigated the role of GPR84 in receptor activator of nuclear factor-κB ligand (RANKL)-induced osteoclast differentiation. Our microarray data showed that GPR84 was significantly downregulated in osteoclasts compared to in their precursors, macrophages. The overexpression of GPR84 in bone marrow-derived macrophages suppressed the formation of multinucleated osteoclasts without affecting precursor proliferation. In addition, GPR84 overexpression attenuated the induction of c-Fos and nuclear factor of activated T cells, cytoplasmic 1 (NFATc1), which are transcription factors that are critical for osteoclastogenesis. Furthermore, knockdown of GPR84 using a small hairpin RNA promoted RANKL-mediated osteoclast differentiation and gene expression of osteoclastogenic markers. Mechanistically, GPR84 overexpression blocked RANKL-stimulated phosphorylation of IκBα and three MAPKs, JNK, ERK, and p38. GPR84 also suppressed NF-κB transcriptional activity mediated by RANKL. Conversely, GPR84 knockdown enhanced RANKL-induced activation of IκBα and the three MAPKs. Collectively, our results revealed that GPR84 functions as a negative regulator of osteoclastogenesis, suggesting that it may be a potential therapeutic target for osteoclast-mediated bone-destructive diseases.
[Mh] Termos MeSH primário: Proteínas Quinases Ativadas por Mitógeno/metabolismo
NF-kappa B/metabolismo
Osteoclastos/enzimologia
Osteogênese
Receptores Acoplados a Proteínas-G/metabolismo
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular
Regulação da Expressão Gênica
Camundongos
Camundongos Endogâmicos C57BL
Inibidor de NF-kappaB alfa/genética
Inibidor de NF-kappaB alfa/metabolismo
Fatores de Transcrição NFATC/genética
Fatores de Transcrição NFATC/metabolismo
Fosforilação
Proteínas Proto-Oncogênicas c-fos/genética
Proteínas Proto-Oncogênicas c-fos/metabolismo
Ligante RANK/genética
Ligante RANK/metabolismo
Células RAW 264.7
Interferência de RNA
Receptores Acoplados a Proteínas-G/genética
Transdução de Sinais
Fatores de Tempo
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Gpr84 protein, mouse); 0 (NF-kappa B); 0 (NFATC Transcription Factors); 0 (Nfatc1 protein, mouse); 0 (Nfkbia protein, mouse); 0 (Proto-Oncogene Proteins c-fos); 0 (RANK Ligand); 0 (Receptors, G-Protein-Coupled); 0 (Tnfsf11 protein, mouse); 139874-52-5 (NF-KappaB Inhibitor alpha); EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170603
[St] Status:MEDLINE
[do] DOI:10.1002/jcp.26035


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[PMID]:28916285
[Au] Autor:Zenata O; Dvorak Z; Vrzal R
[Ad] Endereço:Department of Cell Biology Genetics, Faculty of Science, Palacky University in Olomouc, Slechtitelu 27, Olomouc, CZ-783 71, Czech Republic. Electronic address: zenataOndrej@seznam.cz.
[Ti] Título:Profiling of bisphenol S towards nuclear receptors activities in human reporter cell lines.
[So] Source:Toxicol Lett;281:10-19, 2017 Nov 05.
[Is] ISSN:1879-3169
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Bisphenol S (BPS) is heat-stable structural analog of bisphenol A (BPA), a known endocrine disruptor. Due to the effort to replace BPA with BPS, it is essential to know if BPS is suitable non-toxic replacement without reported deleterious effects of BPA. Since most of the BPA effects are ascribed to its ability to activate nuclear receptors, we screened some prominent members of this family in order to confirm or refute some recent findings. We found that BPS insignificantly activated aryl hydrocarbon receptor (AhR) in reporter gene assay and no induction of AhR target gene CYP1A1 was observed in human hepatocytes (HH). BPS was able to act like an antagonist of pregnane X receptor (PXR) in reporter gene assay, but the expression of PXR target gene CYP3A4, was only moderately affected in HH. While BPS antagonized dexamethasone-inducible glucocorticoid receptor (GR)-dependent luciferase activity in reporter gene assay (IC =52µM), it was not able to antagonize dexamethasone effects on GR-target genes, including GILZ, NFKBIA and IL-6. Synergistic effect of BPS (range 0.001-100µM) and DHT (100nM) was observed at androgen receptor (AR) activity level only. In conclusion, we show that BPS had only limited effect on tested nuclear receptors. Moreover, submicromolar concentrations of BPS affected activated AR. Thus, due to the low levels of exposure for humans, BPS is probably of no regulatory concern. However, further investigation should delineate possible impact on male/female development or sexual functions.
[Mh] Termos MeSH primário: Hepatócitos/efeitos dos fármacos
Fenóis/toxicidade
Receptores Citoplasmáticos e Nucleares/metabolismo
Sulfonas/toxicidade
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Citocromo P-450 CYP1A1/genética
Citocromo P-450 CYP1A1/metabolismo
Citocromo P-450 CYP3A/genética
Citocromo P-450 CYP3A/metabolismo
Dexametasona/toxicidade
Di-Hidrotestosterona/toxicidade
Disruptores Endócrinos/toxicidade
Genes Reporter
Células HEK293
Células HeLa
Hepatócitos/metabolismo
Seres Humanos
Interleucina-6/genética
Interleucina-6/metabolismo
Luciferases/genética
Luciferases/metabolismo
Inibidor de NF-kappaB alfa/genética
Inibidor de NF-kappaB alfa/metabolismo
Receptores de Hidrocarboneto Arílico/genética
Receptores de Hidrocarboneto Arílico/metabolismo
Receptores Citoplasmáticos e Nucleares/genética
Receptores de Glucocorticoides/genética
Receptores de Glucocorticoides/metabolismo
Receptores de Esteroides/antagonistas & inibidores
Receptores de Esteroides/genética
Receptores de Esteroides/metabolismo
Fatores de Transcrição/genética
Fatores de Transcrição/metabolismo
Transcrição Genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Endocrine Disruptors); 0 (IL6 protein, human); 0 (Interleukin-6); 0 (NFKBIA protein, human); 0 (Phenols); 0 (Receptors, Aryl Hydrocarbon); 0 (Receptors, Cytoplasmic and Nuclear); 0 (Receptors, Glucocorticoid); 0 (Receptors, Steroid); 0 (Sulfones); 0 (TSC22D3 protein, human); 0 (Transcription Factors); 0 (pregnane X receptor); 08J2K08A3Y (Dihydrotestosterone); 139874-52-5 (NF-KappaB Inhibitor alpha); 7S5I7G3JQL (Dexamethasone); 80-09-1 (bis(4-hydroxyphenyl)sulfone); EC 1.13.12.- (Luciferases); EC 1.14.13.67 (CYP3A4 protein, human); EC 1.14.14.1 (CYP1A1 protein, human); EC 1.14.14.1 (Cytochrome P-450 CYP1A1); EC 1.14.14.1 (Cytochrome P-450 CYP3A)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171106
[Lr] Data última revisão:
171106
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170917
[St] Status:MEDLINE


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[PMID]:28719912
[Au] Autor:Li S; Liu X; Lei J; Yang J; Tian P; Gao Y
[Ad] Endereço:Department of Nephropathy, Xi'an, China.
[Ti] Título:Crocin Protects Podocytes Against Oxidative Stress and Inflammation Induced by High Glucose Through Inhibition of NF-κB.
[So] Source:Cell Physiol Biochem;42(4):1481-1492, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: Diabetic nephropathy (DN) is a microangiopathic disease characterized by excessive urinary albumin excretion, which occurs in 30% of patients with diabetes mellitus. It is the second leading cause of end-stage renal diseases in China. Nuclear factor-kappa B (NF-κB) is reported to be closely correlated with the inflammation underlying diabetes-associated renal damage. Crocin, a plant-derived compound, has antioxidant properties that may inhibit NF-κB. METHODS: In the present study, we used a conditionally immortalized mouse podocyte cell line to explore whether crocin could effectively block albuminuria. Cells were incubated with 15 or 25 mM D-glucose to mimic diabetic conditions. The expression of Wilms tumor 1 (WT-1) and synaptopodin was evaluated to identify differentiated podocytes, and the expression of nephrin, podocin, and CD2ap was measured as markers of slit diaphragms, the main structures within the glomerular filtration barrier. RESULTS: The high-glucose conditions led to reduced nephrin, podocin, and CD2ap expression, which was prevented by pretreatment with crocin. The oxidative stress and pro-inflammatory response of podocytes associated with DN induced by high glucose were also reduced by crocin pretreatment. Phosphorylated IκBα (p-IκBα) expression induced by high glucose was also significantly decreased by crocin pretreatment. Moreover, pyrrolidine dithiocarbamate, a NF-κB inhibitor, pyrrolidine dithio carbamate, augmented the protective effects of crocin. CONCLUSION: Our results demonstrate a protective role of crocin against damage to podocytes and slit diaphragms under high-glucose conditions via inhibition of NF-κB. This study presents a potential therapy for DN and contributes to the understanding of the mechanism underlying DN.
[Mh] Termos MeSH primário: Antioxidantes/farmacologia
Carotenoides/farmacologia
Glucose/antagonistas & inibidores
NF-kappa B/genética
Podócitos/efeitos dos fármacos
Pirrolidinas/farmacologia
Tiocarbamatos/farmacologia
[Mh] Termos MeSH secundário: Proteínas Adaptadoras de Transdução de Sinal/genética
Proteínas Adaptadoras de Transdução de Sinal/metabolismo
Animais
Linhagem Celular Transformada
Proteínas do Citoesqueleto/genética
Proteínas do Citoesqueleto/metabolismo
Combinação de Medicamentos
Sinergismo Farmacológico
Regulação da Expressão Gênica
Glucose/toxicidade
Peptídeos e Proteínas de Sinalização Intracelular/genética
Peptídeos e Proteínas de Sinalização Intracelular/metabolismo
Proteínas de Membrana/genética
Proteínas de Membrana/metabolismo
Camundongos
Proteínas dos Microfilamentos/genética
Proteínas dos Microfilamentos/metabolismo
Inibidor de NF-kappaB alfa/genética
Inibidor de NF-kappaB alfa/metabolismo
NF-kappa B/antagonistas & inibidores
NF-kappa B/metabolismo
Estresse Oxidativo
Podócitos/citologia
Podócitos/metabolismo
Transdução de Sinais
Proteínas WT1/genética
Proteínas WT1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (Antioxidants); 0 (CD2-associated protein); 0 (Cytoskeletal Proteins); 0 (Drug Combinations); 0 (Intracellular Signaling Peptides and Proteins); 0 (Membrane Proteins); 0 (Microfilament Proteins); 0 (NF-kappa B); 0 (NPHS2 protein); 0 (Pyrrolidines); 0 (Synpo protein, mouse); 0 (Thiocarbamates); 0 (WT1 Proteins); 0 (nephrin); 139874-52-5 (NF-KappaB Inhibitor alpha); 25769-03-3 (pyrrolidine dithiocarbamic acid); 36-88-4 (Carotenoids); 877GWI46C2 (crocin); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171026
[Lr] Data última revisão:
171026
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170719
[St] Status:MEDLINE
[do] DOI:10.1159/000479212


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[PMID]:28714847
[Au] Autor:Pollock N; Taylor G; Jobe F; Guzman E
[Ad] Endereço:1​School of Biosciences, Cardiff University, Cardiff, CF10 3AX, UK 2​The Pirbright Institute, Ash Road, Pirbright, Woking, RG8 0JU, UK.
[Ti] Título:Modulation of the transcription factor NF-κB in antigen-presenting cells by bovine respiratory syncytial virus small hydrophobic protein.
[So] Source:J Gen Virol;98(7):1587-1599, 2017 Jul.
[Is] ISSN:1465-2099
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Bovine respiratory syncytial virus (BRSV) is an important cause of respiratory disease in young cattle and is closely related to human RSV (HRSV), which causes severe respiratory disease in infants and the elderly. The RSV genome encodes a small hydrophobic (SH) protein with viroporin activity. Previous studies have shown that recombinant BRSV lacking the SH gene (rBRSVΔSH) is attenuated in the lungs, but not in the upper respiratory tract, of calves and mucosal vaccination with rBRSVΔSH induced long-lasting protective immunity. Attenuation of rBRSVΔSH may be due to the ability of this virus to induce an early innate response as rBRSVΔSH induces higher levels of pro-inflammatory cytokines than wild-type (wt) rBRSV. In this study, we investigated the effects of the BRSV SH protein on NF-κB p65 phosphorylation, a master step in the regulation of pro-inflammatory cytokines. Expression of SH resulted in the inhibition of NF-κB p65 phosphorylation in response to BRSV infection and extracellular lipopolysaccharide, and a reduction in the production of pro-inflammatory cytokines. In contrast, rBRSVΔSH does not inhibit NF-κB p65 phosphorylation in bovine antigen-presenting cells, including monocytes, macrophages and dendritic cells, resulting in increased expression of pro-inflammatory cytokines and increased activation of T cells compared to cells infected with wt BRSV. These findings highlight an important role for the BRSV SH protein in immune modulation.
[Mh] Termos MeSH primário: Citocinas/metabolismo
Células Dendríticas/imunologia
Macrófagos/imunologia
Monócitos/imunologia
Vírus Sincicial Respiratório Bovino/metabolismo
Proteínas Oncogênicas de Retroviridae/imunologia
Fator de Transcrição RelA/metabolismo
[Mh] Termos MeSH secundário: Animais
Bovinos
Doenças dos Bovinos/imunologia
Doenças dos Bovinos/virologia
Linhagem Celular
Células Dendríticas/metabolismo
Células Dendríticas/virologia
Seres Humanos
Lipopolissacarídeos/metabolismo
Ativação Linfocitária/imunologia
Macrófagos/metabolismo
Macrófagos/virologia
Camundongos
Monócitos/metabolismo
Monócitos/virologia
Inibidor de NF-kappaB alfa/metabolismo
Fosforilação
Células RAW 264.7
Vírus Sincicial Respiratório Bovino/genética
Vírus Sincicial Respiratório Bovino/imunologia
Proteínas Oncogênicas de Retroviridae/genética
Proteínas Oncogênicas de Retroviridae/metabolismo
Linfócitos T/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Lipopolysaccharides); 0 (Retroviridae Proteins, Oncogenic); 0 (Transcription Factor RelA); 0 (small hydrophobic protein, virus); 139874-52-5 (NF-KappaB Inhibitor alpha)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171115
[Lr] Data última revisão:
171115
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170718
[St] Status:MEDLINE
[do] DOI:10.1099/jgv.0.000855


  9 / 3963 MEDLINE  
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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]:28676715
[Au] Autor:Quach HT; Tanigaki R; Yokoigawa J; Yamada Y; Niwa M; Hirano S; Shiono Y; Kimura KI; Kataoka T
[Ad] Endereço:Department of Applied Biology, Kyoto Institute of Technology, Kyoto, Japan.
[Ti] Título:Allantopyrone A interferes with multiple components of the TNF receptor 1 complex and blocks RIP1 modifications in the TNF-α-induced signaling pathway.
[So] Source:J Antibiot (Tokyo);70(9):929-936, 2017 Aug.
[Is] ISSN:0021-8820
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Allantopyrone A is a fungal metabolite that uniquely possesses two α,ß-unsaturated carbonyl moieties. We recently reported that allantopyrone A inhibited the nuclear factor-κB (NF-κB) signaling pathway induced by tumor necrosis factor (TNF)-α in human lung carcinoma A549 cells. In the present study, the mechanism by which allantopyrone A inhibits the TNF-α-induced signaling pathway was investigated in more detail. Allantopyrone A blocked extensive modifications to receptor-interacting protein 1 (RIP1) in the TNF receptor 1 (TNF-R1) complex. Allantopyrone A augmented the high-MW bands of TNF-R1, TNF receptor-associated factor 2, RIP1, the NF-κB subunit RelA and inhibitor of NF-κB kinase ß in A549 cells, suggesting that it binds to and promotes the crosslinking of these proteins. The extracellular cysteine-rich domains of TNF-R1 were crosslinked by allantopyrone A more preferentially than its intracellular portion. The present results demonstrate that allantopyrone A interferes with multiple components of the TNF-R1 complex and blocks RIP1 modifications in the TNF-α-induced NF-κB signaling pathway.
[Mh] Termos MeSH primário: Antibióticos Antineoplásicos/farmacologia
Proteínas de Choque Térmico HSP90/antagonistas & inibidores
Pironas/farmacologia
Proteína Serina-Treonina Quinases de Interação com Receptores/antagonistas & inibidores
Receptores Tipo I de Fatores de Necrose Tumoral/antagonistas & inibidores
Transdução de Sinais/efeitos dos fármacos
Fator de Necrose Tumoral alfa/antagonistas & inibidores
[Mh] Termos MeSH secundário: Células A549
Cisteína/química
Cisteína/metabolismo
Genes Reporter/efeitos dos fármacos
Células HEK293
Proteínas de Choque Térmico HSP90/química
Proteínas de Choque Térmico HSP90/genética
Proteínas de Choque Térmico HSP90/metabolismo
Seres Humanos
Peso Molecular
Inibidor de NF-kappaB alfa/antagonistas & inibidores
Inibidor de NF-kappaB alfa/química
Inibidor de NF-kappaB alfa/metabolismo
Fragmentos de Peptídeos/antagonistas & inibidores
Fragmentos de Peptídeos/química
Fragmentos de Peptídeos/genética
Fragmentos de Peptídeos/metabolismo
Domínios e Motivos de Interação entre Proteínas
Multimerização Proteica/efeitos dos fármacos
Processamento de Proteína Pós-Traducional/efeitos dos fármacos
Proteína Serina-Treonina Quinases de Interação com Receptores/química
Proteína Serina-Treonina Quinases de Interação com Receptores/genética
Proteína Serina-Treonina Quinases de Interação com Receptores/metabolismo
Receptores Tipo I de Fatores de Necrose Tumoral/química
Receptores Tipo I de Fatores de Necrose Tumoral/genética
Receptores Tipo I de Fatores de Necrose Tumoral/metabolismo
Proteínas Recombinantes de Fusão/química
Proteínas Recombinantes de Fusão/metabolismo
Fator 2 Associado a Receptor de TNF/antagonistas & inibidores
Fator 2 Associado a Receptor de TNF/química
Fator 2 Associado a Receptor de TNF/metabolismo
Fator de Transcrição RelA/antagonistas & inibidores
Fator de Transcrição RelA/química
Fator de Transcrição RelA/metabolismo
Fator de Necrose Tumoral alfa/química
Fator de Necrose Tumoral alfa/genética
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibiotics, Antineoplastic); 0 (HSP90 Heat-Shock Proteins); 0 (NFKBIA protein, human); 0 (PSMD2 protein, human); 0 (Peptide Fragments); 0 (Pyrones); 0 (RELA protein, human); 0 (Receptors, Tumor Necrosis Factor, Type I); 0 (Recombinant Fusion Proteins); 0 (TNF Receptor-Associated Factor 2); 0 (TNF protein, human); 0 (TNFRSF1A protein, human); 0 (TRAP1 protein, human); 0 (Transcription Factor RelA); 0 (Tumor Necrosis Factor-alpha); 0 (allantopyrone A); 139874-52-5 (NF-KappaB Inhibitor alpha); EC 2.7.11.1 (RIPK1 protein, human); EC 2.7.11.1 (Receptor-Interacting Protein Serine-Threonine Kinases); K848JZ4886 (Cysteine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170907
[Lr] Data última revisão:
170907
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170706
[St] Status:MEDLINE
[do] DOI:10.1038/ja.2017.74



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