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[PMID]:29348072
[Au] Autor:Liu C; Chen X; Zhi X; Weng W; Li Q; Li X; Zou Y; Su J; Hu HG
[Ad] Endereço:Department of Organic Chemistry, College of Pharmacy, Second Military Medical University, Shanghai 200433, China.
[Ti] Título:Structure-based development of an osteoprotegerin-like glycopeptide that blocks RANKL/RANK interactions and reduces ovariectomy-induced bone loss in mice.
[So] Source:Eur J Med Chem;145:661-672, 2018 Feb 10.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:Osteoporosis is a metabolic bone disease characterized by low bone mass and micro-architectural deterioration of bone, for which the underlying mechanism is an imbalance between bone resorption and bone remodeling. The protein-protein interactions between receptor activator of nuclear factor-κB ligand (RANKL), RANK (its receptor), and osteoprotegerin (OPG), are known to mediate the development and activation of osteoclasts in bone remodeling, and are regarded as a pivotal therapeutic target for the treatment of osteoporosis. Herein, we disclose the successful development of a novel glycopeptide (OM-2), the structure of which is based on the key interacting sites of the reported RANKL and OPG crystal structure. OM-2 exhibited potent binding affinity with RANKL and resistance to degradation by protease enzymes. It also blocked RANKL/RANK interactions, and inhibited osteoclastogenesis in vitro. In vivo studies confirmed that OM-2 could effectively reduce bone loss and inhibit osteoclast activation in ovariectomized (OVX) mice at a dosage of 20.0 mg/kg/day. Accordingly, OM-2 is suggested as a therapeutic candidate for postmenopausal osteoporosis (PMOP) and osteoclastogenesis-related diseases like rheumatoid arthritis (RA). More importantly, its identification validates our structure-based strategy for the development of drugs that target the RANKL/RANK/OPG system.
[Mh] Termos MeSH primário: Glicopeptídeos/farmacologia
Osteoporose/tratamento farmacológico
Osteoprotegerina/farmacologia
Ovariectomia
Ligante RANK/antagonistas & inibidores
Receptores Citoplasmáticos e Nucleares/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Osso e Ossos/efeitos dos fármacos
Osso e Ossos/metabolismo
Osso e Ossos/patologia
Relação Dose-Resposta a Droga
Feminino
Glicopeptídeos/síntese química
Glicopeptídeos/química
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Simulação de Acoplamento Molecular
Estrutura Molecular
Osteoporose/metabolismo
Osteoprotegerina/química
Ligação Proteica/efeitos dos fármacos
Ligante RANK/metabolismo
Receptores Citoplasmáticos e Nucleares/metabolismo
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glycopeptides); 0 (Osteoprotegerin); 0 (RANK Ligand); 0 (Receptors, Cytoplasmic and Nuclear)
[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:180120
[St] Status:MEDLINE


  2 / 6222 MEDLINE  
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[PMID]:29340518
[Au] Autor:Zhang X; Song Y; Song N; Zhang L; Wang Y; Li D; Wang Z; Qu X; Liu Y
[Ad] Endereço:Department of Medical Oncology, The First Hospital of China Medical University, Shenyang, China.
[Ti] Título:Rankl expression predicts poor prognosis in gastric cancer patients: results from a retrospective and single-center analysis.
[So] Source:Braz J Med Biol Res;51(3):e6265, 2018 Jan 11.
[Is] ISSN:1414-431X
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:The receptor activator of nuclear factor κB ligand (RANKL)/RANK pathway plays an important role in the prognosis of several solid tumor types, but its role in gastric cancer prognosis has been poorly characterized. A total of 116 gastric cancer patients who underwent surgical resection were enrolled in this study. Expressions of RANKL and RANK in gastric cancer tissues were detected using immunohistochemical staining. Thirty-eight patients (33%) showed a high level of RANKL expression and 61 patients (53%) showed a high level of RANK expression. There was a positive correlation between expressions of RANKL and RANK (P=0.014, r=0.221). A high level of RANKL expression indicated shorter overall survival (OS) (P=0.008), and was associated with a higher pathological tumor/lymph node/metastasis (pTNM) stage (P=0.035), while no significant correlation was detected between RANK expression and clinicopathological parameters. RANKL also predicted poor prognosis in patients with high RANK expression (P=0.008) and Bormann's type III/IV (P=0.002). Furthermore, RANKL expression correlated with pTNM stage according to high RANK expression (P=0.009), while no significance was found in patients with low RANK expression (P=1.000). Together, our results revealed that high expression of RANKL could predict worse outcomes in gastric cancer especially combined with RANK detection, and thereby this pathway could be a useful prognostic indicator of gastric cancer.
[Mh] Termos MeSH primário: Adenocarcinoma/metabolismo
Proteínas de Neoplasias/metabolismo
Ligante RANK/metabolismo
Neoplasias Gástricas/metabolismo
[Mh] Termos MeSH secundário: Adenocarcinoma/mortalidade
Adenocarcinoma/patologia
Adenocarcinoma/cirurgia
China/epidemiologia
Feminino
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Imuno-Histoquímica
Masculino
Meia-Idade
Gradação de Tumores
Estadiamento de Neoplasias
Prognóstico
Estudos Retrospectivos
Estatísticas não Paramétricas
Neoplasias Gástricas/mortalidade
Neoplasias Gástricas/patologia
Neoplasias Gástricas/cirurgia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Neoplasm Proteins); 0 (RANK Ligand); 0 (TNFSF11 protein, human)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180118
[St] Status:MEDLINE


  3 / 6222 MEDLINE  
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[PMID]:29441931
[Au] Autor:Li N; Tu Y; Shen Y; Qin Y; Lei C; Liu X
[Ti] Título:Calycosin attenuates osteoporosis and regulates the expression of OPG/RANKL in ovariectomized rats MAPK signaling.
[So] Source:Pharmazie;71(10):607-612, 2016 Oct 01.
[Is] ISSN:0031-7144
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:We aimed at exploring the effect of calycosin (CA) on osteoporosis in ovariectomized (OVX) rats. Sprague-Dawley (SD) rats were divided into five groups: Sham group, OVX group, OVX group treated with estradiol valerate (EV), CAL group treated with 15 mg/kg/d of CA and CAH group treated with 30 mg/kg/d of CA for 12 weeks. Bone mineral density (BMD), histopathology, body weight, parameters in serum and urine were observed. Gene expression and protein level of OPG/RANKL were also studied by real-time PCR and western blot, respectively. We further identified the effect of CA on mitogen-activated protein kinase (MAPK) signaling. In comparison with OVX rats, CAL and CAH significantly increased the BMD by 8.3% and 19.0%. Treatment with CA notably inhibited the excretion of Ca, P and Cr. CAH also significantly increased the level of alkaline phosphatase (ALP) and decreased the level of tartrate-resistant acid phosphatase (TRAP) in serum of OVX rats. CA could improve the trabecular bone area, and increased the trabecular number and the trabecular connection after 12-week. CA also increased the expression of osteoprotegerin (OPG) and decreased the Receptor Activator for Nuclear Factor-κB Ligand (RANKL) mRNA expression compared with the OVX rats. In addition, CA could effectively decrease the phosphorylation of MAPKs induced by ovariectomy. In conclusion, CA had remarkable antiosteoporotic activity and therefore can be a promising candidate for the treatment of postmenopausal osteoporosis.
[Mh] Termos MeSH primário: Conservadores da Densidade Óssea/uso terapêutico
Isoflavonas/uso terapêutico
Proteínas Quinases Ativadas por Mitógeno/efeitos dos fármacos
Osteoporose/tratamento farmacológico
Osteoprotegerina/genética
Ligante RANK/genética
Transdução de Sinais/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Densidade Óssea/efeitos dos fármacos
Conservadores da Densidade Óssea/farmacologia
Reabsorção Óssea/prevenção & controle
Feminino
Regulação da Expressão Gênica/efeitos dos fármacos
Proteínas de Choque Térmico HSP90/biossíntese
Proteínas de Choque Térmico HSP90/genética
Isoflavonas/farmacologia
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Osteoporose/genética
Osteoprotegerina/biossíntese
Ovariectomia
Fosforilação
Ligante RANK/biossíntese
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bone Density Conservation Agents); 0 (HSP90 Heat-Shock Proteins); 0 (Isoflavones); 0 (Osteoprotegerin); 0 (RANK Ligand); 0 (TRAP1 protein, rat); 0 (Tnfrsf11b protein, rat); 09N3E8P7TA (7,3'-dihydroxy-4'-methoxyisoflavone); EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
[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.2016.6627


  4 / 6222 MEDLINE  
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[PMID]:29211284
[Au] Autor:Öncel Torun Z; Torun D; Baykal B; Öztuna A; Yesildal F; Avcu F
[Ad] Endereço:Balgat Oral and Dental Health Center, Ankara, Turkey.
[Ti] Título:Effects of triethylene glycol dimethacrylate (TEGDMA) on the odontoclastic differentiation ability of human dental pulp cells.
[So] Source:J Appl Oral Sci;25(6):631-640, 2017 Nov-Dec.
[Is] ISSN:1678-7765
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: The primary purpose of this study was to examine the effects of triethylene glycol dimethacrylate (TEGDMA) on odontoclastic differentiation in the dental pulp tissue. MATERIAL AND METHODS: The effects of different TEGDMA dosages on the odontoclastic differentiation capability of dental pulp cells were analyzed in vitro using the following methodologies: i) flow cytometry and tartrate-resistant acid phosphatase (TRAP) staining; ii) apoptotic effects using Annexin V staining; iii) mRNA expression of osteoprotegerin (OPG) and receptor activator of nuclear factor (NF)-kB ligand (RANKL) genes by quantitative Real-time PCR (qRT-PCR); and iv) OPG and RANKL protein expression by enzyme-linked immunosorbent assay (ELISA). RESULTS: TEGDMA caused relatively less odontoclastic differentiation in comparison with the control group; however, odontoclastic differentiation augmented with increasing doses of TEGDMA (p<0.05). The mRNA and protein expression of OPG was lower in TEGDMA treated pulp cells than in the control group (p<0.05). While the mRNA expression of RANKL remained unchanged compared to the control group (p>0.05), its protein expression was higher than the control group (p<0.05). In addition, TEGDMA increased the apoptosis of dental pulp cells dose dependently. CONCLUSIONS: TEGDMA reduced the odontoclastic differentiation ability of human dental pulp cells. However, odontoclastic differentiation ratios increased proportionally with the increasing dose of TEGDMA.
[Mh] Termos MeSH primário: Diferenciação Celular/efeitos dos fármacos
Polpa Dentária/efeitos dos fármacos
Polietilenoglicóis/farmacologia
Ácidos Polimetacrílicos/farmacologia
Fosfatase Ácida Resistente a Tartarato/efeitos dos fármacos
[Mh] Termos MeSH secundário: Polpa Dentária/citologia
Ensaio de Imunoadsorção Enzimática
Citometria de Fluxo
Seres Humanos
Receptores de Lipopolissacarídeos/metabolismo
Ligante RANK/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Lipopolysaccharide Receptors); 0 (Polymethacrylic Acids); 0 (RANK Ligand); 14I47YJ5EY (triethylene glycol dimethacrylate); 30IQX730WE (Polyethylene Glycols); EC 3.1.3.2 (Tartrate-Resistant Acid Phosphatase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:D; IM
[Da] Data de entrada para processamento:171207
[St] Status:MEDLINE


  5 / 6222 MEDLINE  
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[PMID]:28455312
[Au] Autor:Lopes N; Vachon H; Marie J; Irla M
[Ad] Endereço:Centre d'Immunologie de Marseille-Luminy, Aix Marseille Université, INSERM, CNRS, Marseille Cedex 09, France.
[Ti] Título:Administration of RANKL boosts thymic regeneration upon bone marrow transplantation.
[So] Source:EMBO Mol Med;9(6):835-851, 2017 Jun.
[Is] ISSN:1757-4684
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Cytoablative treatments lead to severe damages on thymic epithelial cells (TECs), which result in delayed thymopoiesis and a prolonged period of T-cell immunodeficiency. Understanding the mechanisms that govern thymic regeneration is of paramount interest for the recovery of a functional immune system notably after bone marrow transplantation (BMT). Here, we show that RANK ligand (RANKL) is upregulated in CD4 thymocytes and lymphoid tissue inducer (LTi) cells during the early phase of thymic regeneration. Importantly, whereas RANKL neutralization alters TEC recovery after irradiation, RANKL administration during BMT boosts the regeneration of TEC subsets including thymic epithelial progenitor-enriched cells, thymus homing of lymphoid progenitors, and thymopoiesis. RANKL increases specifically in LTi cells, lymphotoxin α, which is critical for thymic regeneration. RANKL treatment, dependent on lymphotoxin α, is beneficial upon BMT in young and aged individuals. This study thus indicates that RANKL may be clinically useful to improve T-cell function recovery after BMT by controlling multiple facets of thymic regeneration.
[Mh] Termos MeSH primário: Transplante de Medula Óssea/efeitos adversos
Células Epiteliais/fisiologia
Ligante RANK/administração & dosagem
Radioterapia/efeitos adversos
Regeneração
Timo/fisiologia
[Mh] Termos MeSH secundário: Animais
Linfotoxina-alfa/metabolismo
Camundongos
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Lymphotoxin-alpha); 0 (RANK Ligand)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180219
[Lr] Data última revisão:
180219
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170430
[St] Status:MEDLINE
[do] DOI:10.15252/emmm.201607176


  6 / 6222 MEDLINE  
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[PMID]:29269297
[Au] Autor:Wang J; Fu B; Lu F; Hu X; Tang J; Huang L
[Ad] Endereço:Department of Orthopaedic Surgery, The First Affiliated Hospital of Soochow University, Suzhou 215006, China; Department of Orthopaedic Surgery, Huai'an Second People's Hospital, The Affiliated Huaian Hospital of Xuzhou Medical University, Huai'an 223000, China.
[Ti] Título:Inhibitory activity of linarin on osteoclastogenesis through receptor activator of nuclear factor κB ligand-induced NF-κB pathway.
[So] Source:Biochem Biophys Res Commun;495(3):2133-2138, 2018 01 15.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Linarin, a natural flavonoid glycoside widely found in plants, has been reported to possess anti-inflammation, neuroprotection and osteogenic properties. However, its impact on osteoclast remains unclear. In the present study, the effects of linarin on osteoclastogenesis and its underlying molecular mechanisms of action were investigated. Using the culture systems of osteoclasts derived from bone marrow macrophages (BMMs), we found that linarin dose-dependently inhibited osteoclasts formation and bone resorptive activity. The Cell Counting Kit-8 test displayed that the viability of cells was not influenced by linarin at doses up to 10 µg/mL. In addition, linarin downregulated osteoclast-related genes expression, including nuclear factor of activated T cells cytoplasmic 1 (NFATc1), tartrate resistant acid phosphatase (TRAP), osteoclast-associated receptor (OSCAR) and c-Fos, as shown by quantitative real time polymerase chain reaction (RT-qPCR). Western blot analysis further showed that linarin inhibited receptor activator of nuclear factor κB ligand (RANKL)-induced nuclear factor kappa B (NF-κB) p65 and NFATc1 activity. The present findings show that linarin exerted a potent inhibitory effect on osteoclastogenesis through RANKL-induced NF-κB signaling pathway. In conclusion, the results suggest that linarin has anti-osteoclastic effects and may serve as potential modulatory agents for the prevention and treatment of bone loss-associated diseases.
[Mh] Termos MeSH primário: Glicosídeos/administração & dosagem
NF-kappa B/metabolismo
Osteoblastos/efeitos dos fármacos
Osteoblastos/metabolismo
Osteogênese/fisiologia
Ligante RANK/metabolismo
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Relação Dose-Resposta a Droga
Macrófagos/citologia
Macrófagos/efeitos dos fármacos
Macrófagos/fisiologia
Camundongos
Camundongos Endogâmicos C57BL
Osteoblastos/citologia
Osteogênese/efeitos dos fármacos
Células RAW 264.7
Transdução de Sinais/efeitos dos fármacos
Transdução de Sinais/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glycosides); 0 (NF-kappa B); 0 (RANK Ligand); 0 (TNFSF11 protein, human); HBH2I685IU (linarin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171223
[St] Status:MEDLINE


  7 / 6222 MEDLINE  
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[PMID]:28458359
[Au] Autor:Takeda H; Tominari T; Hirata M; Watanabe K; Matsumoto C; Grundler FMW; Inada M; Miyaura C
[Ad] Endereço:Cooperative Major of Advanced Health Science, Tokyo University of Agriculture and Technology.
[Ti] Título:Lutein Enhances Bone Mass by Stimulating Bone Formation and Suppressing Bone Resorption in Growing Mice.
[So] Source:Biol Pharm Bull;40(5):716-721, 2017.
[Is] ISSN:1347-5215
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Lutein is a member of the xanthophyll family of carotenoids, which are known to prevent hypoxia-induced cell damage in the eye by removing free radicals. However, its role in other tissues is controversial, and the effects of lutein on bone tissues are unknown. To identify a possible role of lutein in bone tissues, we examined the effects of lutein on bone formation and bone resorption and on femoral bone mass in mice. Lutein enhanced the formation of mineralized bone nodules in cultures of osteoblasts. On the other hand, lutein clearly suppressed 1α, 25-dihydroxyvitamin D -induced bone resorption as measured by pit formation in organ culture of mouse calvaria. In co-cultures of bone marrow cells and osteoblasts, lutein suppressed 1α, 25-dihydroxyvitamin D -induced osteoclast formation. In cultures of bone marrow macrophages, lutein suppressed soluble RANKL, the receptor activator of nuclear factor-kappaB (NF-κB) ligand, induced osteoclast formation. When five-week-old male mice were orally administered lutein for 4 weeks, the femoral bone mass was clearly enhanced in cortical bone, as measured by bone mineral density in dual X-ray absorptiometry and micro computed tomography (µCT) analyses. The present study indicates that lutein enhances bone mass in growing mice by suppressing bone resorption and stimulating bone formation. Lutein may be a natural agent that promotes bone turnover and may be beneficial for bone health in humans.
[Mh] Termos MeSH primário: Desenvolvimento Ósseo/efeitos dos fármacos
Reabsorção Óssea/prevenção & controle
Osso e Ossos/anatomia & histologia
Luteína/farmacologia
[Mh] Termos MeSH secundário: Absorciometria de Fóton
Animais
Densidade Óssea/efeitos dos fármacos
Osso e Ossos/diagnóstico por imagem
Calcificação Fisiológica/efeitos dos fármacos
Calcitriol/antagonistas & inibidores
Calcitriol/farmacologia
Células Cultivadas
Fêmur/anatomia & histologia
Fêmur/efeitos dos fármacos
Luteína/uso terapêutico
Masculino
Camundongos
NF-kappa B/antagonistas & inibidores
Osteoblastos/efeitos dos fármacos
Ligante RANK/antagonistas & inibidores
Tomografia Computadorizada por Raios X
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (NF-kappa B); 0 (RANK Ligand); 0 (Tnfsf11 protein, mouse); FXC9231JVH (Calcitriol); X72A60C9MT (Lutein)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE
[do] DOI:10.1248/bpb.b16-00897


  8 / 6222 MEDLINE  
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[PMID]:28458348
[Au] Autor:Lee DI; Jang SK; Park DW; Kim ST; Park JS; Jo BR; Park JY; Park HY; Joo SS
[Ad] Endereço:College of Pharmacy, Chung-Ang University.
[Ti] Título:Diarylheptanoid Hirsutenone Attenuates Osteoclastogenesis by Suppressing IFNγ and NF-κB Signaling in Th1 and Preosteoclastic Cells.
[So] Source:Biol Pharm Bull;40(5):630-637, 2017.
[Is] ISSN:1347-5215
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:The aim of the present study was to examine the inhibitory roles and mechanisms of hirsutenone (HTN) in the regulation of osteoclastogenesis. Gene levels were compared to assure the effects of HTN on osteoclastogenesis in mouse splenocytes/CD4 T cells, mouse macrophage-like cell line RAW264.7 (preosteoclast), MG63 (osteoblast), and RPMI1788 (B cell) cells. The mechanism by which HTN regulates the degradation of tumor necrosis factor receptor-associated factor 6 (TRAF6) and inhibits inhibitor of kappaB (IκB) and nuclear factor-kappaB (NF-κB) signaling was examined by Western blotting and luciferase reporter assays. Our results demonstrated that HTN effectively downregulated the expression of interferon γ (IFNγ), interleukin-22 (IL-22), IL-1ß, and tartrate-resistant acid phosphatase (TRAP) in splenocyte-/CD4 -RAW264.7 co-culture system. Moreover, receptor activator of nuclear factor-κB ligand (RANKL) and CD25 expression were also significantly inhibited in MG63 and CD4 single culture system, suggesting an additional independent effect of HTN on osteoclastogenesis. Notably, TRAF6 was markedly degraded along with a decrease in nuclear factor of activated T-cells (NFATc) and NF-κB activities in RAW264.7 cells. Finally, we concluded that HTN directly or indirectly inhibits osteoclastogenesis via the inhibition of NF-κB signaling by promoting TRAF6 degradation, and plays a crucial role in suppressing the expression of RANKL and cytokines expressed in IFNγ-producing T-helper 1 (Th1) cells. These findings suggest that HTN may be a promising therapeutic candidate for diseases resulting from bone loss.
[Mh] Termos MeSH primário: Catecóis/farmacologia
Diarileptanoides/farmacologia
Interferon gama/antagonistas & inibidores
NF-kappa B/antagonistas & inibidores
Osteoclastos/efeitos dos fármacos
Células Th1/efeitos dos fármacos
[Mh] Termos MeSH secundário: Alnus/química
Animais
Linfócitos T CD4-Positivos/metabolismo
Sobrevivência Celular/efeitos dos fármacos
Citocinas/antagonistas & inibidores
Citocinas/farmacologia
Camundongos
Camundongos Endogâmicos BALB C
Osteogênese/efeitos dos fármacos
Casca de Planta/química
Ligante RANK/genética
Células RAW 264.7
Transdução de Sinais/efeitos dos fármacos
Baço/química
Baço/citologia
Células-Tronco/efeitos dos fármacos
Fosfatase Ácida Resistente a Tartarato/biossíntese
Fosfatase Ácida Resistente a Tartarato/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Catechols); 0 (Cytokines); 0 (Diarylheptanoids); 0 (NF-kappa B); 0 (RANK Ligand); 0 (Tnfsf11 protein, mouse); 0 (hirsutenone); 82115-62-6 (Interferon-gamma); EC 3.1.3.2 (Acp5 protein, mouse); EC 3.1.3.2 (Tartrate-Resistant Acid Phosphatase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE
[do] DOI:10.1248/bpb.b16-00876


  9 / 6222 MEDLINE  
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[PMID]:29025654
[Au] Autor:Cheng Z; Landish B; Chi Z; Nannan C; Jingyu D; Sen L; Xiangjin L
[Ad] Endereço:Department of Orthopaedic Orthopaedics, First Affiliated Hospital, College of Medicine, Zhejiang University, Qingchun Road 79, Hangzhou 310003, People's Republic of China; The Sport Medicine Center of the First Affiliated Hospital, College of Medicine, Zhejiang University, Qingchun Road 79, Hangzhou
[Ti] Título:3D printing hydrogel with graphene oxide is functional in cartilage protection by influencing the signal pathway of Rank/Rankl/OPG.
[So] Source:Mater Sci Eng C Mater Biol Appl;82:244-252, 2018 Jan 01.
[Is] ISSN:1873-0191
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:3Dprinting is defined as the use of printing technology to deposit living cells, and biomaterials on a given /a substrate. Graphene oxide nanoparticles (GO-np) have been used as a delivery vehicle for small molecule drugs in order to investigate the state of GO-np within 3D tissue constructs in terms of a composite 3D printing scaffold, which in turn is relevant to the protection of cartilage. We transplanted rats with hydrogel/GO-np and hydrogel, which in turn showed that hydrogel/GO-np protected the tissue of cartilage by the signal pathway of Rank/Rankl/OPG. Those findings indicated that GO-np may be potentially used to control the release of carrier materials and influence the signal pathway of Rank/Rankl/OPG.
[Mh] Termos MeSH primário: Materiais Biocompatíveis/química
Cartilagem/metabolismo
Grafite/química
Hidrogéis/química
Osteoprotegerina/metabolismo
Ligante RANK/metabolismo
Receptor Ativador de Fator Nuclear kappa-B/metabolismo
[Mh] Termos MeSH secundário: Animais
Materiais Biocompatíveis/farmacologia
Proteína Morfogenética Óssea 7/química
Proteína Morfogenética Óssea 7/metabolismo
Proteína Morfogenética Óssea 7/farmacologia
Cartilagem/efeitos dos fármacos
Linhagem Celular
Sobrevivência Celular/efeitos dos fármacos
Condrócitos/citologia
Condrócitos/efeitos dos fármacos
Condrócitos/metabolismo
Portadores de Fármacos/química
Seres Humanos
Masculino
Nanopartículas/química
Óxidos/química
Ratos
Ratos Sprague-Dawley
Transdução de Sinais/efeitos dos fármacos
Tecidos Suporte/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biocompatible Materials); 0 (Bone Morphogenetic Protein 7); 0 (Drug Carriers); 0 (Hydrogels); 0 (Osteoprotegerin); 0 (Oxides); 0 (RANK Ligand); 0 (Receptor Activator of Nuclear Factor-kappa B); 7782-42-5 (Graphite)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180205
[Lr] Data última revisão:
180205
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171014
[St] Status:MEDLINE


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[PMID]:29238019
[Au] Autor:Yokota K
[Ad] Endereço:Department of Rheumatology and Applied Immunology, Faculty of Medicine, Saitama Medical University.
[Ti] Título:[Inflammation and osteoclasts].
[So] Source:Nihon Rinsho Meneki Gakkai Kaishi;40(5):367-376, 2017.
[Is] ISSN:1349-7413
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Ab] Resumo:  Osteoclasts are differentiated from precursors of the monocyte/macrophage lineage originated from bone marrow hematopoietic stem cells and are the sole bone-resorbing cells in the body. Osteoclast differentiation is thought to require M-CSF (macrophage colony-stimulating factor) and RANKL (receptor activator of nuclear factor kappa-B ligand) signaling. However, it has recently been proposed that under chronic inflammatory conditions, such as systemic autoimmune diseases (e.g., rheumatoid arthritis), an increase in inflammatory cytokine levels within joints induces pathological osteoclast differentiation, causing excessive bone resorption. In addition, the authors have reported that stimulating mouse bone marrow monocytes and human CD14 monocytes with combination of TNFα and IL-6 can induce differentiation of osteoclast-like cells, which are cells with bone resorption activity. In the present article, we discuss the mechanism of osteoclast differentiation of RANKL-independent bone-resorbing cells, using both data from the aforementioned report as well as the latest findings. Understanding the mechanisms underlying RANKL-independent, cytokine-mediated osteoclast differentiation could facilitate the development of novel therapies for inflammatory joint diseases.
[Mh] Termos MeSH primário: Diferenciação Celular/genética
Inflamação/etiologia
Inflamação/patologia
Osteoclastos/citologia
Osteoclastos/fisiologia
[Mh] Termos MeSH secundário: Animais
Artrite Reumatoide/etiologia
Artrite Reumatoide/patologia
Reabsorção Óssea/etiologia
Citocinas/fisiologia
Descoberta de Drogas
Seres Humanos
Mediadores da Inflamação/fisiologia
Interleucina-6/fisiologia
Fator Estimulador de Colônias de Macrófagos
Camundongos
Terapia de Alvo Molecular
Osteoclastos/patologia
Ligante RANK/fisiologia
Transdução de Sinais/fisiologia
Fator de Necrose Tumoral alfa/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Cytokines); 0 (Inflammation Mediators); 0 (Interleukin-6); 0 (RANK Ligand); 0 (Tumor Necrosis Factor-alpha); 81627-83-0 (Macrophage Colony-Stimulating Factor)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180112
[Lr] Data última revisão:
180112
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171215
[St] Status:MEDLINE
[do] DOI:10.2177/jsci.40.367



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