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[PMID]:29172693
[Au] Autor:Ojeda-Montes MJ; Ardid-Ruiz A; Tomás-Hernández S; Gimeno A; Cereto-Massagué A; Beltrán-Debón R; Mulero M; Garcia-Vallvé S; Pujadas G; Valls C
[Ad] Endereço:Research group in Cheminformatics & Nutrition, Departament de Bioquímica i Biotecnologia, Universitat Rovira i Virgili, Campus de Sescelades, Tarragona, Catalonia 43007, Spain.
[Ti] Título:Ephedrine as a lead compound for the development of new DPP-IV inhibitors.
[So] Source:Future Med Chem;9(18):2129-2146, 2017 12.
[Is] ISSN:1756-8927
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:AIM: Extracts from Ephedra species have been reported to be effective as antidiabetics. A previous in silico study predicted that ephedrine and five ephedrine derivatives could contribute to the described antidiabetic effect of Ephedra extracts by inhibiting dipeptidyl peptidase IV (DPP-IV). Finding selective DPP-IV inhibitors is a current therapeutic strategy for Type 2 diabetes mellitus management. Therefore, the main aim of this work is to experimentally determine whether these alkaloids are DPP-IV inhibitors. Materials & methods: The DPP-IV inhibition of Ephedra's alkaloids was determined via a competitive-binding assay. Then, computational analyses were used in order to find out the protein-ligand interactions and to perform a lead optimization. RESULTS: Our results show that all six molecules are DPP-IV inhibitors, with IC ranging from 124 µM for ephedrine to 28 mM for N-methylpseudoephedrine. CONCLUSION: Further computational analysis shows how Ephedra's alkaloids could be used as promising lead molecules for designing more potent and selective DPP-IV inhibitors.
[Mh] Termos MeSH primário: Dipeptidil Peptidase 4/metabolismo
Inibidores da Dipeptidil Peptidase IV/química
Efedrina/análogos & derivados
Hipoglicemiantes/química
[Mh] Termos MeSH secundário: Alcaloides/química
Alcaloides/metabolismo
Sítios de Ligação
Ligação Competitiva
Dipeptidil Peptidase 4/química
Desenho de Drogas
Ephedra/química
Ephedra/metabolismo
Efedrina/metabolismo
Hipoglicemiantes/metabolismo
Concentração Inibidora 50
Simulação de Acoplamento Molecular
Fenilpropanolamina/química
Extratos Vegetais/química
Isoformas de Proteínas/antagonistas & inibidores
Isoformas de Proteínas/metabolismo
Estrutura Terciária de Proteína
Estereoisomerismo
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Alkaloids); 0 (Dipeptidyl-Peptidase IV Inhibitors); 0 (Hypoglycemic Agents); 0 (Plant Extracts); 0 (Protein Isoforms); 33RU150WUN (Phenylpropanolamine); EC 3.4.14.5 (Dipeptidyl Peptidase 4); GN83C131XS (Ephedrine)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE
[do] DOI:10.4155/fmc-2017-0080


  2 / 3309 MEDLINE  
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[PMID]:29374928
[Au] Autor:Song CL; Yao M
[Ad] Endereço:Department of Plastic Surgery and Burns, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 201900, China.
[Ti] Título:[Advances in the research of relationship between CD26 and hypertrophic scar and keloid].
[So] Source:Zhonghua Shao Shang Za Zhi;34(1):54-56, 2018 Jan 20.
[Is] ISSN:1009-2587
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:In recent years, researchers have found that CD26 (dipeptidyl peptidase 4) is closely related to the formation and development of many fibrotic diseases. Hypertrophic scar, keloid, and other skin fibrosis diseases are major problems nowadays, which may affect the patient's appearance and cause joints deformity and dysfunction due to scar contracture. This article briefly reviews the relationship between CD26 and hypertrophic scar and keloid to provide new insights into the treatment of skin fibrotic diseases.
[Mh] Termos MeSH primário: Cicatriz Hipertrófica/patologia
Dipeptidil Peptidase 4/metabolismo
Queloide/patologia
[Mh] Termos MeSH secundário: Fibrose
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
EC 3.4.14.5 (DPP4 protein, human); EC 3.4.14.5 (Dipeptidyl Peptidase 4)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180129
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.1009-2587.2018.01.011


  3 / 3309 MEDLINE  
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[PMID]:29249634
[Au] Autor:Hirose M; Takano H; Hasegawa H; Tadokoro H; Hashimoto N; Takemura G; Kobayashi Y
[Ad] Endereço:Department of Cardiovascular Medicine, Chiba University Graduate School of Medicine, Chiba 260-8670, Japan.
[Ti] Título:The effects of dipeptidyl peptidase-4 on cardiac fibrosis in pressure overload-induced heart failure.
[So] Source:J Pharmacol Sci;135(4):164-173, 2017 Dec.
[Is] ISSN:1347-8648
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Dipeptidyl peptidase-4 (DPP-4) inhibitors are hypoglycemic agents. DPP-4 inhibitor has cardioprotective effects after transverse aortic constriction (TAC), but role of DPP-4 on cardiac fibrosis after TAC is not well known. Our aim was to determine the effects of DPP-4 on cardiac fibrosis in murine TAC model. Wild-type mice and DPP-4 knockout mice were subjected to TAC. Wild-type mice were then treated with vehicle or DPP-4 inhibitor. DPP-4 activities in serum and heart tissue were significantly increased at 2 weeks after TAC, but they were significantly decreased by DPP-4 inhibitor treatment. The inhibition of DPP-4 did not affect left ventricular hypertrophy, but improved cardiac function and decreased myocardial and perivascular fibrosis after TAC. The inhibition of DPP-4 decreased the collagen type III/I ratio in myocardium. These results suggest that DPP-4 inhibition ameliorates the progression of heart failure after TAC by changing the quality and quantity of cardiac fibrosis.
[Mh] Termos MeSH primário: Cardiotônicos
Dipeptidil Peptidase 4/fisiologia
Inibidores da Dipeptidil Peptidase IV/farmacologia
Inibidores da Dipeptidil Peptidase IV/uso terapêutico
Insuficiência Cardíaca/tratamento farmacológico
Insuficiência Cardíaca/etiologia
Miocárdio/patologia
[Mh] Termos MeSH secundário: Animais
Aorta
Estenose da Valva Aórtica/complicações
Colágeno Tipo I/metabolismo
Colágeno Tipo III/metabolismo
Constrição Patológica
Dipeptidil Peptidase 4/metabolismo
Modelos Animais de Doenças
Fibrose
Insuficiência Cardíaca/patologia
Hipertensão/complicações
Hipertrofia
Masculino
Camundongos Endogâmicos C57BL
Miocárdio/metabolismo
Pressão
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cardiotonic Agents); 0 (Collagen Type I); 0 (Collagen Type III); 0 (Dipeptidyl-Peptidase IV Inhibitors); EC 3.4.14.5 (Dipeptidyl Peptidase 4)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171219
[St] Status:MEDLINE


  4 / 3309 MEDLINE  
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[PMID]:29308856
[Au] Autor:Tyurenkov IN; Bakulin DA; Kurkin DV; Volotova EV
[Ti] Título:Cardiovascular Effects of Incretin-Based Therapies and Their Therapeutic Potential.
[So] Source:Vestn Ross Akad Med Nauk;72(1):66-75, 2017.
[Is] ISSN:0869-6047
[Cp] País de publicação:Russia (Federation)
[La] Idioma:eng
[Mh] Termos MeSH primário: Sistema Cardiovascular
Diabetes Mellitus Tipo 2
Inibidores da Dipeptidil Peptidase IV
Receptor do Peptídeo Semelhante ao Glucagon 1/agonistas
Incretinas/metabolismo
[Mh] Termos MeSH secundário: Sistema Cardiovascular/efeitos dos fármacos
Sistema Cardiovascular/metabolismo
Diabetes Mellitus Tipo 2/tratamento farmacológico
Diabetes Mellitus Tipo 2/metabolismo
Diabetes Mellitus Tipo 2/fisiopatologia
Dipeptidil Peptidase 4/metabolismo
Inibidores da Dipeptidil Peptidase IV/metabolismo
Inibidores da Dipeptidil Peptidase IV/farmacologia
Seres Humanos
Substâncias Protetoras/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Dipeptidyl-Peptidase IV Inhibitors); 0 (Glucagon-Like Peptide-1 Receptor); 0 (Incretins); 0 (Protective Agents); EC 3.4.14.5 (Dipeptidyl Peptidase 4)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180109
[St] Status:MEDLINE
[do] DOI:10.15690/vramn732


  5 / 3309 MEDLINE  
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[PMID]:28452143
[Au] Autor:Jain MR; Joharapurkar AA; Kshirsagar SG; Patel VJ; Bahekar RH; Patel HV; Jadav PA; Patel PR; Desai RC
[Ad] Endereço:Zydus Research Centre, Cadila Healthcare Limited, Ahmedabad, India.
[Ti] Título:ZY15557, a novel, long acting inhibitor of dipeptidyl peptidase-4, for the treatment of Type 2 diabetes mellitus.
[So] Source:Br J Pharmacol;174(14):2346-2357, 2017 Jul.
[Is] ISSN:1476-5381
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND PURPOSE: Dipeptidyl peptidase (DPP)-4 inhibitors increase levels of glucagon-like peptide-1 (GLP-1) and provide clinical benefit in the treatment of type 2 diabetes mellitus. As longer acting inhibitors have therapeutic advantages, we developed a novel DPP-4 inhibitor, ZY15557, that has a sustained action and long half-life. EXPERIMENTAL APPROACH: We studied the potency, selectivity, efficacy and duration of action of ZY15557, in vitro, with assays of DPP-4 activity. In vivo, the pharmacodymamics and pharmacokinetics of ZY15557 were studied, using db/db mice and Zucker fatty rats, along with normal mice, rats, dogs and non-human primates. KEY RESULTS: ZY15557 is a potent, competitive and long acting inhibitor of DPP-4 (K 5.53 nM; K 3.2 × 10 ·s , half-life 35.8 min). ZY15557 treatment inhibited DPP-4 activity, and enhanced active GLP-1 and insulin in mice and rats, providing dose-dependent anti-hyperglycaemic effects. Anti-hyperglycaemic effects were also observed in db/db mice and Zucker fatty rats. Following oral dosing, ZY15557 significantly inhibited plasma DPP-4 activity, determined ex vivo, in mice and rats for more than 48 h, and for up to 168 h in dogs and non-human primates. Allometric scaling predicts a half-life for ZY15557 in humans of up to 60 h. CONCLUSIONS AND IMPLICATIONS: ZY15557 is a potent, competitive and long acting DPP-4 inhibitor. ZY15557 showed similar DPP-4 inhibition across different species. ZY15557 showed excellent oral bioavailability in preclinical species. It showed a low plasma clearance (CL) and large volume of distribution (V ) across species, resulting in an extended half-life.
[Mh] Termos MeSH primário: Diabetes Mellitus Experimental/tratamento farmacológico
Diabetes Mellitus Tipo 2/tratamento farmacológico
Dipeptidil Peptidase 4/metabolismo
Inibidores da Dipeptidil Peptidase IV/farmacologia
Piranos/farmacologia
[Mh] Termos MeSH secundário: Animais
Diabetes Mellitus Experimental/metabolismo
Diabetes Mellitus Tipo 2/metabolismo
Inibidores da Dipeptidil Peptidase IV/química
Cães
Relação Dose-Resposta a Droga
Seres Humanos
Macaca mulatta
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Obesos
Estrutura Molecular
Piranos/química
Ratos
Ratos Sprague-Dawley
Ratos Wistar
Ratos Zucker
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Dipeptidyl-Peptidase IV Inhibitors); 0 (Pyrans); 0 (ZY15557); EC 3.4.14.5 (Dipeptidyl Peptidase 4)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180216
[Lr] Data última revisão:
180216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1111/bph.13842


  6 / 3309 MEDLINE  
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[PMID]:28471520
[Au] Autor:Bansho Y; Lee J; Nishida E; Nakajima-Koyama M
[Ad] Endereço:Department of Cell and Developmental Biology, Graduate School of Biostudies, Kyoto University, Japan.
[Ti] Título:Identification and characterization of secreted factors that are upregulated during somatic cell reprogramming.
[So] Source:FEBS Lett;591(11):1584-1600, 2017 06.
[Is] ISSN:1873-3468
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The process of cell reprogramming has been characterized considerably since the successful generation of induced pluripotent stem cells. However, the importance of cell-cell communications for cellular reprogramming remains largely unknown. Secreted factors, which are expressed and secreted during reprogramming, may influence the reprogramming efficiency. Here, we have identified Sostdc1, Glb1l2, Fetub, Dpp4, Gdf3, Trh, and Tdgf1 as prominently upregulated secreted factors during reprogramming. Our detailed analysis reveals that these seven factors may be categorized into four groups based on their expression patterns in relation to the reprogramming stages. Remarkably, knockdown of Sostdc1, which is the most prominently upregulated factor and which is expressed earlier than the other six factors, results in reduced reprogramming efficiency, suggesting its involvement in the reprogramming process.
[Mh] Termos MeSH primário: Reprogramação Celular/genética
Regulação da Expressão Gênica
[Mh] Termos MeSH secundário: Animais
Proteínas Morfogenéticas Ósseas/genética
Proteínas Morfogenéticas Ósseas/metabolismo
Células Cultivadas
Dipeptidil Peptidase 4/genética
Dipeptidil Peptidase 4/metabolismo
Fator de Crescimento Epidérmico/genética
Fator de Crescimento Epidérmico/metabolismo
Fetuína-B/genética
Fetuína-B/metabolismo
Fibroblastos/metabolismo
Citometria de Fluxo
Fator 3 de Diferenciação de Crescimento/genética
Fator 3 de Diferenciação de Crescimento/metabolismo
Immunoblotting
Glicoproteínas de Membrana/genética
Glicoproteínas de Membrana/metabolismo
Camundongos
Análise em Microsséries
Proteínas de Neoplasias/genética
Proteínas de Neoplasias/metabolismo
Reação em Cadeia da Polimerase Via Transcriptase Reversa
[Pt] Tipo de publicação:LETTER; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Bone Morphogenetic Proteins); 0 (Fetub protein, mouse); 0 (Fetuin-B); 0 (Gdf3 protein, mouse); 0 (Growth Differentiation Factor 3); 0 (Membrane Glycoproteins); 0 (Neoplasm Proteins); 0 (Sostdc1 protein, mouse); 0 (Tdgf1 protein, mouse); 62229-50-9 (Epidermal Growth Factor); EC 3.4.14.5 (Dipeptidyl Peptidase 4); EC 3.4.14.5 (Dpp4 protein, mouse)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180130
[Lr] Data última revisão:
180130
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1002/1873-3468.12665


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[PMID]:29244467
[Au] Autor:Dyakova ME
[Ti] Título:Features purine metabolism in patients with pulmonary tuberculosis.
[So] Source:Patol Fiziol Eksp Ter;60(3):36-41, 2016 Jul-Sep.
[Is] ISSN:0031-2991
[Cp] País de publicação:Russia (Federation)
[La] Idioma:eng
[Ab] Resumo:The purpose - comprehensive study of the purine metabolic enzymes in serum and immune cells in patients with pulmonary tuberculosis for the understanding of the pathogenesis of a specific lung disease. Methods: The enzymes of purine metabolism (adenosine deaminase (ADA) and its isoenzymes (ADA-1 and ADA-2), dipeptidylpeptidase IV (DPPIV - CD26), ecto-5'-nucleotidase (5'-NC) in the blood and immune cells was studied in 29 and 76 patients with fibro-cavernous (FCPT) and infiltrative (IPT) pulmonary tuberculosis correspondingly. Results: In patients found changes in purine metabolism, the severity and pathophysiological significance of which depend of clinical forms of tuberculosis, that is, from the gravity specific of the process. Reduced activity of ADA mononuclear cells was accompanied by a decrease in the expression of CD26 in patients with FCPT and the growth of the IPT ectopeptidase patients, that is, the concentration of CD26 mononuclear cells and neutrophils are associated with form of pulmonary tuberculosis. The increased levels of another enzyme purine metabolism - 5'-NC registered in both forms of pulmonary tuberculosis. Conclusion: In the context of the ADA and CD26 association with the IPT can assume increased participation of each of them in the activation of cell proliferation and cytokine production. Low levels of CD26 immune cells in the absence of their connection with the activity of ADA is typical for patients with FCPT and reflects their inherent failure of cellular immunity. We can assume that the formation of complexes with the ADA ectopeptidases (CD26 and 5'-NC) for newly diagnosed IPT provides a balance CD26_ADA extracellular / intracellular adenosine and 5'-NC / adenosine and thereby adequate metabolism of immunocompetent cells.
[Mh] Termos MeSH primário: Dipeptidil Peptidase 4/sangue
Purinas/sangue
Tuberculose Pulmonar/sangue
[Mh] Termos MeSH secundário: Adulto
Dipeptidil Peptidase 4/imunologia
Feminino
Seres Humanos
Masculino
Meia-Idade
Purinas/imunologia
Tuberculose Pulmonar/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Purines); EC 3.4.14.5 (DPP4 protein, human); EC 3.4.14.5 (Dipeptidyl Peptidase 4)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180118
[Lr] Data última revisão:
180118
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171216
[St] Status:MEDLINE


  8 / 3309 MEDLINE  
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[PMID]:29253907
[Au] Autor:Dingenouts CKE; Bakker W; Lodder K; Wiesmeijer KC; Moerkamp AT; Maring JA; Arthur HM; Smits AM; Goumans MJ
[Ad] Endereço:Department of Molecular Cell Biology, Leiden University Medical Center, Leiden, the Netherlands.
[Ti] Título:Inhibiting DPP4 in a mouse model of HHT1 results in a shift towards regenerative macrophages and reduces fibrosis after myocardial infarction.
[So] Source:PLoS One;12(12):e0189805, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:AIMS: Hereditary Hemorrhagic Telangiectasia type-1 (HHT1) is a genetic vascular disorder caused by haploinsufficiency of the TGFß co-receptor endoglin. Dysfunctional homing of HHT1 mononuclear cells (MNCs) towards the infarcted myocardium hampers cardiac recovery. HHT1-MNCs have elevated expression of dipeptidyl peptidase-4 (DPP4/CD26), which inhibits recruitment of CXCR4-expressing MNCs by inactivation of stromal cell-derived factor 1 (SDF1). We hypothesize that inhibiting DPP4 will restore homing of HHT1-MNCs to the infarcted heart and improve cardiac recovery. METHODS AND RESULTS: After inducing myocardial infarction (MI), wild type (WT) and endoglin heterozygous (Eng+/-) mice were treated for 5 days with the DPP4 inhibitor Diprotin A (DipA). DipA increased the number of CXCR4+ MNCs residing in the infarcted Eng+/- hearts (Eng+/- 73.17±12.67 vs. Eng+/- treated 157.00±11.61, P = 0.0003) and significantly reduced infarct size (Eng+/- 46.60±9.33% vs. Eng+/- treated 27.02±3.04%, P = 0.03). Echocardiography demonstrated that DipA treatment slightly deteriorated heart function in Eng+/- mice. An increased number of capillaries (Eng+/- 61.63±1.43 vs. Eng+/- treated 74.30±1.74, P = 0.001) were detected in the infarct border zone whereas the number of arteries was reduced (Eng+/- 11.88±0.63 vs. Eng+/- treated 6.38±0.97, P = 0.003). Interestingly, while less M2 regenerative macrophages were present in Eng+/- hearts prior to DipA treatment, (WT 29.88±1.52% vs. Eng+/- 12.34±1.64%, P<0.0001), DPP4 inhibition restored the number of M2 macrophages to wild type levels. CONCLUSIONS: In this study, we demonstrate that systemic DPP4 inhibition restores the impaired MNC homing in Eng+/- animals post-MI, and enhances cardiac repair, which might be explained by restoring the balance between the inflammatory and regenerative macrophages present in the heart.
[Mh] Termos MeSH primário: Dipeptidil Peptidase 4/química
Inibidores da Dipeptidil Peptidase IV/química
Macrófagos/metabolismo
Infarto do Miocárdio/metabolismo
Telangiectasia Hemorrágica Hereditária/genética
[Mh] Termos MeSH secundário: Animais
Quimiocina CXCL12/metabolismo
Modelos Animais de Doenças
Endoglina/metabolismo
Fibrose/metabolismo
Haploinsuficiência
Ventrículos do Coração/patologia
Heterozigoto
Seres Humanos
Masculino
Camundongos
Camundongos Transgênicos
Infarto do Miocárdio/complicações
Miocárdio/metabolismo
Miocárdio/patologia
Regeneração
Telangiectasia Hemorrágica Hereditária/patologia
Fator de Crescimento Transformador beta/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chemokine CXCL12); 0 (Cxcl12 protein, mouse); 0 (Dipeptidyl-Peptidase IV Inhibitors); 0 (Endoglin); 0 (Transforming Growth Factor beta); EC 3.4.14.5 (Dipeptidyl Peptidase 4); EC 3.4.14.5 (Dpp4 protein, mouse)
[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:171219
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189805


  9 / 3309 MEDLINE  
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[PMID]:28454879
[Au] Autor:Xin Y; Wang X; Zhu M; Qu M; Bogari M; Lin L; Mar Aung Z; Chen W; Chen X; Chai G; Zhang Y
[Ad] Endereço:Department of Plastic and Reconstructive Surgery, Shanghai 9th People's Hospital, China; Shanghai Tissue Engineering Key Laboratory, Shanghai Jiao Tong University School of Medicine, Shanghai 200011, China.
[Ti] Título:Expansion of CD26 positive fibroblast population promotes keloid progression.
[So] Source:Exp Cell Res;356(1):104-113, 2017 07 01.
[Is] ISSN:1090-2422
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Keloid is a skin fibrosis disease that characterised by invasive growth of fibroblasts and aberrant deposition of extracellular matrix. Studies indicated that keloid fibroblasts (KFs) is a class of 'activated' fibroblasts, which show accelerated proliferation and excessive extracellular matrix formation as compared with normal fibroblasts (NFs). However, the mechanism underlying keloid fibroblasts dysfunction is still unknown. OBJECTIVE: To verify CD26 expression difference between KFs and NFs, and investigate the function of CD26 positive fibroblasts in keloid progression. METHODS: KFs and NFs were isolated from Keloid tissues and normal skin tissues respectively. Flow cytometry was performed to isolate CD26+/CD26- fibroblasts from KFs and NFs. Proliferation of different fibroblasts were analyzed by CCK8 assay and Ki 67 straining. Profibrotic phenotype difference was detected by qRT-PCR, western blot, ELISA and immunofluorescence. Scratching experiment and transwell assay were used to assess invasion ability of CD26+/CD26- fibroblasts. Diprotin A was used as a CD26 inhibitor to further investigated the function of CD26 fibroblasts in keloid disease. RESULT: CD26 expression was increased in KFs, and the proportion of CD26+ fibroblasts was significantly increased in KFs. Cell viability analysis showed that CD26+ fibroblasts was more active in proliferation. Furthermore, the expression of profibrotic genes were increased in CD26+ fibroblasts, including TGF-ß1, IGF-1, IL6, collagen 1, collagen 3 and fibronectin. And meanwhile, CD26+ fibroblasts showed stronger invasion ability as compared to CD26- fibroblasts. Moreover, Diprotin A significantly suppressed proliferation and extracellular matrix secretion of CD26+ fibroblasts isolated from keloid tissues. CONCLUSION: Our findings suggest that CD26+ fibroblasts possess proliferation advantage in compare to CD26- fibroblasts, and the advantage caused expansion of CD26 positive fibroblast population promotes keloid progression.
[Mh] Termos MeSH primário: Proliferação Celular/fisiologia
Citocinas/metabolismo
Dipeptidil Peptidase 4/metabolismo
Matriz Extracelular/metabolismo
Fibroblastos/metabolismo
Queloide/patologia
Pele/patologia
[Mh] Termos MeSH secundário: Movimento Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Células Cultivadas
Dipeptidil Peptidase 4/efeitos dos fármacos
Progressão da Doença
Feminino
Seres Humanos
Masculino
Oligopeptídeos/farmacologia
Transdução de Sinais
Pele/citologia
Pele/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cytokines); 0 (Oligopeptides); 90614-48-5 (diprotin A); EC 3.4.14.5 (DPP4 protein, human); EC 3.4.14.5 (Dipeptidyl Peptidase 4)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171209
[Lr] Data última revisão:
171209
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170430
[St] Status:MEDLINE


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[PMID]:29148282
[Au] Autor:Kato E; Kawakami K; Kawabata J
[Ad] Endereço:a Laboratory of Food Biochemistry, Division of Applied Bioscience, Graduate School of Agriculture , Hokkaido University , Kita-ku , Hokkaido , Japan Sapporo.
[Ti] Título:Macrocarpal C isolated from Eucalyptus globulus inhibits dipeptidyl peptidase 4 in an aggregated form.
[So] Source:J Enzyme Inhib Med Chem;33(1):106-109, 2018 Dec.
[Is] ISSN:1475-6374
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Dipeptidyl peptidase 4 (DPP-4) inhibitors are used for the treatment of type-2 diabetes mellitus. Various synthetic inhibitors have been developed to date, and plants containing natural DPP-4 inhibitors have also been identified. Here, 13 plant samples were tested for their DPP-4 inhibitory activity. Macrocarpals A-C were isolated from Eucalyptus globulus through activity-guided fractionation and shown to be DPP-4 inhibitors. Of these, macrocarpal C showed the highest inhibitory activity, demonstrating an inhibition curve characterised by a pronounced increase in activity within a narrow concentration range. Evaluation of macrocarpal C solution by turbidity, nuclear magnetic resonance spectroscopy and mass spectrometry indicated its aggregation, which may explain the characteristics of the inhibition curve. These findings will be valuable for further study of potential small molecule DPP-4 inhibitors.
[Mh] Termos MeSH primário: Dipeptidil Peptidase 4/metabolismo
Inibidores da Dipeptidil Peptidase IV/farmacologia
Eucalyptus/química
Floroglucinol/análogos & derivados
Sesquiterpenos/isolamento & purificação
Sesquiterpenos/farmacologia
[Mh] Termos MeSH secundário: Inibidores da Dipeptidil Peptidase IV/química
Inibidores da Dipeptidil Peptidase IV/isolamento & purificação
Relação Dose-Resposta a Droga
Seres Humanos
Conformação Molecular
Floroglucinol/química
Floroglucinol/isolamento & purificação
Floroglucinol/farmacologia
Sesquiterpenos/química
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Dipeptidyl-Peptidase IV Inhibitors); 0 (Sesquiterpenes); 0 (macrocarpal C); DHD7FFG6YS (Phloroglucinol); EC 3.4.14.5 (DPP4 protein, human); EC 3.4.14.5 (Dipeptidyl Peptidase 4)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171118
[St] Status:MEDLINE
[do] DOI:10.1080/14756366.2017.1396458



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