Base de dados : MEDLINE
Pesquisa : D09.400.500 [Categoria DeCS]
Referências encontradas : 68798 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 6880 ir para página                         

  1 / 68798 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29320816
[Au] Autor:Ismail HAHA; Kang BH; Kim JS; Lee JH; Choi IW; Cha GH; Yuk JM; Lee YH
[Ad] Endereço:Department of Infection Biology, Chungnam National University School of Medicine, Daejeon 34134, Korea.
[Ti] Título:IL-12 and IL-23 Production in Toxoplasma gondii- or LPS-Treated Jurkat T Cells via PI3K and MAPK Signaling Pathways.
[So] Source:Korean J Parasitol;55(6):613-622, 2017 Dec.
[Is] ISSN:1738-0006
[Cp] País de publicação:Korea (South)
[La] Idioma:eng
[Ab] Resumo:IL-12 and IL-23 are closely related in structure, and have been shown to play crucial roles in regulation of immune responses. However, little is known about the regulation of these cytokines in T cells. Here, we investigated the roles of PI3K and MAPK pathways in IL-12 and IL-23 production in human Jurkat T cells in response to Toxoplasma gondii and LPS. IL-12 and IL-23 production was significantly increased in T cells after stimulation with T. gondii or LPS. T. gondii and LPS increased the phosphorylation of AKT, ERK1/2, p38 MAPK, and JNK1/2 in T cells from 10 min post-stimulation, and peaked at 30-60 min. Inhibition of the PI3K pathway reduced IL-12 and IL-23 production in T. gondii-infected cells, but increased in LPS-stimulated cells. IL-12 and IL-23 production was significantly reduced by ERK1/2 and p38 MAPK inhibitors in T. gondii- and LPS-stimulated cells, but not in cells treated with a JNK1/2 inhibitor. Collectively, IL-12 and IL-23 production was positively regulated by PI3K and JNK1/2 in T. gondii-infected Jurkat cells, but negatively regulated in LPS-stimulated cells. And ERK1/2 and p38 MAPK positively regulated IL-12 and IL-23 production in Jurkat T cells. These data indicate that T. gondii and LPS induced IL-12 and IL-23 production in Jurkat T cells through the regulation of the PI3K and MAPK pathways; however, the mechanism underlying the stimulation of IL-12 and IL-23 production by T. gondii in Jurkat T cells is different from that of LPS.
[Mh] Termos MeSH primário: Interleucina-12/metabolismo
Interleucina-23/metabolismo
Lipopolissacarídeos/imunologia
Sistema de Sinalização das MAP Quinases/imunologia
Sistema de Sinalização das MAP Quinases/fisiologia
Fosfatidilinositol 3-Quinases/imunologia
Fosfatidilinositol 3-Quinases/fisiologia
Toxoplasma/imunologia
[Mh] Termos MeSH secundário: Células Cultivadas
Seres Humanos
Células Jurkat
Proteína Quinase 3 Ativada por Mitógeno/metabolismo
Proteína Quinase 3 Ativada por Mitógeno/fisiologia
Proteína Quinase 8 Ativada por Mitógeno/metabolismo
Proteína Quinase 8 Ativada por Mitógeno/fisiologia
Proteína Quinase 9 Ativada por Mitógeno/metabolismo
Proteína Quinase 9 Ativada por Mitógeno/fisiologia
Fosforilação
Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
Proteínas Quinases p38 Ativadas por Mitógeno/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukin-23); 0 (Lipopolysaccharides); 187348-17-0 (Interleukin-12); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.1.24 (Mitogen-Activated Protein Kinase 9); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 8); EC 2.7.11.24 (p38 Mitogen-Activated Protein 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:180112
[St] Status:MEDLINE
[do] DOI:10.3347/kjp.2017.55.6.613


  2 / 68798 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[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


  3 / 68798 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29031765
[Au] Autor:Boakye YD; Groyer L; Heiss EH
[Ad] Endereço:Department of Pharmacognosy, University of Vienna, Althanstrasse 14, 1090 Vienna, Austria.
[Ti] Título:An increased autophagic flux contributes to the anti-inflammatory potential of urolithin A in macrophages.
[So] Source:Biochim Biophys Acta;1862(1):61-70, 2018 01.
[Is] ISSN:0006-3002
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: An extract of Phyllanthus muellerianus and its constituent geraniin have been reported to exert anti-inflammatory activity in vivo. However, orally consumed geraniin, an ellagitannin, shows low bioavailability and undergoes metabolization to urolithins by gut microbiota. This study aimed at comparing geraniin and urolithin A with respect to inhibition of M1 (LPS) polarization of murine J774.1 macrophages and shedding more light on possible underlying mechanisms. METHODS: Photometric, fluorimetric as well as luminescence-based assays monitored production of reactive oxygen species (ROS) and nitric oxide (NO), cell viability or reporter gene expression. Western blot analyses and confocal microscopy showed abundance and localization of target proteins, respectively. RESULTS: Urolithin A is a stronger inhibitor of M1 (LPS) macrophage polarization (production of NO, ROS and pro-inflammatory proteins) than geraniin. Urolithin A leads to an elevated autophagic flux in macrophages. Inhibition of autophagy in M1 (LPS) macrophages overcomes the suppressed nuclear translocation of p65 (NF-kB; nuclear factor kB), the reduced expression of pro-inflammatory genes as well as the diminished NO production brought about by urolithin A. The increased autophagic flux is furthermore associated with impaired Akt/mTOR (mammalian target of rapamycin) signaling in urolithin A-treated macrophages. CONCLUSIONS AND GENERAL SIGNIFICANCE: Intestinal metabolization may boost the potential health benefit of widely consumed dietary ellagitannins, as suggested by side by side comparison of geraniin and urolithin A in M1(LPS) macrophages. Increased activity of the autophagic cellular recycling machinery aids the anti-inflammatory bioactivity of urolithin A.
[Mh] Termos MeSH primário: Anti-Inflamatórios/farmacologia
Autofagia/efeitos dos fármacos
Cumarínicos/farmacologia
Macrófagos/metabolismo
[Mh] Termos MeSH secundário: Transporte Ativo do Núcleo Celular/efeitos dos fármacos
Animais
Células CHO
Núcleo Celular/metabolismo
Cricetinae
Cricetulus
Células HEK293
Seres Humanos
Lipopolissacarídeos/toxicidade
Camundongos
Óxido Nítrico/metabolismo
Espécies Reativas de Oxigênio/metabolismo
Fator de Transcrição RelA/metabolismo
Proteínas ral de Ligação ao GTP/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Coumarins); 0 (Lipopolysaccharides); 0 (RELA protein, human); 0 (Reactive Oxygen Species); 0 (Transcription Factor RelA); 1143-70-0 (3,8-dihydroxy-6H-dibenzo(b,d)pyran-6-one); 31C4KY9ESH (Nitric Oxide); EC 3.6.1.- (Rala protein, mouse); EC 3.6.5.2 (ral GTP-Binding Proteins)
[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:171017
[St] Status:MEDLINE


  4 / 68798 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29441970
[Au] Autor:Ohkura N; Ohnishi K; Taniguchi M; Nakayama A; Usuba Y; Fujita M; Fujii A; Ishibashi K; Baba K; Atsumi G
[Ti] Título:Anti-platelet effects of chalcones from Koidzumi (Ashitaba) .
[So] Source:Pharmazie;71(11):651-654, 2016 Nov 02.
[Is] ISSN:0031-7144
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Angelica keiskei Koidzumi (Ashitaba) is a traditional folk medicine that is also regarded in Japan as a health food with potential antithrombotic properties. The ability of the major chalcones, xanthoangelol (XA) and 4-hydroxyderricin (4-HD) extracted from Ashitaba roots to inhibit platelet aggregation activity in vitro was recently determined. However, the anti-platelet activities of Ashitaba chalcones in vivo have remained unclear. The present study examines the anti-platelet effects of Ashitaba exudate and its constituent chalcones using mouse tail-bleeding models that reflect platelet aggregation in vivo. Ashitaba exudate and the major chalcone subtype XA, suppressed the lipopolysaccharide (LPS)-induced shortening of mouse tail bleeding. However, trace amounts of other Ashitaba chalcone subtypes including xanthoangelols B (XB), D (XD), E (XE) and F (XF) did not affect tail bleeding. These results suggest that the major chalcone subtype in Ashitaba, XA, has anti-platelet-activities in vivo.
[Mh] Termos MeSH primário: Angelica/química
Chalconas/farmacologia
Inibidores da Agregação de Plaquetas/farmacologia
[Mh] Termos MeSH secundário: Animais
Chalconas/química
Hemorragia/tratamento farmacológico
Lipopolissacarídeos/antagonistas & inibidores
Lipopolissacarídeos/farmacologia
Masculino
Camundongos
Camundongos Endogâmicos ICR
Raízes de Plantas/química
Agregação Plaquetária/efeitos dos fármacos
Inibidores da Agregação de Plaquetas/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chalcones); 0 (Lipopolysaccharides); 0 (Platelet Aggregation Inhibitors)
[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:180215
[St] Status:MEDLINE
[do] DOI:10.1691/ph.2016.6678


  5 / 68798 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29441967
[Au] Autor:Sheng F; Han M; Huang Z; Zhang L
[Ti] Título:Interleukin 6 receptor inhibitor tocilizumab suppresses cytokine expression, inflammasome activation and phagocytosis in a cell model of sepsis.
[So] Source:Pharmazie;71(11):636-639, 2016 Nov 02.
[Is] ISSN:0031-7144
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Sepsis is a life-threatening condition, usually accompanied by excessive inflammation. Tocilizumab (TCZ) is a humanized monoclonal antibody against the interleukin (IL) 6 receptor and has been studied in various inflammatory diseases, but little is known about its effects in sepsis. This study aims to reveal the role of TCZ in inflammation during sepsis. METHODS: Human monocyte cell line THP-1 was stimulated by lipopolysaccharide (LPS) as a cell model for sepsis. After TCZ treatment, the expression of cytokines tumor necrosis factor (TNF) and IL10, the production of chemokine (C-C motif) ligand 2 (CCL2) and IL1B, and the expression of inflammasome factors NLR family pyrin domain containing 3 (NLRP3) and caspase 1 (CASP1), were detected by qRT-PCR and ELISA. Phagocytosis assay was also performed to assess the phagocytosis activity of TCZ-treated cells. RESULTS: LPS stimulation significantly upregulated TNF and IL10 mRNA levels (P < 0.01) and CCL2 and IL1B production (P < 0.001), promoted NLRP3 and CASP1 levels (P < 0.01) and elevated phagocytosis activity of THP-1 cells (P < 0.001). TCZ treatment had the opposite effects of decreasing TNF and IL10 mRNA levels (P < 0.05), CCL2 and IL1B production (P < 0.001), inhibiting NLRP3 and CASP1 (P < 0.01), and suppressing phagocytosis activity (P < 0.001) compared to the LPS group. CONCLUSION: These results indicate the suppressive role of TCZ in cytokine production, inflammation activation and phagocytosis in sepsis cell model, implying its effects on controlling "cytokine storm" during sepsis. Thus TCZ provides a promising strategy for treating sepsis.
[Mh] Termos MeSH primário: Anticorpos Monoclonais Humanizados/farmacologia
Citocinas/antagonistas & inibidores
Inflamassomos/efeitos dos fármacos
Fagocitose/efeitos dos fármacos
Receptores de Interleucina-6/antagonistas & inibidores
Sepse/patologia
[Mh] Termos MeSH secundário: Linhagem Celular
Citocinas/biossíntese
Seres Humanos
Lipopolissacarídeos/antagonistas & inibidores
Lipopolissacarídeos/farmacologia
Monócitos/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal, Humanized); 0 (Cytokines); 0 (Inflammasomes); 0 (Lipopolysaccharides); 0 (Receptors, Interleukin-6); I031V2H011 (tocilizumab)
[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:180215
[St] Status:MEDLINE
[do] DOI:10.1691/ph.2016.6713


  6 / 68798 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29441964
[Au] Autor:Kono Y; Miyoshi S; Fujita T
[Ti] Título:Dextran sodium sulfate alters cytokine production in macrophages .
[So] Source:Pharmazie;71(11):619-624, 2016 Nov 02.
[Is] ISSN:0031-7144
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Macrophages have been assumed to have a crucial role in the development of inflammatory bowel disease (IBD). However, involvement of intestinal macrophages in IBD onset and functional alterations of macrophages during IBD development has not been clarified. We investigated the effect of exposure of compounds used in the induction of colitis in mice on the immune responses of peritoneal macrophages in mice. 2,4,6- trinitrobenzenesulfonic acid and oxazolone did not affect the production of interleukin (IL)-10 and IL-12 from lipopolysaccharide (LPS)-stimulated peritoneal macrophages from BALB/c mice. A significant increase in IL-10 secretion and decrease in IL-12 production from LPS-stimulated macrophages were observed upon exposure to dextran sodium sulfate (DSS). TNF-α production was enhanced significantly by exposure to DSS and LPS. The level of nitric-oxide production from macrophages was increased slightly by exposure to DSS and LPS. Expression of sphingosine kinase-1 and LIGHT (both of which are specific biomarkers of M2b macrophages) was observed in macrophages upon DSS exposure. Alteration of cytokine production in macrophages was observed upon DSS exposure in the absence of LPS stimulation. Peritoneal macrophages from C57BL/6 mice showed similar responses to peritoneal macrophages from BALB/c mice against DSS. These results suggest that DSS directs the immune response of macrophages towards the M2b phenotype.
[Mh] Termos MeSH primário: Citocinas/biossíntese
Sulfato de Dextrana/farmacologia
Macrófagos Peritoneais/metabolismo
[Mh] Termos MeSH secundário: Animais
Colite/induzido quimicamente
Colite/patologia
Feminino
Técnicas In Vitro
Interleucina-10/biossíntese
Interleucina-10/genética
Interleucina-12/biossíntese
Interleucina-12/genética
Lipopolissacarídeos/farmacologia
Macrófagos Peritoneais/efeitos dos fármacos
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C57BL
Óxido Nítrico/biossíntese
Fosfotransferases (Aceptor do Grupo Álcool)/biossíntese
Fosfotransferases (Aceptor do Grupo Álcool)/genética
Especificidade da Espécie
Membro 14 da Superfamília de Ligantes de Fatores de Necrose Tumoral/biossíntese
Membro 14 da Superfamília de Ligantes de Fatores de Necrose Tumoral/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (IL10 protein, mouse); 0 (Lipopolysaccharides); 0 (Tnfsf14 protein, mouse); 0 (Tumor Necrosis Factor Ligand Superfamily Member 14); 130068-27-8 (Interleukin-10); 187348-17-0 (Interleukin-12); 31C4KY9ESH (Nitric Oxide); 9042-14-2 (Dextran Sulfate); EC 2.7.1.- (Phosphotransferases (Alcohol Group Acceptor)); EC 2.7.1.- (sphingosine kinase)
[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:180215
[St] Status:MEDLINE
[do] DOI:10.1691/ph.2016.6688


  7 / 68798 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29357800
[Au] Autor:Siverio-Mota D; Andujar I; Marrero-Ponce Y; Giner RM; Diaz-Mendoza C; Paba GM; Vicet-Muro L; Cordero-Maldonado ML; de Witte PAM; Crawford AD; Veitia MS; Perez-Jimenez F; Aran VJ
[Ad] Endereço:Laboratory for Molecular Biodiscovery, Department of Pharmaceutical and Pharmacological Sciences, University of Leuven, Herestraat 49, 3000 Leuven, Belgium.
[Ti] Título:Anti-Inflammatory Activity and Cheminformatics Analysis of New Poten t 2-Substituted 1-Methyl-5-Nitroindazolinones.
[So] Source:Curr Top Med Chem;17(30):3236-3248, 2018 Feb 09.
[Is] ISSN:1873-4294
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:After the identification of the anti-inflammatory properties of VA5-13l (2-benzyl-1- methyl-5-nitroindazolinone) in previous investigations, some of its analogous compounds were designed, synthesized and evaluated in two anti-inflammatory methods: LPS-enhanced leukocyte migration assay in zebrafish; and 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced mouse ear edema. The products evaluated (3, 6, 8, 9 and 10) showed the lower values of relative leukocyte migration at 30 µM (0.14, 0.07, 0.10, 0.13 and 0.07, respectively), while in ear edema and myeloperoxidase activity methods, all the compounds reduced inflammation, only 4 and 16 yielded unsatisfactory results. The relationship linking structure and activity (SAR analysis) was determinate by using SARANEA software. The importance of the 5-Nitro group of the indazole ring for the activity was evident, and showed modest reduction when benzyl (Bn) is changed by alkyl group. A substituted Bn moiety at N2 (R) is the best substituent (5-10); nevertheless, if methylene group of Bn is deleted, the activity is affected. Also, introduction of halogen atoms mainly at positions 3 or 4 of the benzyl moiety (6 and 10) leads in general to strong activities. In fact, compounds 7 and 8 (R = 4-FBn or 4-ClBn, respectively) exhibit satisfactory results in in vivo tests and appear promising. The production of IL-6 at all doses assayed was significantly reduced, except with 16. Nonetheless, the production of TNF-α was significantly inhibited only by this chemical (16) at concentration of 50 µM. On the other hand, compound 2 was the one that mostly inhibited the expression of COX-2 and iNOS. From these results, it can be concluded that the inhibition in the release of cytokines can be one of the mechanisms of action responsible for the anti-inflammatory effect for 2-benzyl derivates while other 2-alkyl derivatives can inhibit production of NO. Therefore, nitroindazolinone chemical prototype could be an interesting structural group with anti-inflammatory purposes in the therapeutic.
[Mh] Termos MeSH primário: Anti-Inflamatórios não Esteroides/farmacologia
Inibidores de Ciclo-Oxigenase 2/farmacologia
Indazóis/farmacologia
Informática
Nitrocompostos/farmacologia
[Mh] Termos MeSH secundário: Animais
Anti-Inflamatórios não Esteroides/química
Ciclo-Oxigenase 2/metabolismo
Inibidores de Ciclo-Oxigenase 2/química
Relação Dose-Resposta a Droga
Seres Humanos
Indazóis/química
Lipopolissacarídeos/antagonistas & inibidores
Lipopolissacarídeos/farmacologia
Estrutura Molecular
Óxido Nítrico/antagonistas & inibidores
Óxido Nítrico/biossíntese
Óxido Nítrico Sintase Tipo II/antagonistas & inibidores
Óxido Nítrico Sintase Tipo II/metabolismo
Nitrocompostos/química
Relação Estrutura-Atividade
Fator de Necrose Tumoral alfa/antagonistas & inibidores
Peixe-Zebra
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Cyclooxygenase 2 Inhibitors); 0 (Indazoles); 0 (Lipopolysaccharides); 0 (Nitro Compounds); 0 (Tumor Necrosis Factor-alpha); 31C4KY9ESH (Nitric Oxide); EC 1.14.13.39 (Nitric Oxide Synthase Type II); 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:180124
[St] Status:MEDLINE
[do] DOI:10.2174/1568026618666180119125255


  8 / 68798 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo SciELO Brasil
[PMID]:29267498
[Au] Autor:Ni XJ; Xu ZQ; Jin H; Zheng SL; Cai Y; Wang JJ
[Ad] Endereço:Transplantation Center, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
[Ti] Título:Ginsenoside Rg1 protects human renal tubular epithelial cells from lipopolysaccharide-induced apoptosis and inflammation damage.
[So] Source:Braz J Med Biol Res;51(2):e6611, 2017 Dec 11.
[Is] ISSN:1414-431X
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:Ginsenoside Rg1, one of the most notable active components of Panax ginseng, has been widely reported to exert anti-inflammatory actions. This study aimed to reveal whether ginsenoside Rg1 also exhibits beneficial roles against lipopolysaccharide (LPS)-induced apoptosis and inflammation in human renal tubular epithelial cells, and to evaluate the potential role of the component on tubulointerstitial nephritis treatment. HK-2 cells were treated with various doses of ginsenoside Rg1 (0, 50, 100, 150, and 200 µM) in the absence or presence of 5 µg/mL LPS. Thereafter, CCK-8 assay, flow cytometry, western blot, migration assay, reactive oxygen species (ROS) assay, and ELISA were carried out to respectively assess cell viability, apoptosis, migration, ROS activity, and the release of inflammatory cytokines. As a result, ginsenoside Rg1 protected HK-2 cells from LPS-induced injury, as cell viability was increased, cell apoptosis was decreased, and the release of MCP-1, IL-1ß, IL-6, and TNF-α was reduced. Ginsenoside Rg1 functioned to HK-2 cells in a dose-dependent manner, and the 150 µM dose exhibited the most protective functions. Ginsenoside Rg1 had no significant impact on cell migration and ROS activity, while it alleviated LPS-induced ROS release and migration impairment. Furthermore, the down-regulations of p-PI3K, p-AKT, and up-regulations of PTEN, p-IκBα, p-p65, Bcl-3 induced by LPS were recovered to some extent after ginsenoside Rg1 treatment. In conclusion, ginsenoside Rg1 protects HK-2 cells against LPS-induced inflammation and apoptosis via activation of the PI3K/AKT pathway and suppression of NF-κB pathway.
[Mh] Termos MeSH primário: Anti-Inflamatórios/farmacologia
Apoptose/efeitos dos fármacos
Células Epiteliais/efeitos dos fármacos
Ginsenosídeos/farmacologia
Túbulos Renais/citologia
Lipopolissacarídeos
Nefrite/prevenção & controle
[Mh] Termos MeSH secundário: Análise de Variância
Western Blotting
Linhagem Celular
Ensaios de Migração Celular
Sobrevivência Celular/efeitos dos fármacos
Citocinas/análise
Citocinas/efeitos dos fármacos
Ensaio de Imunoadsorção Enzimática
Seres Humanos
Túbulos Renais/efeitos dos fármacos
Fosfatidilinositol 3-Quinases/análise
Fosfatidilinositol 3-Quinases/efeitos dos fármacos
Substâncias Protetoras/farmacologia
Proteínas Proto-Oncogênicas c-akt/análise
Proteínas Proto-Oncogênicas c-akt/efeitos dos fármacos
Espécies Reativas de Oxigênio/análise
Reprodutibilidade dos Testes
[Pt] Tipo de publicação:EVALUATION STUDIES; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Cytokines); 0 (Ginsenosides); 0 (Lipopolysaccharides); 0 (Protective Agents); 0 (Reactive Oxygen Species); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); PJ788634QY (ginsenoside Rg1)
[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


  9 / 68798 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[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


  10 / 68798 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28456012
[Au] Autor:Alizadeh A; Dyck SM; Kataria H; Shahriary GM; Nguyen DH; Santhosh KT; Karimi-Abdolrezaee S
[Ad] Endereço:Regenerative Medicine Program, Department of Physiology and Pathophysiology, Spinal Cord Research Centre, University of Manitoba, Winnipeg, Manitoba, R3E 0J9, Canada.
[Ti] Título:Neuregulin-1 positively modulates glial response and improves neurological recovery following traumatic spinal cord injury.
[So] Source:Glia;65(7):1152-1175, 2017 Jul.
[Is] ISSN:1098-1136
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Spinal cord injury (SCI) results in glial activation and neuroinflammation, which play pivotal roles in the secondary injury mechanisms with both pro- and antiregeneration effects. Presently, little is known about the endogenous molecular mechanisms that regulate glial functions in the injured spinal cord. We previously reported that the expression of neuregulin-1 (Nrg-1) is acutely and chronically declined following traumatic SCI. Here, we investigated the potential ramifications of Nrg-1 dysregulation on glial and immune cell reactivity following SCI. Using complementary in vitro approaches and a clinically-relevant model of severe compressive SCI in rats, we demonstrate that immediate delivery of Nrg-1 (500 ng/day) after injury enhances a neuroprotective phenotype in inflammatory cells associated with increased interleukin-10 and arginase-1 expression. We also found a decrease in proinflammatory factors including IL-1ß, TNF-α, matrix metalloproteinases (MMP-2 and 9) and nitric oxide after injury. In addition, Nrg-1 modulates astrogliosis and scar formation by reducing inhibitory chondroitin sulfate proteoglycans after SCI. Mechanistically, Nrg-1 effects on activated glia are mediated through ErbB2 tyrosine phosphorylation in an ErbB2/3 heterodimer complex. Furthermore, Nrg-1 exerts its effects through downregulation of MyD88, a downstream adaptor of Toll-like receptors, and increased phosphorylation of Erk1/2 and STAT3. Nrg-1 treatment with the therapeutic dosage of 1.5 µg/day significantly improves tissue preservation and functional recovery following SCI. Our findings for the first time provide novel insights into the role and mechanisms of Nrg-1 in acute SCI and suggest a positive immunomodulatory role for Nrg-1 that can harness the beneficial properties of activated glia and inflammatory cells in recovery following SCI.
[Mh] Termos MeSH primário: Doenças do Sistema Nervoso/tratamento farmacológico
Doenças do Sistema Nervoso/etiologia
Neuregulina-1/uso terapêutico
Neuroglia/fisiologia
Recuperação de Função Fisiológica/fisiologia
Traumatismos da Medula Espinal/complicações
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Arginase/metabolismo
Células Cultivadas
Meios de Cultivo Condicionados/farmacologia
Modelos Animais de Doenças
Feminino
Regulação da Expressão Gênica/efeitos dos fármacos
Regulação da Expressão Gênica/fisiologia
Proteína Glial Fibrilar Ácida/metabolismo
Interleucina-10/metabolismo
Lipopolissacarídeos/toxicidade
Locomoção/efeitos dos fármacos
Camundongos
Camundongos Endogâmicos C57BL
Neuregulina-1/metabolismo
Neuregulina-1/farmacologia
Neuroglia/efeitos dos fármacos
Ratos
Recuperação de Função Fisiológica/efeitos dos fármacos
Transdução de Sinais/efeitos dos fármacos
Traumatismos da Medula Espinal/patologia
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Culture Media, Conditioned); 0 (Glial Fibrillary Acidic Protein); 0 (Lipopolysaccharides); 0 (Neuregulin-1); 130068-27-8 (Interleukin-10); EC 3.5.3.1 (Arginase); EC 3.5.3.1 (arginase I, rat)
[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:170430
[St] Status:MEDLINE
[do] DOI:10.1002/glia.23150



página 1 de 6880 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde