Base de dados : MEDLINE
Pesquisa : A08.637.400 [Categoria DeCS]
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  1 / 14514 MEDLINE  
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[PMID]:29353043
[Au] Autor:Tanaka M; Ishihara Y; Mizuno S; Ishida A; Vogel CF; Tsuji M; Yamazaki T; Itoh K
[Ad] Endereço:Laboratory of Molecular Brain Science, Graduate School of Integrated Arts and Sciences, Hiroshima University, Hiroshima, 739-8521, Japan; Laboratory for Pharmacotherapy and Experimental Neurology, Kagawa School of Pharmaceutical Sciences, Tokushima Bunri University, Kagawa, 769-2193, Japan.
[Ti] Título:Progression of vasogenic edema induced by activated microglia under permanent middle cerebral artery occlusion.
[So] Source:Biochem Biophys Res Commun;496(2):582-587, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Brain edema is a severe complication that accompanies ischemic stroke. Increasing evidence shows that inflammatory cytokines impair tight junctions of the blood-brain barrier, suggesting the involvement of microglia in brain edema. In this study, we examined the role of microglia in the progression of ischemic brain edema using mice with permanent middle cerebral artery occlusion. The intensity of T2-weighted imaging (T2WI) in the cerebral cortex and the striatum was elevated 3 h after occlusion and spread to peripheral regions of the ischemic hemisphere. Merged images of 2,3,5-triphenyl tetrazolium chloride staining and T2WI revealed the exact vasogenic edema region, which spread from the ischemic core to outside the ischemic region. Microglia were strongly activated in the ischemic region 3 h after occlusion and, notably, activated microglia were observed in the non-ischemic region 24 h after occlusion. Pretreatment with minocycline, an inhibitor of microglial activation clearly suppressed not only vasogenic edema but also infarct formation. We demonstrated in this study that vasogenic edema spreads from the ischemic core to the peripheral region, which can be elicited, at least in part, by microglial activation induced by ischemia.
[Mh] Termos MeSH primário: Edema Encefálico/etiologia
Encéfalo/patologia
Infarto da Artéria Cerebral Média/complicações
Microglia/patologia
[Mh] Termos MeSH secundário: Animais
Edema Encefálico/patologia
Progressão da Doença
Infarto da Artéria Cerebral Média/patologia
Masculino
Camundongos Endogâmicos ICR
Água/análise
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
059QF0KO0R (Water)
[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:180122
[St] Status:MEDLINE


  2 / 14514 MEDLINE  
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[PMID]:28471051
[Au] Autor:Döring C; Regen T; Gertig U; van Rossum D; Winkler A; Saiepour N; Brück W; Hanisch UK; Janova H
[Ad] Endereço:Institute of Neuropathology, University Medical Center Göttingen, Göttingen, 37075, Germany.
[Ti] Título:A presumed antagonistic LPS identifies distinct functional organization of TLR4 in mouse microglia.
[So] Source:Glia;65(7):1176-1185, 2017 Jul.
[Is] ISSN:1098-1136
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Microglia as principle innate immune cells of the central nervous system (CNS) are the first line of defense against invading pathogens. They are capable of sensing infections through diverse receptors, such as Toll-like receptor 4 (TLR4). This receptor is best known for its ability to recognize bacterial lipopolysaccharide (LPS), a causative agent of gram-negative sepsis and septic shock. A putative, naturally occurring antagonist of TLR4 derives from the photosynthetic bacterium Rhodobacter sphaeroides. However, the antagonistic potential of R. sphaeroides LPS (Rs-LPS) is no universal feature, since several studies suggested agonistic rather than antagonistic actions of this molecule depending on the investigated mammalian species. Here we show the agonistic versus antagonistic potential of Rs-LPS in primary mouse microglia. We demonstrate that Rs-LPS efficiently induces the release of cytokines and chemokines, which depends on TLR4, MyD88, and TRIF, but not CD14. Furthermore, Rs-LPS is able to regulate the phagocytic capacity of microglia as agonist, while it antagonizes Re-LPS-induced MHC I expression. Finally, to our knowledge, we are the first to provide in vivo evidence for an agonistic potential of Rs-LPS, as it efficiently triggers the recruitment of peripheral immune cells to the endotoxin-challenged CNS. Together, our results argue for a versatile and complex organization of the microglial TLR4 system, which specifically translates exogenous signals into cellular functions. Importantly, as demonstrated here for microglia, the antagonistic potential of Rs-LPS needs to be considered with caution, as reactions to Rs-LPS not only differ by cell type, but even by function within one cell type.
[Mh] Termos MeSH primário: Lipopolissacarídeos/farmacologia
Microglia/efeitos dos fármacos
Receptor 4 Toll-Like/antagonistas & inibidores
Receptor 4 Toll-Like/metabolismo
[Mh] Termos MeSH secundário: Proteínas Adaptadoras de Transporte Vesicular/genética
Proteínas Adaptadoras de Transporte Vesicular/metabolismo
Animais
Animais Recém-Nascidos
Encéfalo/citologia
Células Cultivadas
Corpo Estriado/efeitos dos fármacos
Citocinas/metabolismo
Relação Dose-Resposta a Droga
Receptores de Lipopolissacarídeos/genética
Receptores de Lipopolissacarídeos/metabolismo
Macrófagos/efeitos dos fármacos
Macrófagos/fisiologia
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Bainha de Mielina/efeitos dos fármacos
Bainha de Mielina/patologia
Fator 88 de Diferenciação Mieloide/genética
Fator 88 de Diferenciação Mieloide/metabolismo
Fagocitose/efeitos dos fármacos
Fagocitose/fisiologia
Receptor 4 Toll-Like/genética
Regulação para Cima/efeitos dos fármacos
Regulação para Cima/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adaptor Proteins, Vesicular Transport); 0 (Cytokines); 0 (Lipopolysaccharide Receptors); 0 (Lipopolysaccharides); 0 (Myeloid Differentiation Factor 88); 0 (TICAM-1 protein, mouse); 0 (Tlr4 protein, mouse); 0 (Toll-Like Receptor 4)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1002/glia.23151


  3 / 14514 MEDLINE  
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[PMID]:27778395
[Au] Autor:Michailidou I; Naessens DM; Hametner S; Guldenaar W; Kooi EJ; Geurts JJ; Baas F; Lassmann H; Ramaglia V
[Ad] Endereço:Department of Genome Analysis, Academic Medical Center, Meibergdreef 9, Amsterdam, 1105, The Netherlands.
[Ti] Título:Complement C3 on microglial clusters in multiple sclerosis occur in chronic but not acute disease: Implication for disease pathogenesis.
[So] Source:Glia;65(2):264-277, 2017 02.
[Is] ISSN:1098-1136
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Microglial clusters with C3d deposits are observed in the periplaque of multiple sclerosis (MS) brains and were proposed as early stage of lesion formation. As such they should appear in the brain of MS donors with acute disease but thus far this has not been shown. Using postmortem brain tissue from acute (n = 10) and chronic (n = 15) MS cases we investigated whether C3d+ microglial clusters are part of an acute attack against myelinated axons, which could have implications for disease pathogenesis. The specificity of our findings to MS was tested in ischemic stroke cases (n = 8) with initial or advanced lesions and further analyzed in experimental traumatic brain injury (TBI, n = 26), as both conditions are primarily nondemyelinating but share essential features of neurodegeneration with MS lesions. C3d+ microglial clusters were found in chronic but not acute MS. They were not associated with antibody deposits or terminal complement activation. They were linked to slowly expanding lesions, localized on axons with impaired transport and associated with neuronal C3 production. C3d+ microglial clusters were not specific to MS as they were also found in stroke and experimental TBI. We conclude that C3d+ microglial clusters in MS are not part of an acute attack against myelinated axons. As such it is unlikely that they drive formation of new lesions but could represent a physiological mechanism to remove irreversibly damaged axons in chronic disease. GLIA 2017;65:264-277.
[Mh] Termos MeSH primário: Complemento C3/metabolismo
Microglia/metabolismo
Esclerose Múltipla/patologia
[Mh] Termos MeSH secundário: Doença Aguda
Adulto
Idoso
Idoso de 80 Anos ou mais
Animais
Autopsia
Doença Crônica
Complemento C3/genética
Citocinas/metabolismo
Proteínas de Ligação a DNA/metabolismo
Modelos Animais de Doenças
Feminino
Traumatismos Cranianos Fechados/patologia
Seres Humanos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Meia-Idade
Proteínas da Mielina/metabolismo
Proteínas do Tecido Nervoso/metabolismo
Neurônios/patologia
Acidente Vascular Cerebral/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (AIF1 protein, human); 0 (C3 protein, human); 0 (Complement C3); 0 (Cytokines); 0 (DNA-Binding Proteins); 0 (Myelin Proteins); 0 (Nerve Tissue Proteins)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE
[do] DOI:10.1002/glia.23090


  4 / 14514 MEDLINE  
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[PMID]:28747383
[Au] Autor:McDonough A; Lee RV; Noor S; Lee C; Le T; Iorga M; Phillips JLH; Murphy S; Möller T; Weinstein JR
[Ad] Endereço:Department of Neurology and.
[Ti] Título:Ischemia/Reperfusion Induces Interferon-Stimulated Gene Expression in Microglia.
[So] Source:J Neurosci;37(34):8292-8308, 2017 Aug 23.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Innate immune signaling is important in the pathophysiology of ischemia/reperfusion (stroke)-induced injury and recovery. Several lines of evidence support a central role for microglia in these processes. Recent work has identified Toll-like receptors (TLRs) and type I interferon (IFN) signaling in both ischemia/reperfusion-induced brain injury and ischemic preconditioning-mediated neuroprotection. To determine the effects of "ischemia/reperfusion-like" conditions on microglia, we performed genomic analyses on wild-type (WT) and cultured microglia after sequential exposure to hypoxia/hypoglycemia and normoxia/normoglycemia (H/H-N/N). We observed increased expression of type 1 IFN-stimulated genes (ISGs) as the predominant transcriptomal feature of H/H-N/N-exposed WT, but not , microglia. Microarray analysis on sorted microglia from ipsilateral male mouse cortex after a transient ischemic pulse also demonstrated robust expression of ISGs. Type 1 IFNs, including the IFN-αs and IFN-ß, activate the interferon-α/ß receptor (IFNAR) complex. We confirmed both H/H-N/N- and ischemia/reperfusion-induced microglial ISG responses by quantitative real-time PCR and demonstrated that both were dependent on IFNAR1. We characterized the effects of hypoxia/hypoglycemia on phosphorylation of signal transducer and activator of transcription 1 (STAT1), release of type 1 IFNs, and surface expression of IFNAR1 in microglia. We demonstrated that IFN-ß induces dose-dependent secretion of ISG chemokines in cultured microglia and robust ISG expression in microglia both and Finally, we demonstrated that the microglial ISG chemokine responses to TLR4 agonists were dependent on TLR4 and IFNAR1. Together, these data suggest novel ischemia/reperfusion-induced pathways for both TLR4-dependent and -independent, IFNAR1-dependent, type 1 IFN signaling in microglia. Stroke is the fifth leading cause of death in the United States and is a leading cause of serious long-term disability worldwide. Innate immune responses are critical in stroke pathophysiology, and microglia are key cellular effectors in the CNS response to ischemia/reperfusion. Using a transcriptional analysis approach, we identified a robust interferon (IFN)-stimulated gene response within microglia exposed to ischemia/reperfusion in both and experimental paradigms. Using a number of complementary techniques, we have demonstrated that these responses are dependent on innate immune signaling components including Toll-like receptor-4 and type I IFNs. We have also elucidated several novel ischemia/reperfusion-induced microglial signaling mechanisms.
[Mh] Termos MeSH primário: Isquemia Encefálica/metabolismo
Interferons/farmacologia
Microglia/metabolismo
Receptor de Interferon alfa e beta/biossíntese
Traumatismo por Reperfusão/metabolismo
Receptor 4 Toll-Like/deficiência
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Isquemia Encefálica/genética
Células Cultivadas
Relação Dose-Resposta a Droga
Feminino
Expressão Gênica
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Microglia/efeitos dos fármacos
Receptor de Interferon alfa e beta/genética
Traumatismo por Reperfusão/genética
Receptor 4 Toll-Like/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ifnar1 protein, mouse); 0 (Tlr4 protein, mouse); 0 (Toll-Like Receptor 4); 156986-95-7 (Receptor, Interferon alpha-beta); 9008-11-1 (Interferons)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180303
[Lr] Data última revisão:
180303
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170728
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.0725-17.2017


  5 / 14514 MEDLINE  
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[PMID]:28468668
[Au] Autor:Flowers A; Bell-Temin H; Jalloh A; Stevens SM; Bickford PC
[Ad] Endereço:Department of Neurosurgery and Brain Repair, USF Health Morsani College of Medicine, University of South Florida, 12901 Bruce B Downs Blvd., Campus Box MDC-78, Tampa, FL, 33570, USA.
[Ti] Título:Proteomic anaysis of aged microglia: shifts in transcription, bioenergetics, and nutrient response.
[So] Source:J Neuroinflammation;14(1):96, 2017 May 03.
[Is] ISSN:1742-2094
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Age is the primary risk factor for many diseases. As such, age is a critical co-factor for examination in order to understand the progression and potential intervention in disease progression. Studies examining both the phenotype and transcriptome of aged microglia demonstrated a propensity for the development of a pro-inflammatory phenotype. Less well studied is the concomitant blunting of anti-inflammatory aspects of microglial function with age which also impact plasticity and repair in the CNS. METHODS: This study utilizes mass spectrometry-based proteomics to compare primary microglia from young and aged animals. RESULTS: This study revealed alterations in three clusters of inter-related proteins. The three pathways were inflammatory signaling, mitochondrial function, and cellular metabolism. Analysis of these clusters identified the protein rapamycin-insensitive companion of mTOR (RICTOR), a component of the mTORC2 complex, as a novel upstream regulator of several biological functions that are altered with age and potentially linked to phenotype development. A decrease in mTORC2-dependent AKT S473 phosphorylation, as assessed by insulin growth factor (IGF) treatment, was observed in aged microglia. This novel finding was confirmed by genetic manipulation of the microglial cell line. BV2 cells with diminished RICTOR displayed a phenotype that was strikingly similar to that of aged microglia. This finding is particularly relevant as the mTOR pathway already has a number of pharmacological modulators used clinically. CONCLUSIONS: The results suggest that microglia from aged mice show changes in cellular metabolism and energy regulation that might underlie the alterations in inflammatory signaling. Modulation of one pathway identified in our bioinformatic analysis, RICTOR, may provide an avenue by which deleterious aspects of the aging microglia can be attenuated. If successful, this could mean potentially delaying or diminishing the progress of diseases for which progressive inflammation is involved.
[Mh] Termos MeSH primário: Senescência Celular/fisiologia
Metabolismo Energético/fisiologia
Microglia/metabolismo
Mapas de Interação de Proteínas/fisiologia
Proteômica/métodos
Transcrição Genética/fisiologia
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Ácidos Graxos/metabolismo
Alimentos
Glucose/metabolismo
Camundongos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fatty Acids); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1186/s12974-017-0840-7


  6 / 14514 MEDLINE  
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[PMID]:29441925
[Au] Autor:Cai QY; Liu XL; Zhang XQ; Liu YX; Li M; Zhao CZ; Zhang XM; Meng QH
[Ti] Título:Anti-neuroinflammation activity of acetylpuerarin mediated by a PKC-δ-dependent caspase signaling pathway: and studies.
[So] Source:Pharmazie;71(10):575-582, 2016 Oct 01.
[Is] ISSN:0031-7144
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: This study was performed to evaluate the regulating effects of acetylpuerarin on inflammation in an Alzheimer's disease (AD) rat model and an inflammatory cell model. METHODS: Healthy female Wistar rats and mouse BV2 microglia cells were selected. AD rat models were established with the method of bilateral intrahippocampal amyloid-ß(Aß)1-42 injections and the inflammatory cell models were established using Aß25-35-induced mouse BV2 microglia cells. The cytotoxicity of acetylpuerarin on BV2 microglial cells was detected by MTT assay and the morphological changes of BV2 microglia cells were observed under inverted phase contrast microscope. As inflammatory parameters, the expressions of IL-1ß, iNOS, IL-6 and TNF-α were examined by Elisa, Immunohistochemistry, Quantitative real-time PCR (qRT-PCR), Western blot and Immunofluorescence analyses. We also examined the acetylpuerarin's effect on the activity of PKC-δ, IKKß and caspase-8/caspase-3 pathway. RESULTS: Acetylpuerarin exerted no significant cytotoxicity on BV2 microglia cells and was applied in all subsequent experiments. Acetylpuerarin treatment mitigated Aß25-35-induced morphological changes associated with microglia activation. Moreover, the expressions of caspase-8, cleaved caspase-3, PKC-δ, IKKß, iNOS, IL-1ß and TNF-α in Aß25-35-stimulated BV2 microglia cells were significantly suppressed by acetylpuerarin and in a dose-dependent manner. Additionally, the expression of IL-1ß in hippocampus and the level of IL-6 in serum of Aß1-42 treated rat were reduced by acetylpuerarin and in a concentration-dependent manner. CONCLUSION: Our results suggest that acetylpuerarin's anti-inflammation mechanism on AD may be mediated through the PKC-δ-dependent caspase signalling pathway.
[Mh] Termos MeSH primário: Caspases/efeitos dos fármacos
Encefalite/tratamento farmacológico
Isoflavonas/farmacologia
Proteína Quinase C-delta/efeitos dos fármacos
[Mh] Termos MeSH secundário: Doença de Alzheimer/induzido quimicamente
Doença de Alzheimer/tratamento farmacológico
Doença de Alzheimer/patologia
Peptídeos beta-Amiloides
Animais
Sobrevivência Celular/efeitos dos fármacos
Citocinas/metabolismo
Encefalite/induzido quimicamente
Feminino
Ativação de Macrófagos/efeitos dos fármacos
Camundongos
Microglia/efeitos dos fármacos
Fragmentos de Peptídeos
Ratos
Ratos Wistar
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amyloid beta-Peptides); 0 (Cytokines); 0 (Isoflavones); 0 (Peptide Fragments); 0 (acetylpuerarin); 0 (amyloid beta-protein (1-42)); 0 (amyloid beta-protein (25-35)); EC 2.7.1.- (Prkcd protein, rat); EC 2.7.11.13 (Protein Kinase C-delta); EC 3.4.22.- (Caspases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180215
[St] Status:MEDLINE
[do] DOI:10.1691/ph.2016.6660


  7 / 14514 MEDLINE  
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[PMID]:29194444
[Au] Autor:Bollinger JL; Collins KE; Patel R; Wellman CL
[Ad] Endereço:Department of Psychological and Brain Sciences, Indiana University, Bloomington, IN, United States of America.
[Ti] Título:Behavioral stress alters corticolimbic microglia in a sex- and brain region-specific manner.
[So] Source:PLoS One;12(12):e0187631, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Women are more susceptible to numerous stress-linked psychological disorders (e.g., depression) characterized by dysfunction of corticolimbic brain regions critical for emotion regulation and cognitive function. Although sparsely investigated, a number of studies indicate sex differences in stress effects on neuronal structure, function, and behaviors associated with these regions. We recently demonstrated a basal sex difference in- and differential effects of stress on- microglial activation in medial prefrontal cortex (mPFC). The resident immune cells of the brain, microglia are implicated in synaptic and dendritic plasticity, and cognitive-behavioral function. Here, we examined the effects of acute (3h/day, 1 day) and chronic (3h/day, 10 days) restraint stress on microglial density and morphology, as well as immune factor expression in orbitofrontal cortex (OFC), basolateral amygdala (BLA), and dorsal hippocampus (DHC) in male and female rats. Microglia were visualized, classified based on their morphology, and stereologically counted. Microglia-associated transcripts (CD40, iNOS, Arg1, CX3CL1, CX3CR1, CD200, and CD200R) were assessed in brain punches from each region. Expression of genes linked with cellular stress, neuroimmune state, and neuron-microglia communication varied between unstressed male and female rats in a region-specific manner. In OFC, chronic stress upregulated a wider variety of immune factors in females than in males. Acute stress increased microglia-associated transcripts in BLA in males, whereas chronic stress altered immune factor expression in BLA more broadly in females. In DHC, chronic stress increased immune factor expression in males but not females. Moreover, acute and chronic stress differentially affected microglial morphological activation state in male and female rats across all brain regions investigated. In males, chronic stress altered microglial activation in a pattern consistent with microglial involvement in stress-induced dendritic remodeling across OFC, BLA, and DHC. Together, these data suggest the potential for microglia-mediated sex differences in stress effects on neural structure, function, and behavior.
[Mh] Termos MeSH primário: Encéfalo/metabolismo
Microglia/metabolismo
Estresse Psicológico
[Mh] Termos MeSH secundário: Animais
Feminino
Sistema Límbico/metabolismo
Masculino
Reação em Cadeia da Polimerase
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180228
[Lr] Data última revisão:
180228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171202
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0187631


  8 / 14514 MEDLINE  
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[PMID]:28451639
[Au] Autor:Kanda H; Kobayashi K; Yamanaka H; Okubo M; Noguchi K
[Ad] Endereço:Department of Anatomy and Neuroscience, Hyogo College of Medicine, Nishinomiya, Hyogo 663-8501, Japan.
[Ti] Título:Microglial TNFα Induces COX2 and PGI2 Synthase Expression in Spinal Endothelial Cells during Neuropathic Pain.
[So] Source:eNeuro;4(2), 2017 Mar-Apr.
[Is] ISSN:2373-2822
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Prostaglandins (PGs) are typical lipid mediators that play a role in homeostasis and disease. They are synthesized from arachidonic acid by cyclooxygenase 1 (COX1) and COX2. Although COX2 has been reported to be upregulated in the spinal cord after nerve injury, its expression and functional roles in neuropathic pain remain unclear. In this study, we investigated the expression of Cox2, PGI2 synthase (Pgis), and prostaglandin I2 receptor (IP receptor) mRNA in the rat spinal cord after spared nerve injury (SNI). Levels of Cox2 and Pgis mRNA increased in endothelial cells from 24 to 48 h after nerve injury. IP receptor mRNA was constitutively expressed in dorsal horn neurons. A COX2 inhibitor and IP receptor antagonists attenuated pain behavior in the early phase of neuropathic pain. Furthermore, we examined the relationship between COX2 and tumor necrosis factor-α (TNFα) in the spinal cord of a rat SNI model. Levels of TNFα mRNA transiently increased in the spinal microglia 24 h after SNI. The TNF receptors Tnfr1 and Tnfr2 mRNA were colocalized with COX2. Intrathecal injection of TNFα induced Cox2 and Pgis mRNA expression in endothelial cells. These results revealed that microglia-derived TNFα induced COX2 and PGIS expression in spinal endothelial cells and that endothelial PGI2 played a critical role in neuropathic pain via neuronal IP receptor. These findings further suggest that the glia-endothelial cell interaction of the neurovascular unit via transient TNFα is involved in the generation of neuropathic pain.
[Mh] Termos MeSH primário: Ciclo-Oxigenase 2/metabolismo
Sistema Enzimático do Citocromo P-450/metabolismo
Células Endoteliais/enzimologia
Oxirredutases Intramoleculares/metabolismo
Microglia/metabolismo
Neuralgia/metabolismo
Medula Espinal/metabolismo
Fator de Necrose Tumoral alfa/metabolismo
[Mh] Termos MeSH secundário: Animais
Inflamação/enzimologia
Masculino
Traumatismos dos Nervos Periféricos/metabolismo
RNA Mensageiro
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (RNA, Messenger); 0 (Tumor Necrosis Factor-alpha); 9035-51-2 (Cytochrome P-450 Enzyme System); EC 1.14.99.1 (Cyclooxygenase 2); EC 1.14.99.1 (Ptgs2 protein, rat); EC 5.3.- (Intramolecular Oxidoreductases); EC 5.3.99.4 (prostacyclin synthetase)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180228
[Lr] Data última revisão:
180228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE


  9 / 14514 MEDLINE  
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[PMID]:29351316
[Au] Autor:Yeh CH; Hsieh LP; Lin MC; Wei TS; Lin HC; Chang CC; Hsing CH
[Ad] Endereço:Department of Medicinal Botanicals and Health applications, Da-Yeh University, Changhua, Taiwan.
[Ti] Título:Dexmedetomidine reduces lipopolysaccharide induced neuroinflammation, sickness behavior, and anhedonia.
[So] Source:PLoS One;13(1):e0191070, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Peripheral innate immune response may induce sickness behavior through activating microglia, excessive cytokines production, and neuroinflammation. Dexmedetomidine (Dex) has anti-inflammatory effect. We investigated the effects of Dex on lipopolysaccharide (LPS)-induced neuroinflammation and sickness behavior in mice. MATERIALS AND METHODS: BALB/c mice were intraperitoneally (i.p.) injected with Dex (50 ug/kg) or vehicle. One hour later, the mice were injected (i.p.) with Escherichia coli LPS (0.33 mg/kg) or saline (n = 6 in each group). We analyzed the food and water intake, body weight loss, and sucrose preference of the mice for 24h. We also determined microglia activation and cytokines expression in the brains of the mice. In vitro, we determine cytokines expression in LPS-treated BV-2 microglial cells with or without Dex treatment. RESULTS: In the Dex-pretreated mice, LPS-induced sickness behavior (anorexia, weight loss, and social withdrawal) were attenuated and microglial activation was lower than vehicle control. The mRNA expression of TNF-α, MCP-1, indoleamine 2, 3 dioxygenase (IDO), caspase-3, and iNOS were increased in the brain of LPS-challenged mice, which were reduced by Dex but not vehicle. CONCLUSION: Dexmedetomidine diminished LPS-induced neuroinflammation in the mouse brain and modulated the cytokine-associated changes in sickness behavior.
[Mh] Termos MeSH primário: Anedonia/efeitos dos fármacos
Encéfalo/efeitos dos fármacos
Dexmedetomidina/farmacologia
Comportamento de Doença/efeitos dos fármacos
Inflamação/induzido quimicamente
Lipopolissacarídeos/toxicidade
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Encéfalo/patologia
Inflamação/patologia
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Microglia/efeitos dos fármacos
Reação em Cadeia da Polimerase em Tempo Real
Reação em Cadeia da Polimerase Via Transcriptase Reversa
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Lipopolysaccharides); 67VB76HONO (Dexmedetomidine)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180120
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191070


  10 / 14514 MEDLINE  
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[PMID]:29248573
[Au] Autor:Takahashi M; Komada M; Miyazawa K; Goto S; Ikeda Y
[Ad] Endereço:Department of Anatomy, School of Dentistry, Aichi Gakuin University, 1-100 Kusumoto-cho, Chikusa-ku, Nagoya, Aichi 464-8650, Japan; Department of Orthodontics, School of Dentistry, Aichi Gakuin University, 2-11 Suemori-dori, Chikusa-ku, Nagoya, Aichi 464-8650, Japan.
[Ti] Título:Bisphenol A exposure induces increased microglia and microglial related factors in the murine embryonic dorsal telencephalon and hypothalamus.
[So] Source:Toxicol Lett;284:113-119, 2018 Mar 01.
[Is] ISSN:1879-3169
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Bisphenol A (BPA) is a widely used compound in the food packaging industry. Prenatal exposure to BPA induces histological abnormalities in the neocortex and hypothalamus in association with abnormal behaviors. Yet, the molecular and cellular neurodevelopmental toxicological mechanisms of BPA are incompletely characterized on neuroinflammatory-related endopoints. To evaluate the neurodevelopmental effects of BPA exposure in mouse embryos, we examined microglial numbers as well as the expression of microglial-related factors in the E15.5 embryonic brain. BPA-exposed embryos exhibited significant increases in Iba1-immunoreactive microglial numbers in the dorsal telencephalon and the hypothalamus compared to control embryos. Further, the expression levels of microglial markers (Iba1, CD16, iNOS, and CD206), inflammatory factors (TNFα and IL4), signal transducing molecules (Cx3Cr1 and Cx3Cl1), and neurotrophic factor (IGF1) were altered in BPA-exposed embryos. These findings suggest that BPA exposure increases microglial numbers in the brain and alters the neuroinflammatory status at a transcriptional level. Together, these changes may represent a novel target for neurodevelopmental toxicity assessment after BPA exposure.
[Mh] Termos MeSH primário: Compostos Benzidrílicos/toxicidade
Poluentes Ambientais/toxicidade
Hipotálamo/efeitos dos fármacos
Microglia/efeitos dos fármacos
Fenóis/toxicidade
Efeitos Tardios da Exposição Pré-Natal/induzido quimicamente
Telencéfalo/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Comportamento Animal/efeitos dos fármacos
Biomarcadores/análise
Contagem de Células
Relação Dose-Resposta a Droga
Feminino
Embalagem de Alimentos
Expressão Gênica/efeitos dos fármacos
Hipotálamo/embriologia
Mediadores da Inflamação/imunologia
Masculino
Camundongos Endogâmicos ICR
Microglia/imunologia
Microglia/metabolismo
Microglia/patologia
Neurogênese/efeitos dos fármacos
Gravidez
Efeitos Tardios da Exposição Pré-Natal/imunologia
Efeitos Tardios da Exposição Pré-Natal/metabolismo
Efeitos Tardios da Exposição Pré-Natal/patologia
Telencéfalo/embriologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benzhydryl Compounds); 0 (Biomarkers); 0 (Environmental Pollutants); 0 (Inflammation Mediators); 0 (Phenols); MLT3645I99 (bisphenol A)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171218
[St] Status:MEDLINE



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