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[PMID]:29380441
[Au] Autor:Waugh CA; Arukwe A; Jaspers VLB
[Ad] Endereço:Environmental Toxicology, Department of Biology, Faculty of Natural Sciences, Norwegian University of Science and Technology, Trondheim, Norway.
[Ti] Título:Deregulation of microRNA-155 and its transcription factor NF-kB by polychlorinated biphenyls during viral infections.
[So] Source:APMIS;126(3):234-240, 2018 Mar.
[Is] ISSN:1600-0463
[Cp] País de publicação:Denmark
[La] Idioma:eng
[Ab] Resumo:Polychlorinated biphenyls (PCBs), and similar environmental contaminants, have been linked to virus outbreaks and increased viral induced mortality since the 1970s. Yet the mechanisms behind this increased susceptibility remain elusive. It has recently been illustrated that the innate immune viral detection system is tightly regulated by small non-coding RNAs, including microRNAs (miRNAs). For virus infections miRNA-155 expression is an important host response against infection, and deregulation of this miRNA is closely associated with adverse outcomes. Thus, we designed a targeted in vitro study using primary chicken fibroblasts, first exposed to a mixture of PCBs (Arochlor-1250) before being stimulated with a synthetic RNA virus (poly I:C), to determine if PCBs have the potential to deregulate miRNA-155. In this paper, we provide the first data for the deregulation of miRNA-155 when a host is exposed to a mixture of PCBs before a virus infection. Thus, we provide important evidence that PCBs can be involved in the deregulation of important miRNA pathways involved in the immune system; thereby demonstrating novel insights into the mechanism of PCB toxicity on the immune system.
[Mh] Termos MeSH primário: Imunidade Inata/genética
MicroRNAs/genética
NF-kappa B/genética
Poli I-C/farmacologia
Bifenilos Policlorados/química
Vírus/imunologia
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Embrião de Galinha
Galinhas/genética
Galinhas/imunologia
Regulação da Expressão Gênica/imunologia
Seres Humanos
Viroses/genética
Viroses/imunologia
Viroses/virologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MIRN155 microRNA, human); 0 (MicroRNAs); 0 (NF-kappa B); DFC2HB4I0K (Polychlorinated Biphenyls); O84C90HH2L (Poly I-C)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180131
[St] Status:MEDLINE
[do] DOI:10.1111/apm.12811


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[PMID]:29351887
[Au] Autor:Jin R; Chen Q; Yao S; Bai E; Fu W; Wang L; Wang J; Du X; Wei T; Xu H; Jiang C; Qiu P; Wu J; Li W; Liang G
[Ad] Endereço:Department of Digestive Diseases, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325000, China; Chemical Biology Research Center, College of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang 325035, China.
[Ti] Título:Synthesis and anti-tumor activity of EF24 analogues as IKKß inhibitors.
[So] Source:Eur J Med Chem;144:218-228, 2018 Jan 20.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:EF24 is an IKKß inhibitor (IC : 72 µM) containing various anti-tumor activities. In this study, a series of EF24 analogs targeting IKKß were designed and synthesized. Several IKKß inhibitors with better activities than EF24 were screened out and B3 showed best IKKß inhibitory (IC : 6.6 µM). Molecular docking and dynamic simulation experiments further confirmed this inhibitory effect. B3 obviously suppressed the viability of Hela229, A549, SGC-7901 and MGC-803 cells. Then, in SGC-7901 and MGC-803 cells, B3 blocked the NF-κB signal pathway by inhibiting IKKß phosphorylation, and followed arrested the cell cycle at G2/M phase by suppressing the Cyclin B1 and Cdc2 p34 expression, induced the cell apoptosis by down-regulating Bcl-2 protein and up-regulating cleaved-caspase3. Moreover, B3 significantly reduced tumor growth and suppressed the IKKß-NF-κB signal pathway in SGC-7901 xenograft model. In total, this study present a potential IKKß inhibitor as anti-tumor precursor.
[Mh] Termos MeSH primário: Antineoplásicos/química
Antineoplásicos/farmacologia
Compostos de Benzilideno/química
Compostos de Benzilideno/farmacologia
Quinase I-kappa B/antagonistas & inibidores
Piperidonas/química
Piperidonas/farmacologia
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/síntese química
Antineoplásicos/uso terapêutico
Apoptose/efeitos dos fármacos
Compostos de Benzilideno/síntese química
Compostos de Benzilideno/uso terapêutico
Linhagem Celular Tumoral
Pontos de Checagem da Fase G2 do Ciclo Celular/efeitos dos fármacos
Seres Humanos
Quinase I-kappa B/metabolismo
Camundongos Nus
Simulação de Acoplamento Molecular
NF-kappa B/metabolismo
Neoplasias/tratamento farmacológico
Neoplasias/metabolismo
Neoplasias/patologia
Fosforilação/efeitos dos fármacos
Piperidonas/síntese química
Piperidonas/uso terapêutico
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3,5-bis(2-fluorobenzylidene)piperidin-4-one); 0 (Antineoplastic Agents); 0 (Benzylidene Compounds); 0 (NF-kappa B); 0 (Piperidones); EC 2.7.11.10 (I-kappa B Kinase)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180121
[St] Status:MEDLINE


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[PMID]:29268132
[Au] Autor:Xu XJ; Wang F; Zeng T; Lin J; Liu J; Chang YQ; Sun PH; Chen WM
[Ad] Endereço:College of Pharmacy, Jinan University, Guangzhou, 510632, PR China.
[Ti] Título:4-arylamidobenzyl substituted 5-bromomethylene-2(5H)-furanones for chronic bacterial infection.
[So] Source:Eur J Med Chem;144:164-178, 2018 Jan 20.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:Bacterial quorum-sensing (QS) can cause bacterial biofilm formation, thus induce antibiotic resistance and inflammation in chronic bacterial infections. A series of novel 4-arylamidobenzyl substituted 5-bromomethylene-2(5H)-furanones were designed by introducing of brominated furanones into rosiglitazone skeleton, and their potential application in the treatment of chronic bacterial infection was evaluated with regard to their disruption of quorum sensing and anti-inflammatory activities in vitro as well as in animal infection model. Compound 2e displayed both potent QS inhibitory activity and anti-inflammatory activity. Further mechanism studies revealed that the biological effects of 2e and 2k could be attributed, at least in part, to their interaction with PPARγ, and consequent suppression of the activation of NF-κB and MAPK cascades. Importantly, pretreatment with 2e significantly protects mice from lethal-dose LPS challenge. Thus, these data suggest that the dual effective derivative 2e may serve as a valuable candidate for the treatment of chronic bacterial infection.
[Mh] Termos MeSH primário: 4-Butirolactona/análogos & derivados
Antibacterianos/química
Antibacterianos/farmacologia
Anti-Inflamatórios/química
Anti-Inflamatórios/farmacologia
Pseudomonas aeruginosa/efeitos dos fármacos
[Mh] Termos MeSH secundário: 4-Butirolactona/química
4-Butirolactona/farmacologia
Animais
Antibacterianos/uso terapêutico
Anti-Inflamatórios/uso terapêutico
Doença Crônica
Seres Humanos
Lipopolissacarídeos/imunologia
Masculino
Camundongos
Simulação de Acoplamento Molecular
NF-kappa B/imunologia
Óxido Nítrico/imunologia
PPAR gama/imunologia
Infecções por Pseudomonas/tratamento farmacológico
Infecções por Pseudomonas/imunologia
Infecções por Pseudomonas/microbiologia
Pseudomonas aeruginosa/imunologia
Pseudomonas aeruginosa/fisiologia
Percepção de Quorum/efeitos dos fármacos
Células RAW 264.7
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (5-bromomethylene-2(5H)-furanone); 0 (Anti-Bacterial Agents); 0 (Anti-Inflammatory Agents); 0 (Lipopolysaccharides); 0 (NF-kappa B); 0 (PPAR gamma); 31C4KY9ESH (Nitric Oxide); OL659KIY4X (4-Butyrolactone)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171222
[St] Status:MEDLINE


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[PMID]:28471399
[Au] Autor:Wang CC; Wang YX; Yu NQ; Hu D; Wang XY; Chen XG; Liao YW; Yao J; Wang H; He L; Wu L
[Ad] Endereço:School of Pharmacy, China Pharmaceutical University, Nanjing 210009, China. w940984614@hotmail.com.
[Ti] Título:Brazilian Green Propolis Extract Synergizes with Protoporphyrin IX-mediated Photodynamic Therapy via Enhancement of Intracellular Accumulation of Protoporphyrin IX and Attenuation of NF-κB and COX-2.
[So] Source:Molecules;22(5), 2017 May 04.
[Is] ISSN:1420-3049
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Brazilian green propolis (BGP) is noted for its impressive antitumor effects and has been used as a folk medicine in various cultures for many years. It has been demonstrated that BGP could enhance the cytotoxic effect of cytostatic drugs on tumor cells. Photodynamic therapy (PDT) is a therapeutic approach used against malignant cells. To assess the synergistic effect of BGP extract on protoporphyrin IX (PpIX)-mediated photocytotoxicity, MTT assays were performed using A431 and HeLa cells. TUNEL assay and Annexin V-FITC/PI staining were performed to confirm the induction of apoptosis. Western blotting analysis was performed to examine the pro-apoptotic proteins, anti-apoptotic proteins and inflammation related proteins in A431 cells. Intracellular accumulation of PpIX was examined by flow cytometry. The synergistic effect of BGP extract in PpIX-PDT was also evaluated with a xenograft model. Our findings reveal that BGP extract increased PpIX-mediated photocytotoxicity in A431 and HeLa cells. PpIX-PDT with BGP extract treatment resulted in a decrease in Bcl-xL and an increase in NOXA, Bax and caspase-3 cleavage. The protein expression levels of p-IKKα/ß, NF-κB and COX-2 were upregulated by PpIX-PDT but significantly attenuated when in combination with BGP extract. BGP extract was also found to significantly enhance the intracellular accumulation of PpIX in A431 cells. BGP extract increased PpIX-mediated photocytotoxicity in a xenograft model as well. Our findings provide evidence for a synergistic effect of BGP extract in PpIX-PDT both in vitro and in vivo.
[Mh] Termos MeSH primário: Ciclo-Oxigenase 2/metabolismo
NF-kappa B/metabolismo
Fotoquimioterapia
Própole
Protoporfirinas/farmacologia
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Brasil
Linhagem Celular Tumoral
Cromatografia Líquida de Alta Pressão
Sinergismo Farmacológico
Citometria de Fluxo
Xenoenxertos
Seres Humanos
Camundongos Endogâmicos BALB C
Camundongos Nus
Protoporfirinas/farmacocinética
Espectrofotometria Ultravioleta
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (NF-kappa B); 0 (Protoporphyrins); 9009-62-5 (Propolis); C2K325S808 (protoporphyrin IX); EC 1.14.99.1 (Cyclooxygenase 2)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE


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[PMID]:28452703
[Au] Autor:Shin JM; Park JH; Kim HJ; Park IH; Lee HM
[Ad] Endereço:Department of Otorhinolaryngology-Head and Neck Surgery, Korea University College of Medicine, Seoul, South Korea.
[Ti] Título:Cigarette smoke extract increases vascular endothelial growth factor production TLR4/ROS/MAPKs/NF-kappaB pathway in nasal fibroblast.
[So] Source:Am J Rhinol Allergy;31(2):78-84, 2017 Mar 01.
[Is] ISSN:1945-8932
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Cigarette smoke is a complex mixture of various chemical compounds, including free radicals and highly toxic compounds. Cigarette smoke exposure has been shown to be associated with chronic rhinosinusitis and tissue remodeling in upper airway. Vascular endothelial growth factor (VEGF) is one of the cytokines with a crucial role in tissue remodeling of airway. The aims of this study were to determine the effects of cigarette smoke extract (CSE) on VEGF expression and to investigate the underlying molecular mechanisms of CSE in nasal fibroblasts. METHODS: Nasal fibroblasts were stimulated with CSE. Cytotoxicity was evaluated by 3-(4,5- dimethylthiazol-2yl)-2,5-diphenyl-tetrazolium bromide assay. The expression level of VEGF was measured using reverse transcription-polymerase chain reaction (RT-PCR), and enzyme-linked immunosorbent assay. Messenger RNA (mRNA) expression level of TLR4 were determined by RT-PCR. Small interfering RNA (siRNA) for TLR4 was transfected to suppress TLR4 expression. Activation of reactive oxygen species (ROS) was analyzed by using dichloro-dihydro-fluorescein diacetate assay. Mitogen-activated protein kinase (MAPK) and NF-kappaB activations were determined by using western blot and/or luciferase assay. RESULTS: CSE had no significant cytotoxic effect in nasal fibroblast up to 5%. CSE significantly increased both VEGF mRNA and protein expression dose-dependently. The down-regulation of TLR4 transcription by siRNA treatment suppressed CSE-induced expressions of both TLR4 and VEGF. Pretreatment with ROS scavengers, specific inhibitors of each MAPK, and NF-kappaB inhibitor significantly decreased CSE-induced VEGF expression. CONCLUSIONS: CSE has a stimulatory effect on VEGF expression through the TLR4, ROS, MAPK, and NF-kappaB signaling pathway in nasal fibroblasts.
[Mh] Termos MeSH primário: Fibroblastos/fisiologia
Nariz/patologia
Receptor 4 Toll-Like/metabolismo
Fator A de Crescimento do Endotélio Vascular/metabolismo
[Mh] Termos MeSH secundário: Adulto
Morte Celular
Células Cultivadas
Fumar Cigarros/efeitos adversos
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Feminino
Regulação da Expressão Gênica
Seres Humanos
Masculino
NF-kappa B/metabolismo
RNA Interferente Pequeno/genética
Espécies Reativas de Oxigênio/metabolismo
Transdução de Sinais
Receptor 4 Toll-Like/genética
Fator A de Crescimento do Endotélio Vascular/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (NF-kappa B); 0 (RNA, Small Interfering); 0 (Reactive Oxygen Species); 0 (TLR4 protein, human); 0 (Toll-Like Receptor 4); 0 (Vascular Endothelial Growth Factor A); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.2500/ajra.2017.31.4415


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[PMID]:29267505
[Au] Autor:Hai W; Ping X; Zhi-Wen Y; Chun Z
[Ad] Endereço:Department of Shanghai East Hospital, Tongji University, Shanghai, China.
[Ti] Título:Therapeutic effect and potential mechanism of pioglitazone in rats with severe acute pancreatitis.
[So] Source:Braz J Med Biol Res;51(2):e6812, 2017 Dec 11.
[Is] ISSN:1414-431X
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:Caspase recruitment domain-containing protein 9 (Card9) is located upstream of the nuclear factor kappa B (NF-κB) and p38 mitogen-activated protein kinase (MAPK) inflammatory pathways. This study investigated the therapeutic effect and potential mechanism of pioglitazone in rats with severe acute pancreatitis (SAP). SAP was induced by a retrograde infusion of 5.0% sodium taurocholate into the biliopancreatic duct of Sprague Dawley rats (n=54), which were then treated with pioglitazone. Blood and pancreatic tissues were harvested at 3, 6, and 12 h after SAP induction. Pancreatic pathological damage was evaluated by hematoxylin and eosin staining. Serum amylase, serum pro-inflammatory cytokines, and pancreatic myeloperoxidase (MPO) activities were determined by enzyme-linked immunosorbent assay. The expression of Card9 mRNA and protein in pancreatic tissues was detected by real-time polymerase chain reaction and western blotting. Pioglitazone had a therapeutic effect in treating rats with SAP by decreasing the level of amylase activity, ameliorating pancreatic histological damage, decreasing serum pro-inflammatory cytokine levels and tissue MPO activity, and downregulating the expression of NF-κB, p38MAPK, and Card9 mRNAs and proteins (P<0.05). The present study demonstrated that the inhibition of Card9 expression could reduce the severity of SAP. Card9 has a role in the pathogenic mechanism of SAP.
[Mh] Termos MeSH primário: Anti-Inflamatórios/farmacologia
Pancreatite/tratamento farmacológico
Pancreatite/patologia
Tiazolidinedionas/farmacologia
[Mh] Termos MeSH secundário: Amilases/sangue
Amilases/efeitos dos fármacos
Animais
Anti-Inflamatórios/uso terapêutico
Western Blotting
Proteínas Adaptadoras de Sinalização CARD/análise
Proteínas Adaptadoras de Sinalização CARD/efeitos dos fármacos
Citocinas/sangue
Citocinas/efeitos dos fármacos
Ensaio de Imunoadsorção Enzimática
Masculino
NF-kappa B/análise
Peroxidase/análise
Distribuição Aleatória
Ratos Sprague-Dawley
Reação em Cadeia da Polimerase em Tempo Real
Reprodutibilidade dos Testes
Índice de Gravidade de Doença
Tiazolidinedionas/uso terapêutico
Fatores de Tempo
Resultado do Tratamento
Proteínas Quinases p38 Ativadas por Mitógeno/análise
[Pt] Tipo de publicação:EVALUATION STUDIES; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (CARD Signaling Adaptor Proteins); 0 (Card9 protein, mouse); 0 (Cytokines); 0 (NF-kappa B); 0 (Thiazolidinediones); EC 1.11.1.7 (Peroxidase); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases); EC 3.2.1.- (Amylases); X4OV71U42S (pioglitazone)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171222
[St] Status:MEDLINE


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[PMID]:29188362
[Au] Autor:Slattery ML; Mullany LE; Sakoda L; Samowitz WS; Wolff RK; Stevens JR; Herrick JS
[Ad] Endereço:Department of Medicine, University of Utah, 383 Colorow, Salt Lake City, UT, 84108, USA. marty.slattery@hsc.utah.edu.
[Ti] Título:The NF-κB signalling pathway in colorectal cancer: associations between dysregulated gene and miRNA expression.
[So] Source:J Cancer Res Clin Oncol;144(2):269-283, 2018 Feb.
[Is] ISSN:1432-1335
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The nuclear factor-kappa B (NF-κB) signalling pathway is a regulator of immune response and inflammation that has been implicated in the carcinogenic process. We examined differentially expressed genes in this pathway and miRNAs to determine associations with colorectal cancer (CRC). METHODS: We used data from 217 CRC cases to evaluate differences in NF-κB signalling pathway gene expression between paired carcinoma and normal mucosa and identify miRNAs that are associated with these genes. Gene expression data from RNA-Seq and miRNA expression data from Agilent Human miRNA Microarray V19.0 were analysed. We evaluated genes most strongly associated and differentially expressed (fold change (FC) of > 1.5 or < 0.67) that were statistically significant after adjustment for multiple comparisons. RESULTS: Of the 92 genes evaluated, 22 were significantly downregulated and nine genes were significantly upregulated in all tumours. Two additional genes (CD14 and CSNK2A1) were dysregulated in MSS tumours and two genes (CARD11 and VCAM1) were downregulated and six genes were upregulated (LYN, TICAM2, ICAM1, IL1B, CCL4 and PTGS2) in MSI tumours. Sixteen of the 21 dysregulated genes were associated with 40 miRNAs. There were 76 miRNA:mRNA associations of which 38 had seed-region matches. Genes were associated with multiple miRNAs, with TNFSRF11A (RANK) being associated with 15 miRNAs. Likewise several miRNAs were associated with multiple genes (miR-150-5p with eight genes, miR-195-5p with four genes, miR-203a with five genes, miR-20b-5p with four genes, miR-650 with six genes and miR-92a-3p with five genes). CONCLUSIONS: Focusing on the genes and their associated miRNAs within the entire signalling pathway provides a comprehensive understanding of this complex pathway as it relates to CRC and offers insight into potential therapeutic agents.
[Mh] Termos MeSH primário: Neoplasias Colorretais/genética
Neoplasias Colorretais/metabolismo
Regulação Neoplásica da Expressão Gênica
MicroRNAs/genética
NF-kappa B/metabolismo
[Mh] Termos MeSH secundário: Adulto
Idoso
Estudos de Casos e Controles
Feminino
Seres Humanos
Masculino
MicroRNAs/biossíntese
Meia-Idade
NF-kappa B/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MicroRNAs); 0 (NF-kappa B)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171201
[St] Status:MEDLINE
[do] DOI:10.1007/s00432-017-2548-6


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[PMID]:28987401
[Au] Autor:Li B; Guo L; Ku T; Chen M; Li G; Sang N
[Ad] Endereço:College of Environment and Resource, Research Center of Environment and Health, Shanxi University, Taiyuan, Shanxi 030006, PR China.
[Ti] Título:PM exposure stimulates COX-2-mediated excitatory synaptic transmission via ROS-NF-κB pathway.
[So] Source:Chemosphere;190:124-134, 2018 Jan.
[Is] ISSN:1879-1298
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Long-term exposure to fine particulate matter (PM ) has been reported to be closely associated with the neuroinflammation and synaptic dysfunction, but the mechanisms underlying the process remain unclear. Cyclooxygenase-2 (COX-2) is a key player in neuroinflammation, and has been also implicated in the glutamatergic excitotoxicity and synaptic plasticity. Thus, we hypothesized that COX-2 was involved in PM -promoted neuroinflammation and synaptic dysfunction. Our results revealed that PM elevated COX-2 expression in primary cultured hippocampal neurons and increased the amplitude of field excitatory postsynaptic potentials (fEPSPs) in hippocampal brain slices. And the administration of NS398 (a COX-2 inhibitor) prevented the increased fEPSPs. PM also induced intracellular reactive oxygen species (ROS) generation accompanied with glutathione (GSH) depletion and the loss of mitochondrial membrane potential (MMP), and the ROS inhibitor, N-acetyl-L-cystein (NAC) suppressed the COX-2 overexpression and the increased fEPSPs. Furthermore, the nuclear factor kappa B (NF-κB) was involved in ROS-induced COX-2 and fEPSP in response to PM exposure. These findings indicated that PM activated COX-2 expression and enhanced the synaptic transmission through ROS-NF-κB pathway, and provided possible biomarkers and specific interventions for PM -induced neurological damage.
[Mh] Termos MeSH primário: Ciclo-Oxigenase 2/fisiologia
NF-kappa B/metabolismo
Material Particulado/toxicidade
Espécies Reativas de Oxigênio/metabolismo
Transmissão Sináptica
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Ciclo-Oxigenase 2/metabolismo
Hipocampo/citologia
Inflamação/etiologia
Camundongos
Neurônios/patologia
Material Particulado/farmacologia
Transmissão Sináptica/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (NF-kappa B); 0 (Particulate Matter); 0 (Reactive Oxygen Species); EC 1.14.99.1 (Cyclooxygenase 2)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171009
[St] Status:MEDLINE


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[PMID]:28453760
[Au] Autor:Hibiya S; Tsuchiya K; Hayashi R; Fukushima K; Horita N; Watanabe S; Shirasaki T; Nishimura R; Kimura N; Nishimura T; Gotoh N; Oshima S; Okamoto R; Nakamura T; Watanabe M
[Ad] Endereço:Department of Gastroenterology and Hepatology, Graduate School, Tokyo Medical and Dental University (TMDU), Tokyo, Japan.
[Ti] Título:Long-term Inflammation Transforms Intestinal Epithelial Cells of Colonic Organoids.
[So] Source:J Crohns Colitis;11(5):621-630, 2017 May 01.
[Is] ISSN:1876-4479
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Background and Aims: Patients with ulcerative colitis [UC] are at an increased risk of developing colitis-associated cancer [CAC], suggesting that continuous inflammation in the colon promotes the transformation of colonic epithelial cells. However, the mechanisms underlying cell transformation in UC remain unknown. We therefore aimed to investigate the effect of long-term inflammation on intestinal epithelial cells [IECs] using organoid culture. Methods: IECs were isolated from mouse colon, and were cultured according to a method for a three-dimensional [3D] organoid culture. To mimic chronic inflammation, a mixture of cytokines and bacterial components were added to the medium for over a year. Cell signal intensity was assessed by 3D immunofluorescence. Cell transformation was assessed by microarray with gene set enrichment analysis. Results: Stimulation with cytokines resulted in a significant induction of target genes for the nuclear factor [NF]-κB pathway in colonic organoids. Following 60 weeks of continuous stimulation, cell differentiation was suppressed. Continuous stimulation also resulted in significant amplification of NF-κB signalling. Amplified NF-κB signalling by long-term stimulation remained in colonic organoids even 11 weeks after the removal of all cytokines. Some genes were specifically upregulated only in colonic organoids after the removal all cytokines following long-term stimulation. Conclusions: Colonic organoids stimulated with cytokines for a prolonged period were established as in vitro model to assess long-term epithelial responses to inflammatory cytokines. Chronic inflammation led to sustained NF-κB signalling activation in colonic organoids, resulting in cell transformation that might be related to the carcinogenesis of CAC in UC.
[Mh] Termos MeSH primário: Transformação Celular Neoplásica/patologia
Colite/patologia
Mucosa Intestinal/citologia
Organoides/patologia
[Mh] Termos MeSH secundário: Animais
Colo/citologia
Colo/patologia
Citocinas/metabolismo
Feminino
Mucosa Intestinal/patologia
Camundongos
Camundongos Endogâmicos C57BL
NF-kappa B/metabolismo
Análise de Sequência com Séries de Oligonucleotídeos
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (NF-kappa B)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1093/ecco-jcc/jjw186


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[PMID]:29241192
[Au] Autor:Mao G; Wu P; Zhang Z; Zhang Z; Liao W; Li Y; Kang Y
[Ad] Endereço:Department of Joint Surgery, First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
[Ti] Título:MicroRNA-92a-3p Regulates Aggrecanase-1 and Aggrecanase-2 Expression in Chondrogenesis and IL-1ß-Induced Catabolism in Human Articular Chondrocytes.
[So] Source:Cell Physiol Biochem;44(1):38-52, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: Aggrecanase-1 (ADAMTS-4) and aggrecanase-2 (ADAMTS-5) are secreted enzymes belonging to the ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs) family that play significant roles in the progression of osteoarthritis (OA). Here, we aimed to determine whether the expression of ADAMTS-4/5 in chondrogenesis and inflammation is regulated by microRNA-92a-3p (miR-92a-3p). METHODS: MiR-92a-3p and ADAMTS-4/5 expressions were determined by quantitative polymerase chain reaction (qPCR). To investigate the repressive effect of miR-92a-3p on ADAMTS-4/5 expression, chondrogenic human mesenchymal stem cells (hMSCs) and human chondrocytes were transfected with mature miR-92a-3p or an antisense inhibitor (anti-miR-92a-3p), respectively. ADAMTS-4/5 protein production was quantified by enzyme-linked immunosorbent assay (ELISA), and miR-92a-3p involvement in IL-1ß-mediated catabolic effects was examined by immunoblotting. The roles of activated MAP kinases (MAPK) and nuclear factor (NF)-κB were evaluated by using specific inhibitors. Interaction between miR-92a-3p and its putative binding site in the 3'-untranslated region (3'-UTR) of ADAMTS-4/5 mRNA was confirmed by luciferase reporter assay. RESULTS: miR-92a-3p expression was elevated in chondrogenic hMSCs, with significantly lower expression in OA cartilage than in normal cartilage. Stimulation with IL-1ß significantly reduced miR-92a-3p expression in primary human chondrocytes (PHCs). Transfection of chondrocytes with miR-92a-3p downregulated IL-1ß-induced ADAMTS-4/5 expression, and the activity of a reporter construct containing the 3'-UTR of human ADAMTS-4/5 mRNA. MiR-92a-3p expression was suppressed upon IL-1ß-induced activation of MAPK and NF-κB in chondrocytes. CONCLUSION: MiR-92a-3p is an important regulator of ADAMTS-4/5 in human chondrocytes and may contribute to the development of OA.
[Mh] Termos MeSH primário: Proteína ADAMTS4/metabolismo
Proteína ADAMTS5/metabolismo
Condrogênese/efeitos dos fármacos
Condrogênese/genética
Interleucina-1beta/farmacologia
MicroRNAs/metabolismo
[Mh] Termos MeSH secundário: Proteína ADAMTS4/antagonistas & inibidores
Proteína ADAMTS4/genética
Proteína ADAMTS5/antagonistas & inibidores
Proteína ADAMTS5/genética
Adulto
Idoso
Antagomirs/metabolismo
Células da Medula Óssea/citologia
Cartilagem Articular/metabolismo
Cartilagem Articular/patologia
Células Cultivadas
Condrócitos/citologia
Condrócitos/efeitos dos fármacos
Condrócitos/metabolismo
Feminino
Expressão Gênica/efeitos dos fármacos
Seres Humanos
Masculino
Células Mesenquimais Estromais/citologia
Células Mesenquimais Estromais/efeitos dos fármacos
Células Mesenquimais Estromais/metabolismo
MicroRNAs/antagonistas & inibidores
MicroRNAs/genética
Meia-Idade
Proteínas Quinases Ativadas por Mitógeno/antagonistas & inibidores
Proteínas Quinases Ativadas por Mitógeno/metabolismo
NF-kappa B/antagonistas & inibidores
NF-kappa B/metabolismo
Osteoartrite do Joelho/genética
Osteoartrite do Joelho/metabolismo
Osteoartrite do Joelho/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antagomirs); 0 (Interleukin-1beta); 0 (MIRN92 microRNA, human); 0 (MicroRNAs); 0 (NF-kappa B); EC 2.7.11.24 (Mitogen-Activated Protein Kinases); EC 3.4.24.- (ADAMTS5 Protein); EC 3.4.24.82 (ADAMTS4 Protein)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171215
[St] Status:MEDLINE
[do] DOI:10.1159/000484579



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