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[PMID]:29390478
[Au] Autor:Mizuno S; Wakui M; Machida Y; Hosoe N; Hisamatsu T; Ishida T; Kameyama K; Naganuma M; Kanai T
[Ad] Endereço:Division of Gastroenterology and Hepatology, Department of Internal Medicine.
[Ti] Título:Increased levels of prostaglandin E-major urinary metabolite (PGE-MUM) in active mesenteric panniculitis patients: A case report.
[So] Source:Medicine (Baltimore);96(51):e9237, 2017 Dec.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Mesenteric panniculitis (MP) is a rare disease with abdominal and systemic symptoms and is characterized by nonspecific inflammation, fat necrosis, and fibrosis in mesenteric fat. Active inflammatory responses may increase levels of prostaglandin E-major urinary metabolite (PGE-MUM), which was reported to reflect the disease activity of ulcerative colitis and chronic fibrosing interstitial pneumonia. We recently experienced a case with elevated PGE-MUM at the time of diagnosis of MP and we investigated the potential of PGE-MUM as a biomarker. PATIENT CONCERN: In this report we described 2 active mesenteric panniculitis patients with high PGE-MUM levels. DIAGNOSES: Mesenteric panniculitis INTERVENTIONS:: Both MP patients were measured the levels of PGE-MUM. OUTCOMES: Both MP patients exhibited high levels of PGE-MUM before treatment. In one, the levels were sensitively correlated with clinical symptoms and serological markers on steroids. LESSONS: The study observations suggest the potential of PGE-MUM to reflect the disease activity of MP. To verify its use, more findings based on clinical studies should be accumulated.
[Mh] Termos MeSH primário: Corticosteroides/uso terapêutico
Paniculite Peritoneal/tratamento farmacológico
Paniculite Peritoneal/metabolismo
Prostaglandinas E/metabolismo
[Mh] Termos MeSH secundário: Idoso
Biomarcadores/metabolismo
Feminino
Seguimentos
Seres Humanos
Masculino
Meia-Idade
Paniculite Peritoneal/urina
Medição de Risco
Índice de Gravidade de Doença
Resultado do Tratamento
Urinálise
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Adrenal Cortex Hormones); 0 (Biomarkers); 0 (Prostaglandins E)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180214
[Lr] Data última revisão:
180214
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180203
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009237


  2 / 14335 MEDLINE  
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[PMID]:27578923
[Au] Autor:Filho EG; da Silva EZ; Zanotto CZ; Oliver C; Jamur MC
[Ad] Endereço:Department of Cell and Molecular Biology and Pathogenic Bioagents, Ribeirão Preto Medical School, University of São Paulo, Avenida Bandeirantes 3900, 14049-900 Ribeirão Preto, SP, Brazil.
[Ti] Título:Cross-Linking Mast Cell Specific Gangliosides Stimulates the Release of Newly Formed Lipid Mediators and Newly Synthesized Cytokines.
[So] Source:Mediators Inflamm;2016:9160540, 2016.
[Is] ISSN:1466-1861
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mast cells are immunoregulatory cells that participate in inflammatory processes. Cross-linking mast cell specific GD1b derived gangliosides by mAbAA4 results in partial activation of mast cells without the release of preformed mediators. The present study examines the release of newly formed and newly synthesized mediators following ganglioside cross-linking. Cross-linking the gangliosides with mAbAA4 released the newly formed lipid mediators, prostaglandins D2 and E2, without release of leukotrienes B4 and C4. The effect of cross-linking these gangliosides on the activation of enzymes in the arachidonate cascade was then investigated. Ganglioside cross-linking resulted in phosphorylation of cytosolic phospholipase A2 and increased expression of cyclooxygenase-2. Translocation of 5-lipoxygenase from the cytosol to the nucleus was not induced by ganglioside cross-linking. Cross-linking of GD1b derived gangliosides also resulted in the release of the newly synthesized mediators, interleukin-4, interleukin-6, and TNF-α. The effect of cross-linking the gangliosides on the MAP kinase pathway was then investigated. Cross-linking the gangliosides induced the phosphorylation of ERK1/2, JNK1/2, and p38 as well as activating both NFκB and NFAT in a Syk-dependent manner. Therefore, cross-linking the mast cell specific GD1b derived gangliosides results in the activation of signaling pathways that culminate with the release of newly formed and newly synthesized mediators.
[Mh] Termos MeSH primário: Citocinas/metabolismo
Gangliosídeos/metabolismo
Mastócitos/metabolismo
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Fosfolipases A2 do Grupo IV/metabolismo
Immunoblotting
Interleucina-4/metabolismo
Interleucina-6/metabolismo
Leucotrienos/metabolismo
Proteína Quinase 1 Ativada por Mitógeno/metabolismo
Proteína Quinase 3 Ativada por Mitógeno/metabolismo
Proteína Quinase 8 Ativada por Mitógeno/metabolismo
Proteína Quinase 9 Ativada por Mitógeno/metabolismo
NF-kappa B/metabolismo
Fatores de Transcrição NFATC/metabolismo
Fosforilação
Prostaglandinas D/metabolismo
Prostaglandinas E/metabolismo
Ratos
Fator de Necrose Tumoral alfa/metabolismo
Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Gangliosides); 0 (Interleukin-6); 0 (Leukotrienes); 0 (NF-kappa B); 0 (NFATC Transcription Factors); 0 (Prostaglandins D); 0 (Prostaglandins E); 0 (Tumor Necrosis Factor-alpha); 207137-56-2 (Interleukin-4); EC 2.7.1.24 (Mitogen-Activated Protein Kinase 9); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1); 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); EC 3.1.1.4 (Group IV Phospholipases A2)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170515
[Lr] Data última revisão:
170515
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160901
[St] Status:MEDLINE
[do] DOI:10.1155/2016/9160540


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[PMID]:27329879
[Au] Autor:Liu XY; Pan KQ; Zhang L; Liu WS; Song FL
[Ad] Endereço:The Affiliated Hospital of Qingdao University. Qingdao 266003, China. E-mail:593866072@qq.com.
[Ti] Título:[The effect of carboxymethyl chitosan zinc and peptide on IL-1,TNF-α and PGE-2 in gingival crevicular fluid of miniature pigs].
[So] Source:Shanghai Kou Qiang Yi Xue;25(2):172-6, 2016 Apr.
[Is] ISSN:1006-7248
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:PURPOSE: This experiment was aimed at exploring whether carboxymethyl chitosan zinc and peptide (CMC-Zn(+)-P) can reduce the occurrence and development of periodontal tissue inflammation effectively by observing the change of IL-1,TNF-α and PGE-2 level in gingival crevicular fluid (GCF) before and after brushing, so as to find a new effective material in preventing and treating periodontal diseases. METHODS: Miniature pigs were selected as experimental subjects and divided into 4 groups randomly: the control group; CMC-Zn(+)-P group (material group);brushing group; brushing + CMC-Zn(+)-P group (composite group). Gingival crevicular fluid before and one month after the experiment was collected. The levels of IL-1, TNF-α and PGE-2 were examined by enzyme-linked immune-sorbent assay, while the clinical periodontal index was recorded. SPSS 18.0 software package was used for statistical analysis. RESULTS: There was no significant difference in levels of IL-1, TNF-α and PGE-2 and clinical periodontal index between the 4 groups before experiment. After one month, the levels of IL-1, TNF-α, PGE-2 in GCF had significant difference between 4 groups. The levels of IL-1, TNF-α, PGE-2 in composite group were significant lower than that of the other three groups (P<0.008).The levels of IL-1, TNF-α and PGE-2 in the material group and brushing group were significantly lower than that of the control group (P<0.008). Compared with materials group, the brushing group had significantly lower level of IL-1,significantly higher level of PGE-2 ,but no difference in the level of TNF-α.In addition, the teeth calculus index of composite group was significantly lower than that of other groups (P<0.05). CONCLUSIONS: CMC-Zn(+)-P can effectively reduce periodontal tissue inflammation and cut down the speed of deposition of dental calculus. If used cooperatively with brushing, the effect will be better.
[Mh] Termos MeSH primário: Quitosana/química
Líquido do Sulco Gengival/metabolismo
Interleucina-1/metabolismo
Prostaglandinas E/metabolismo
Fator de Necrose Tumoral alfa/metabolismo
[Mh] Termos MeSH secundário: Animais
Quitosana/análogos & derivados
Cálculos Dentários
Doenças Periodontais
Índice Periodontal
Periodonto
Suínos
Porco Miniatura
Zinco
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukin-1); 0 (Prostaglandins E); 0 (Tumor Necrosis Factor-alpha); 0 (carboxymethyl-chitosan); 9012-76-4 (Chitosan); J41CSQ7QDS (Zinc)
[Em] Mês de entrada:1610
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:D; IM
[Da] Data de entrada para processamento:160623
[St] Status:MEDLINE


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[PMID]:27160444
[Au] Autor:Sirotkin AV; Mertin D; Süvegová K; Lauricik J; Morovic M; Harrath AH; Kotwica J
[Ad] Endereço:Constantine the Philosopher University, Nitra, Slovakia; Research Institute of Animal Production, Luzianky, Slovakia. Electronic address: asirotkin@ukf.sk.
[Ti] Título:Mink aging is associated with a reduction in ovarian hormone release and the response to FSH and ghrelin.
[So] Source:Theriogenology;86(5):1175-81, 2016 Sep 15.
[Is] ISSN:1879-3231
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The endocrine mechanisms of mink ovarian hormones release and reproductive aging are poorly investigated. The aims of our study were to: (1) identify hormones produced by mink ovaries (the steroids progesterone [P] and estradiol [E], the peptide hormone oxytocin [OT], and the prostaglandin F [PGF] and prostaglandin E [PGE]); (2) examine the effect of FSH and ghrelin on the release of the hormones listed previously; and (3) understand whether these hormones can be involved in the control of mink reproductive aging, i.e., whether aging can be associated with changes (a) in the basal release of P, E, OT, PGF, or PGE and (b) their response to FSH and ghrelin. Fragments of ovaries of young (yearlings) and old (3-5 years of age) minks were cultured with and without FSH and ghrelin (0, 1, 10, or 100 ng/mL), and the release of hormones was analyzed by EIA/RIA. We found that isolated ovaries were able to release P, E, OT, PGF, and PGE, and the levels of P produced in the ovaries of old animals were lower than those produced in the ovaries of young animals, whereas the levels of other hormones did not differ. FSH was able to stimulate P and E and suppress OT and PGF and did not affect PGE release. Aging was associated with the inhibition of the effect of FSH on ovarian P and E, the appearance of the inhibitory action of FSH on OT, and the disappearance of this action on ovarian PGF. PGE was not affected by FSH, irrespective of animal age. Ghrelin was able to promote E (but not P) and suppress OT, PGF, and PGE output. Aging was associated with the appearance of an inhibitory influence of ghrelin on ovarian OT and PGE and with the disappearance of this influence on PGF output. Aging did not affect the action of ghrelin on ovarian P and E. Our observations (1) confirm the production of P and E and show that OT, PGF, and PGE are released from mink ovaries, (2) confirm the involvement of FSH and demonstrate the involvement of ghrelin in the control of mink ovarian hormone release, and (3) suggest that reproductive aging in minks is due to a reduction in basal P release and alterations in the response of E, OT, PGF (but not of PGE) to FSH and ghrelin.
[Mh] Termos MeSH primário: Envelhecimento/fisiologia
Hormônio Foliculoestimulante/farmacologia
Grelina/farmacologia
Vison/fisiologia
Ovário/efeitos dos fármacos
Ovário/fisiologia
[Mh] Termos MeSH secundário: Animais
Estradiol/metabolismo
Feminino
Ocitocina/metabolismo
Progesterona/metabolismo
Prostaglandinas E/metabolismo
Prostaglandinas F/metabolismo
Técnicas de Cultura de Tecidos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ghrelin); 0 (Prostaglandins E); 0 (Prostaglandins F); 4G7DS2Q64Y (Progesterone); 4TI98Z838E (Estradiol); 50-56-6 (Oxytocin); 9002-68-0 (Follicle Stimulating Hormone)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170413
[Lr] Data última revisão:
170413
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160511
[St] Status:MEDLINE


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[PMID]:26616878
[Au] Autor:Cho CH; Kim J; Ahn JY; Hahn HG; Cho SW
[Ad] Endereço:Department of Biochemistry and Molecular Biology, University of Ulsan College of Medicine, Seoul 138-736, Republic of Korea.
[Ti] Título:N-adamantyl-4-methylthiazol-2-amine suppresses lipopolysaccharide-induced brain inflammation by regulating NF-κB signaling in mice.
[So] Source:J Neuroimmunol;289:98-104, 2015 Dec 15.
[Is] ISSN:1872-8421
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:We report that N-adamantyl-4-methylthiazol-2-amine (KHG26693), a novel thiazole derivative, can prevent lipopolysaccharide (LPS)-induced brain inflammation in mice. In this LPS-induced model of brain inflammation, administration of KHG26693 effectively prevented increases in the levels of IL-1ß, TNF-α, prostaglandin E2, malondialdehyde, and nitric oxide, and mitigated reductions in the levels of superoxide dismutase in the hippocampus. KHG26693 also prevented reductions in the levels of hippocampal brain-derived neurotrophic factors. Furthermore, pretreatment with KHG26693 prior to LPS treatment dramatically attenuated the elevation of inducible nitric oxide synthase and cyclooxygenase-2 protein levels. Moreover, pretreatment with KHG26693 significantly suppressed LPS-induced phosphorylation of NF-κB and IκBα through the inactivation of IKKß. Additionally, KHG26693 caused the downregulation of LPS-induced cystathionine-b-synthase gene expression in the brain. Although the clinical relevance of our findings remains to be determined, our data suggest that KHG26693 might prevent neuronal cell injury via the reduction of inflammation and oxidative stress in the brain.
[Mh] Termos MeSH primário: Adamantano/análogos & derivados
Anti-Inflamatórios/uso terapêutico
Encefalite/induzido quimicamente
Encefalite/prevenção & controle
Lipopolissacarídeos/toxicidade
Tiazóis/uso terapêutico
[Mh] Termos MeSH secundário: Adamantano/uso terapêutico
Análise de Variância
Animais
Encéfalo/efeitos dos fármacos
Encéfalo/metabolismo
Fator Neurotrófico Derivado do Encéfalo/metabolismo
Ciclo-Oxigenase 1/metabolismo
Ciclo-Oxigenase 2/metabolismo
Modelos Animais de Doenças
Relação Dose-Resposta a Droga
Esquema de Medicação
Interações Medicamentosas
Encefalite/metabolismo
Feminino
Regulação da Expressão Gênica/efeitos dos fármacos
Interleucina-1beta/metabolismo
Malondialdeído/metabolismo
Proteínas de Membrana/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Óxido Nítrico/metabolismo
Prostaglandinas E
Superóxido Dismutase/metabolismo
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Brain-Derived Neurotrophic Factor); 0 (Interleukin-1beta); 0 (Lipopolysaccharides); 0 (Membrane Proteins); 0 (N-adamantyl-4-methylthiazol-2-amine); 0 (Prostaglandins E); 0 (Thiazoles); 0 (Tumor Necrosis Factor-alpha); 31C4KY9ESH (Nitric Oxide); 4Y8F71G49Q (Malondialdehyde); EC 1.14.99.- (Ptgs2 protein, mouse); EC 1.14.99.1 (Cyclooxygenase 1); EC 1.14.99.1 (Cyclooxygenase 2); EC 1.14.99.1 (Ptgs1 protein, mouse); EC 1.15.1.1 (Superoxide Dismutase); PJY633525U (Adamantane)
[Em] Mês de entrada:1603
[Cu] Atualização por classe:151130
[Lr] Data última revisão:
151130
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151201
[St] Status:MEDLINE


  6 / 14335 MEDLINE  
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[PMID]:26538834
[Au] Autor:Yan ZW; Dong J; Qin CH; Zhao CY; Miao LY; He CY
[Ad] Endereço:Department of Clinical Pharmacology, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215006, China.
[Ti] Título:Therapeutic Effect of Chenodeoxycholic Acid in an Experimental Rabbit Model of Osteoarthritis.
[So] Source:Mediators Inflamm;2015:780149, 2015.
[Is] ISSN:1466-1861
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Osteoarthritis (OA) is a slowly progressive joint disease typically seen in middle-age to elderly people. At present, there is no ideal agent to treat OA. Chenodeoxycholic acid (CDCA) was a principal active constituent from animal bile. However, the therapeutic effect of CDCA on OA severity was largely unknown. The purpose of this study was to evaluate the therapeutic effect of intra-articular injection of CDCA in a rabbit OA model. OA was induced in experimental rabbits by anterior cruciate ligament transection (ACLT) and then rabbits were intra-articularly injected with CDCA (10 mg/kg or 50 mg/kg) once per week for 5 weeks. The results showed that CDCA significantly decreased cartilage degradation on the surface of femoral condyles, reducing the pathological changes of articular cartilage and synovial membrane by macroscopic and histological analysis. CDCA also significantly decreased bone destruction and erosion of joint evaluated by micro-CT. Furthermore, CDCA could markedly reduce the release of matrix metalloproteinase-1 (MMP-1), matrix metalloproteinase-3 (MMP-3), interleukin-1ß (IL-1ß), and prostaglandin E2 (PGE2) in synovial fluid. These observations highlight CDCA might be a potential therapeutic agent for OA.
[Mh] Termos MeSH primário: Ácido Quenodesoxicólico/uso terapêutico
Osteoartrite/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Ligamento Cruzado Anterior/cirurgia
Cartilagem Articular/patologia
Modelos Animais de Doenças
Ensaio de Imunoadsorção Enzimática
Fêmur/patologia
Injeções Intra-Articulares
Interleucina-1beta/metabolismo
Masculino
Metaloproteinase 1 da Matriz/metabolismo
Metaloproteinase 3 da Matriz/metabolismo
Prostaglandinas E/metabolismo
Coelhos
Membrana Sinovial/patologia
Microtomografia por Raio-X
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Interleukin-1beta); 0 (Prostaglandins E); 0GEI24LG0J (Chenodeoxycholic Acid); EC 3.4.24.17 (Matrix Metalloproteinase 3); EC 3.4.24.7 (Matrix Metalloproteinase 1)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:170627
[Lr] Data última revisão:
170627
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151106
[St] Status:MEDLINE
[do] DOI:10.1155/2015/780149


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[PMID]:25897683
[Au] Autor:Kwon SH; Ma SX; Hong SI; Lee SY; Jang CG
[Ad] Endereço:1 Department of Pharmacology, School of Pharmacy, Sungkyunkwan University , Suwon, Korea.
[Ti] Título:Lonicera japonica THUNB. Extract Inhibits Lipopolysaccharide-Stimulated Inflammatory Responses by Suppressing NF-κB Signaling in BV-2 Microglial Cells.
[So] Source:J Med Food;18(7):762-75, 2015 Jul.
[Is] ISSN:1557-7600
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In the current study, we evaluated the anti-inflammatory effects of Lonicera japonica THUNB. (LJ) and its underlying molecular mechanism in lipopolysaccharide (LPS)-stimulated BV-2 microglial cells. Our results indicated that LJ significantly inhibits LPS-stimulated production of nitric oxide (NO) and prostaglandin E2 (PGE2). In addition, LJ inhibited inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) at both the protein and mRNA levels. In LPS-stimulated BV-2 microglial cells, LJ inhibited proinflammatory cytokines and chemokines, tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß), monocyte chemoattractant protein-1 (MCP-1), matrix metalloproteinase-9 (MMP-9) enzymatic activities, and/or mRNA expression, as well as reactive oxygen species (ROS) production. LJ significantly suppressed activation of nuclear factor-κB (NF-κB) and its translocation from the cytosol to the nucleus and suppressed the DNA-binding activity of NF-κB. Furthermore, LJ significantly inhibited phosphorylation of c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase 1/2 (ERK 1/2), p38 mitogen-activated protein kinases (MAPKs), phosphatidylinositol 3-kinases (PI3K)/Akt, and Janus kinase 1 (JAK1)/signal transducer and activator of transcription (STAT)1/3. Collectively, our findings indicated that the antineuroinflammatory properties of LJ in LPS-induced BV-2 microglial cells is due to downregulation of proinflammatory cytokines and chemokines downstream of inhibition of NF-κB activation.
[Mh] Termos MeSH primário: Anti-Inflamatórios/farmacologia
Lipopolissacarídeos/farmacologia
Lonicera/química
Microglia/metabolismo
NF-kappa B/antagonistas & inibidores
Extratos Vegetais/farmacologia
[Mh] Termos MeSH secundário: Linhagem Celular
Sobrevivência Celular/efeitos dos fármacos
Quimiocinas/antagonistas & inibidores
Ciclo-Oxigenase 2/genética
Citocinas/antagonistas & inibidores
Expressão Gênica/efeitos dos fármacos
Óxido Nítrico/antagonistas & inibidores
Óxido Nítrico Sintase Tipo II/genética
Fosforilação/efeitos dos fármacos
Prostaglandinas E/antagonistas & inibidores
RNA Mensageiro/análise
Espécies Reativas de Oxigênio/metabolismo
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Chemokines); 0 (Cytokines); 0 (Lipopolysaccharides); 0 (NF-kappa B); 0 (Plant Extracts); 0 (Prostaglandins E); 0 (RNA, Messenger); 0 (Reactive Oxygen Species); 31C4KY9ESH (Nitric Oxide); EC 1.14.13.39 (Nitric Oxide Synthase Type II); EC 1.14.99.1 (Cyclooxygenase 2)
[Em] Mês de entrada:1603
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150422
[St] Status:MEDLINE
[do] DOI:10.1089/jmf.2014.3341


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[PMID]:25893742
[Au] Autor:Kumar V; Al-Abbasi FA; Ahmed D; Verma A; Mujeeb M; Anwar F
[Ad] Endereço:Department of Pharmaceutical Sciences, Faculty of Health Sciences, Sam Higginbottom Institute of Agriculture, Technology & Sciences, Allahabad, Uttar Pradesh 211007, India. phvikas@gmail.com.
[Ti] Título:Paederia foetida Linn. inhibits adjuvant induced arthritis by suppression of PGE(2) and COX-2 expression via nuclear factor-κB.
[So] Source:Food Funct;6(5):1652-66, 2015 May.
[Is] ISSN:2042-650X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The current investigation was undertaken to determine the anti-inflammatory and antioxidant effects of Paederia foetida Linn. (PF) along with its mechanism of action when implemented in tissue protection. HPTLC was used in the identification of the compound quercetin, while in vitro analysis confirmed the significance of the antioxidant and anti-inflammatory action of PF. We initially demonstrated the in vivo anti-inflammatory effect of PF, evaluating it against a variety of phlogistic agents as well as turpentine oil, prostaglandin and arachidonic acid. Groups of rats, fasted overnight, were treated as follows: Group I: normal control (vehicle), Group II: PF (100 mg kg(-1)), Group III: arthritic control (CFA only, 0.05 ml), Group IV, V, VI: CFA (0.05 ml) + PF (25, 50 and 100 mg kg(-1)) and Group VII: CFA (0.05 ml) + indomethacin (10 mg per kg b.w.). PF significantly protected against paw edema, arthritic index and body weight alteration induced by Complete Fruend's Adjuvant (CFA). Other observations, like histological and macroscopic changes, were observed in CFA induced inflammation in knee joints. Subcutaneous administration of CFA was accompanied by proinflammatory cytokine status, as appraised by the amplification of interleukin-2 (IL-2), interleukin-1ß (IL-1ß) and tumor necrosis factor (TNF-α); oxidative stress status was estimated by the enhancement of the level of lipid peroxidation (LPO) and the depletion of superoxide dismutase (SOD), glutathione peroxidase (GPx) and glutathione (GSH). Pre-treatment with PF significantly (P < 0.001) protected against CFA induced oxidative stress and proinflammatory cytokines. More prominently, CFA administration augmented tissue and plasma superoxide (O2) and hydrogen peroxide (H2O2) levels, while the PF pre-treatment significantly (P < 0.001) reversed all CFA induced intracellular interruption. Following CFA induced arthritis, PF was tested for its free radical scavenging activity against the DPPH and ABTS radicals and its inhibitory proficiency against COX-1 and COX-2 in vitro. Considering the above, the current research confirmed momentous protection against CFA induced arthritis, which could be attributed to its anti-inflammatory and pro-oxidant nature.
[Mh] Termos MeSH primário: Anti-Inflamatórios/administração & dosagem
Artrite Experimental/tratamento farmacológico
Ciclo-Oxigenase 2/genética
NF-kappa B/imunologia
Extratos Vegetais/administração & dosagem
Prostaglandinas E/genética
Rubiaceae/química
[Mh] Termos MeSH secundário: Animais
Anti-Inflamatórios/química
Antioxidantes/administração & dosagem
Antioxidantes/química
Artrite Experimental/genética
Artrite Experimental/imunologia
Ciclo-Oxigenase 2/imunologia
Feminino
Seres Humanos
Interleucina-1beta/genética
Interleucina-1beta/imunologia
Interleucina-2/genética
Interleucina-2/imunologia
Masculino
NF-kappa B/genética
Extratos Vegetais/química
Prostaglandinas E/imunologia
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Antioxidants); 0 (Interleukin-1beta); 0 (Interleukin-2); 0 (NF-kappa B); 0 (Plant Extracts); 0 (Prostaglandins E); EC 1.14.99.1 (Cyclooxygenase 2)
[Em] Mês de entrada:1602
[Cu] Atualização por classe:150514
[Lr] Data última revisão:
150514
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150421
[St] Status:MEDLINE
[do] DOI:10.1039/c5fo00178a


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[PMID]:25890183
[Au] Autor:Wang H; Zhang D; Ge M; Li Z; Jiang J; Li Y
[Ad] Endereço:Institute of Medicinal Biotechnology, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100050, China. hq_wangimb@163.com.
[Ti] Título:Formononetin inhibits enterovirus 71 replication by regulating COX- 2/PGE2 expression.
[So] Source:Virol J;12:35, 2015 Mar 01.
[Is] ISSN:1743-422X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The activation of ERK, p38 and JNK signal cascade in host cells has been demonstrated to up-regulate of enterovirus 71 (EV71)-induced cyclooxygenase-2 (COX-2)/ prostaglandins E2 (PGE2) expression which is essential for viral replication. So, we want to know whether a compound can inhibit EV71 infection by suppressing COX-2/PGE2 expression. METHODS: The antiviral effect of formononetin was determined by cytopathic effect (CPE) assay and the time course assays. The influence of formononetin for EV71 replication was determined by immunofluorescence assay, western blotting assay and qRT-PCR assay. The mechanism of the antiviral activity of formononetin was determined by western blotting assay and ELISA assay. RESULTS: Formononetin could reduce EV71 RNA and protein synthesis in a dose-dependent manner. The time course assays showed that formononetin displayed significant antiviral activity both before (24 or 12 h) and after (0-6 h) EV71 inoculation in SK-N-SH cells. Formononetin was also able to prevent EV71-induced cytopathic effect (CPE) and suppress the activation of ERK, p38 and JNK signal pathways. Furthermore, formononetin could suppress the EV71-induced COX-2/PGE2 expression. Also, formononetin exhibited similar antiviral activities against other members of Picornaviridae including coxsackievirus B2 (CVB2), coxsackievirus B3 (CVB3) and coxsackievirus B6 (CVB6). CONCLUSIONS: Formononetin could inhibit EV71-induced COX-2 expression and PGE2 production via MAPKs pathway including ERK, p38 and JNK. Formononetin exhibited antiviral activities against some members of Picornaviridae. These findings suggest that formononetin could be a potential lead or supplement for the development of new anti-EV71 agents in the future.
[Mh] Termos MeSH primário: Antivirais/farmacologia
Ciclo-Oxigenase 2/metabolismo
Enterovirus Humano A/efeitos dos fármacos
Infecções por Enterovirus/genética
Isoflavonas/farmacologia
Prostaglandinas E/metabolismo
Replicação Viral/efeitos dos fármacos
[Mh] Termos MeSH secundário: Ciclo-Oxigenase 2/genética
Enterovirus Humano A/fisiologia
Infecções por Enterovirus/enzimologia
Infecções por Enterovirus/metabolismo
Infecções por Enterovirus/virologia
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antiviral Agents); 0 (Isoflavones); 0 (Prostaglandins E); 295DQC67BJ (formononetin); EC 1.14.99.1 (Cyclooxygenase 2)
[Em] Mês de entrada:1601
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150419
[St] Status:MEDLINE
[do] DOI:10.1186/s12985-015-0264-x


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[PMID]:25751734
[Au] Autor:Guo L; Chen Z; Amarnath V; Yancey PG; Van Lenten BJ; Savage JR; Fazio S; Linton MF; Davies SS
[Ad] Endereço:1Division of Clinical Pharmacology, Vanderbilt University at Nashville, Nashville, Tennessee.
[Ti] Título:Isolevuglandin-type lipid aldehydes induce the inflammatory response of macrophages by modifying phosphatidylethanolamines and activating the receptor for advanced glycation endproducts.
[So] Source:Antioxid Redox Signal;22(18):1633-45, 2015 Jun 20.
[Is] ISSN:1557-7716
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:AIMS: Increased lipid peroxidation occurs in many conditions associated with inflammation. Because lipid peroxidation produces lipid aldehydes that can induce inflammatory responses through unknown mechanisms, elucidating these mechanisms may lead to development of better treatments for inflammatory diseases. We recently demonstrated that exposure of cultured cells to lipid aldehydes such as isolevuglandins (IsoLG) results in the modification of phosphatidylethanolamine (PE). We therefore sought to determine (i) whether PE modification by isolevuglandins (IsoLG-PE) occurred in vivo, (ii) whether IsoLG-PE stimulated the inflammatory responses of macrophages, and (iii) the identity of receptors mediating the inflammatory effects of IsoLG-PE. RESULTS: IsoLG-PE levels were elevated in plasma of patients with familial hypercholesterolemia and in the livers of mice fed a high-fat diet to induce obesity and hepatosteatosis. IsoLG-PE potently stimulated nuclear factor kappa B (NFκB) activation and expression of inflammatory cytokines in macrophages. The effects of IsoLG-PE were blocked by the soluble form of the receptor for advanced glycation endproducts (sRAGE) and by RAGE antagonists. Furthermore, macrophages derived from the bone marrow of Ager null mice failed to express inflammatory cytokines in response to IsoLG-PE to the same extent as macrophages from wild-type mice. INNOVATION: These studies are the first to identify IsoLG-PE as a mediator of macrophage activation and a specific receptor, RAGE, which mediates its biological effects. CONCLUSION: PE modification by IsoLG forms RAGE ligands that activate macrophages, so that the increased IsoLG-PE generated by high circulating cholesterol levels or high-fat diet may play a role in the inflammation associated with these conditions.
[Mh] Termos MeSH primário: Aldeídos/metabolismo
Inflamação/metabolismo
Macrófagos/metabolismo
Fosfatidiletanolaminas/metabolismo
Prostaglandinas E/química
Pirrolidinas/química
Receptor para Produtos Finais de Glicação Avançada/genética
Receptor para Produtos Finais de Glicação Avançada/metabolismo
[Mh] Termos MeSH secundário: Animais
Seres Humanos
Lipídeos/química
Masculino
Camundongos Endogâmicos C57BL
Camundongos Knockout
NF-kappa B/metabolismo
Fosfatidiletanolaminas/química
Receptor para Produtos Finais de Glicação Avançada/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Aldehydes); 0 (Lipids); 0 (NF-kappa B); 0 (Phosphatidylethanolamines); 0 (Prostaglandins E); 0 (Pyrrolidines); 0 (Receptor for Advanced Glycation End Products); 39382-08-6 (phosphatidylethanolamine)
[Em] Mês de entrada:1602
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150310
[St] Status:MEDLINE
[do] DOI:10.1089/ars.2014.6078



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