Base de dados : MEDLINE
Pesquisa : D02.241.223.651 [Categoria DeCS]
Referências encontradas : 1563 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 157 ir para página                         

  1 / 1563 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29389946
[Au] Autor:Okhovat MA; Ziari K; Ranjbaran R; Nikouyan N
[Ad] Endereço:Diagnostic Laboratory Sciences and Technology Research Center, School of Paramedical Sciences, Shiraz University of Medical Sciences, Shiraz, Iran.
[Ti] Título:The effect of histone deacetylase inhibitors on AHSP expression.
[So] Source:PLoS One;13(2):e0189267, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Alpha-hemoglobin stabilizing protein (AHSP) is a molecular chaperone that can reduce the damage caused by excess free α-globin to erythroid cells in patients with impaired ß-globin chain synthesis. We assessed the effect of sodium phenylbutyrate and sodium valproate, two histone deacetylase inhibitors (HDIs) that are being studied for the treatment of hemoglobinopathies, on the expression of AHSP, BCL11A (all isoforms), γ-globin genes (HBG1/2), and some related transcription factors including GATA1, NFE2, EKLF, KLF4, and STAT3. For this purpose, the K562 cell line was cultured for 2, 4, and 6 days in the presence and absence of sodium phenylbutyrate and sodium valproate. Relative real-time qRT-PCR analysis of mRNA levels was performed to determine the effects of the two compounds on gene expression. Expression of all target mRNAs increased significantly (p < 0.05), except for the expression of BCL11A, which was down-regulated (p < 0.05) in the cells treated with both compounds relative to the levels measured for untreated cells. The findings indicated that sodium valproate had a more considerable effect than sodium phenylbutyrate (p < 0.0005) on BCL11A repression and the up-regulation of other studied genes. γ-Globin and AHSP gene expression continuously increased during the culture period in the treated cells, with the highest gene expression observed for 1 mM sodium valproate after 6 days. Both compounds repressed the expression of BCL11A (-XL, -L, -S) and up-regulated GATA1, NFE2, EKLF, KLF4, STAT3, AHSP, and γ-globin genes expression. Moreover, sodium valproate showed a stronger effect on repressing BCL11A and escalating the expression of other target genes. The findings of this in vitro experiment could be considered in selecting drugs for clinical use in patients with ß-hemoglobinopathies.
[Mh] Termos MeSH primário: Proteínas Sanguíneas/metabolismo
Inibidores de Histona Desacetilases/farmacologia
Chaperonas Moleculares/metabolismo
[Mh] Termos MeSH secundário: Regulação da Expressão Gênica/efeitos dos fármacos
Hemoglobinopatias/tratamento farmacológico
Hemoglobinopatias/genética
Inibidores de Histona Desacetilases/uso terapêutico
Seres Humanos
Células K562
Fenilbutiratos/farmacologia
Reação em Cadeia da Polimerase em Tempo Real
Ácido Valproico/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (AHSP protein, human); 0 (Blood Proteins); 0 (Histone Deacetylase Inhibitors); 0 (Molecular Chaperones); 0 (Phenylbutyrates); 614OI1Z5WI (Valproic Acid); 7WY7YBI87E (4-phenylbutyric acid)
[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:180202
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189267


  2 / 1563 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28470097
[Au] Autor:Khan S; Komarya SK; Jena G
[Ad] Endereço:Facility for Risk Assessment & Intervention Studies, Department of Pharmacology & Toxicology, National Institute of Pharmaceutical Education & Research, Sector-67, SAS Nagar, Punjab-160062, India.
[Ti] Título:Phenylbutyrate and ß-cell function: contribution of histone deacetylases and ER stress inhibition.
[So] Source:Epigenomics;9(5):711-720, 2017 May.
[Is] ISSN:1750-192X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Incidences of diabetes are increasing globally due to involvement of genetic and epigenetic factors. Phenylbutyrate (PBA) is a US FDA approved drug for treatment of urea cycle disorder in children. PBA reduces endoplasmic reticulum (ER) stress and is proven as a potent histone deacetylases (HDACs) inhibitor. Chronic ER stress results in unfolding protein response, which triggers apoptosis. Abnormal ER homoeostasis is responsible for defective processing of several genes/proteins and contributes to ß-cell death/failure. Accumulated evidences indicated that HDACs modulate key biochemical pathways and HDAC inhibitors improve ß-cell function and insulin resistance by modulating multiple targets. This review highlights the role of PBA on ß-cell functions, insulin resistance for possible treatment of diabetes through inhibition of ER stress and HDACs.
[Mh] Termos MeSH primário: Diabetes Mellitus/tratamento farmacológico
Estresse do Retículo Endoplasmático
Inibidores de Histona Desacetilases/farmacologia
Histona Desacetilases/metabolismo
Células Secretoras de Insulina/metabolismo
Fenilbutiratos/farmacologia
[Mh] Termos MeSH secundário: Animais
Diabetes Mellitus/metabolismo
Inibidores de Histona Desacetilases/uso terapêutico
Seres Humanos
Células Secretoras de Insulina/efeitos dos fármacos
Fenilbutiratos/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Histone Deacetylase Inhibitors); 0 (Phenylbutyrates); EC 3.5.1.98 (Histone Deacetylases)
[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:170505
[St] Status:MEDLINE
[do] DOI:10.2217/epi-2016-0160


  3 / 1563 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28749244
[Au] Autor:Miller AC; Rivas R; McMahon R; Miller K; Tesoro L; Villa V; Yanushkevich D; Lison P
[Ad] Endereço:a Scientific Research Department , Armed Forces Radiobiology Research Institute (AFRRI), Uniformed Services University of the Health Sciences (USUHS) , Bethesda , MD , USA.
[Ti] Título:Radiation protection and mitigation potential of phenylbutyrate: delivered via oral administration.
[So] Source:Int J Radiat Biol;93(9):907-919, 2017 09.
[Is] ISSN:1362-3095
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Phenylbutyrate (PB), a histone deacetylase inhibitor (HDACi) has demonstrated radiation protection in both in vitro and in vivo models. Studies previously demonstrated that PB and other HDAC inhibitors could inhibit radiation lethality in vivo by subcutaneous (s.c) injection. The objective of this study was to test the ability of oral PB treatment to protect against or to mitigate acute gamma radiation-induced lethality in vivo. MATERIALS AND METHODS: Human osteoblasts cells were used to evaluate radiation survival when PB was delivered pre- or post-radiation. A 30-day radiation lethality study was used to assess the radioprotective (pre-radiation) and radiomitigative (post-radiation) capability of PB. Possible mechanisms evaluated were antioxidant activity effects, HDAC inhibition, DNA damage, and hematological recovery. RESULTS: Treatment of HOS cells with PB 50 µM either before or after radiation increased radiation resistance as assessed by clonogenic survival. Western blot studies showed that PB treatment acetylated histones in vivo and ameliorated the radiation-induced reduction in acetylated histone-4 (H4). Pre-radiation oral administration of PB (10 mg/kg) provided radioprotection against gamma radiation (7-11.5 Gy) with a dose reduction factor of 1.25 (p = 0.001). PB oral administration post-radiation provided moderate radiation mitigation against gamma radiation (7-11.5 Gy) and demonstrated a dose reduction factor of 1.18 (p = 0.05). PB pre-radiation and post-radiation treatment was associated with significant elevations in neutrophils and platelets and attenuation of DNA damage. CONCLUSIONS: These results indicate that oral PB has potential as a radiation protector and a radiation mitigator and that potential mechanisms of action include attenuation of DNA damage, antioxidant activity, and bone marrow protection.
[Mh] Termos MeSH primário: Dano ao DNA/efeitos dos fármacos
Raios gama
Osteoblastos/efeitos dos fármacos
Osteoblastos/efeitos da radiação
Fenilbutiratos/farmacologia
Lesões por Radiação/prevenção & controle
Espécies Reativas de Oxigênio/metabolismo
[Mh] Termos MeSH secundário: Administração Oral
Animais
Linhagem Celular
Relação Dose-Resposta a Droga
Estudos de Viabilidade
Seres Humanos
Dose Letal Mediana
Masculino
Camundongos
Camundongos Endogâmicos DBA
Osteoblastos/citologia
Osteoblastos/fisiologia
Fenilbutiratos/efeitos adversos
Dose de Radiação
Lesões por Radiação/diagnóstico
Protetores contra Radiação/efeitos adversos
Protetores contra Radiação/farmacologia
Taxa de Sobrevida
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (Phenylbutyrates); 0 (Radiation-Protective Agents); 0 (Reactive Oxygen Species)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180111
[Lr] Data última revisão:
180111
[Sb] Subgrupo de revista:IM; S
[Da] Data de entrada para processamento:170728
[St] Status:MEDLINE
[do] DOI:10.1080/09553002.2017.1350301


  4 / 1563 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29028830
[Au] Autor:Ma L; Chu W; Chai J; Shen C; Li D; Wang X
[Ad] Endereço:Department of Burn & Plastic Surgery, Burns Institute, First Hospital affiliated to General Hospital of the Chinese People's Liberation Army, Beijing, China.
[Ti] Título:ER stress and subsequent activated calpain play a pivotal role in skeletal muscle wasting after severe burn injury.
[So] Source:PLoS One;12(10):e0186128, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Severe burns are typically followed by hypermetabolism characterized by significant muscle wasting, which causes considerable morbidity and mortality. The aim of the present study was to explore the underlying mechanisms of skeletal muscle damage/wasting post-burn. Rats were randomized to the sham, sham+4-phenylbutyrate (4-PBA, a pharmacological chaperone promoting endoplasmic reticulum (ER) folding/trafficking, commonly considered as an inhibitor of ER), burn (30% total body surface area), and burn+4-PBA groups; and sacrificed at 1, 4, 7, 14 days after the burn injury. Tibial anterior muscle was harvested for transmission electron microscopy, calcium imaging, gene expression and protein analysis of ER stress / ubiquitin-proteasome system / autophagy, and calpain activity measurement. The results showed that ER stress markers were increased in the burn group compared with the sham group, especially at post-burn days 4 and 7, which might consequently elevate cytoplasmic calcium concentration, promote calpain production as well as activation, and cause skeletal muscle damage/wasting of TA muscle after severe burn injury. Interestingly, treatment with 4-PBA prevented burn-induced ER swelling and altered protein expression of ER stress markers and calcium release, attenuating calpain activation and skeletal muscle damage/wasting after severe burn injury. Atrogin-1 and LC3-II/LC3-I ratio were also increased in the burn group compared with the sham group, while MuRF-1 remained unchanged; 4-PBA decreased atrogin-1 in the burn group. Taken together, these findings suggested that severe burn injury induces ER stress, which in turns causes calpain activation. ER stress and subsequent activated calpain play a critical role in skeletal muscle damage/wasting in burned rats.
[Mh] Termos MeSH primário: Queimaduras/enzimologia
Queimaduras/patologia
Calpaína/metabolismo
Estresse do Retículo Endoplasmático
Músculo Esquelético/patologia
[Mh] Termos MeSH secundário: Animais
Queimaduras/complicações
Queimaduras/metabolismo
Cálcio/metabolismo
Estresse do Retículo Endoplasmático/efeitos dos fármacos
Ativação Enzimática/efeitos dos fármacos
Homeostase/efeitos dos fármacos
Masculino
Músculo Esquelético/efeitos dos fármacos
Fenilbutiratos/farmacologia
Proteólise/efeitos dos fármacos
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Phenylbutyrates); 7WY7YBI87E (4-phenylbutyric acid); EC 3.4.22.- (Calpain); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171014
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0186128


  5 / 1563 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28930444
[Au] Autor:Al-Keilani MS; Al-Sawalha NA
[Ad] Endereço:Jordan University of Science and Technology , College of Pharmacy, Department of Clinical Pharmacy, P.O. Box 3030, Irbid 22110, Jordan.
[Ti] Título:Potential of Phenylbutyrate as Adjuvant Chemotherapy: An Overview of Cellular and Molecular Anticancer Mechanisms.
[So] Source:Chem Res Toxicol;30(10):1767-1777, 2017 Oct 16.
[Is] ISSN:1520-5010
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Despite the advancement in cancer therapy, a high number of patients fail treatment because of drug resistance. Several preclinical in vitro data suggest that phenylbutyrate has antiproliferative, antiangiogenic, antimetastatic, immunomodulatory, and differentiating properties. Moreover, phenylbutyrate administration in vivo provided an oncoprotective effect. However, the results of clinical trials indicate that the antineoplastic potential of phenylbutyrate is hindered by its pharmacokinetic and pharmacodynamic properties. Thus, understanding the exact mechanisms of the anticancer effect of phenylbutyrate could assist in the selection of patients who will best benefit from this drug. The present review discusses the proposed mechanisms of antineoplastic effect of phenylbutyrate and the preclinical and clinical evidence suggesting its potential role as anticancer in different types of cancer.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Neoplasias/tratamento farmacológico
Fenilbutiratos/farmacologia
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/química
Proliferação Celular/efeitos dos fármacos
Quimioterapia Adjuvante
Seres Humanos
Neoplasias/patologia
Fenilbutiratos/química
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Phenylbutyrates)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171101
[Lr] Data última revisão:
171101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170921
[St] Status:MEDLINE
[do] DOI:10.1021/acs.chemrestox.7b00149


  6 / 1563 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:28875973
[Au] Autor:Plusa T
[Ad] Endereço:EMC Medical Institute SA - Department of Internal Medicine and Lung Disease, Hospital st. Anna in Piaseczno, Poland.
[Ti] Título:[Butamirate citrate in control of cough in respiratory tract inflammation].
[Ti] Título:Miejsce cytrynianu butamiratu w kontrolowaniu kaszlu w zapaleniu dróg oddechowych..
[So] Source:Pol Merkur Lekarski;43(254):69-74, 2017 Aug 21.
[Is] ISSN:1426-9686
[Cp] País de publicação:Poland
[La] Idioma:pol
[Ab] Resumo:Cough is the reflex defense response of the respiratory tract to the present secretions in the throat, trachea and bronchi, and ongoing inflammation in the mucous membranes of the upper and lower respiratory tract. From a practical point of view, cough is dry (unproductive) and productive cough with expulsion of significant amounts of secretion. Drugs used to treat cough differ in both mechanism of action and pharmacokinetic activity. Butamirate citrate belongs to a new class of cough suppressants acting centrally through the receptors in the brainstem. In addition, it has a very beneficial effect, because it reduces the resistance in the airways by inhibiting bronchospasm and anti-inflammatory effect. It is rapidly absorbed after oral administration and its therapeutic plasma concentration is determined after 5-10 minutes of administration, irrespective of the dose. Possible side effects are rarely seen in 0.5-1% of patients, mainly in the form of skin rash, nausea, diarrhea, dizziness, which usually resolves during treatment. The cough effect of most cough suppressants is good, but their mechanisms are different and for that reason they should be individually selected. An important asset of this group of drugs is peripheral activity and effects on bronchodilator muscles, such as in the case of butamirate. Inclusion of this feature is particularly beneficial in chronic inflammatory bronchial diseases.
[Mh] Termos MeSH primário: Antitussígenos/uso terapêutico
Tosse/tratamento farmacológico
Fenilbutiratos/uso terapêutico
[Mh] Termos MeSH secundário: Administração Oral
Antitussígenos/administração & dosagem
Antitussígenos/efeitos adversos
Antitussígenos/farmacologia
Seres Humanos
Inflamação/tratamento farmacológico
Fenilbutiratos/administração & dosagem
Fenilbutiratos/efeitos adversos
Fenilbutiratos/farmacologia
Doenças Respiratórias/tratamento farmacológico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antitussive Agents); 0 (Phenylbutyrates); M75MZG2236 (butamirate)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170907
[St] Status:MEDLINE


  7 / 1563 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28869398
[Au] Autor:Dichiara M; Amata E; Rescifina A; Prezzavento O; Floresta G; Parenti C; Pittalà V; Marrazzo A
[Ad] Endereço:Dipartimento di Scienze del Farmaco, Università di Catania, Viale Andrea Doria 6, 95125 Catania, Italy.
[Ti] Título:Synthesis and evaluation of haloperidol metabolite II prodrugs as anticancer agents.
[So] Source:Future Med Chem;9(15):1749-1764, 2017 Oct.
[Is] ISSN:1756-8927
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The use of haloperidol metabolite II (HP-metabolite II) prodrugs is an emerging strategy in the treatment of cancer. HP-metabolite II exhibits antiproliferative properties at micromolar concentrations inducing apoptosis in different types of cancer. Thus, the application of the prodrug approach appears as a useful method leading to much more desirable pharmacokinetic and pharmacodynamic properties. Some studies have shown that the esterification of the hydroxyl group of HP-metabolite II with 4-phenylbutiric acid (4-PBA) or valproic acid enhances the anticancer therapeutic potency. The current progresses in the design, synthesis and evaluation of anticancer activity of HP metabolite II prodrugs will be discussed in this review.
[Mh] Termos MeSH primário: Haloperidol/farmacologia
Pró-Fármacos/síntese química
Pró-Fármacos/farmacologia
[Mh] Termos MeSH secundário: Antineoplásicos/síntese química
Antineoplásicos/farmacologia
Sobrevivência Celular/efeitos dos fármacos
Haloperidol/química
Haloperidol/metabolismo
Inibidores de Histona Desacetilases/síntese química
Inibidores de Histona Desacetilases/química
Inibidores de Histona Desacetilases/farmacologia
Seres Humanos
Fenilbutiratos/química
Fenilbutiratos/farmacologia
Receptores sigma/antagonistas & inibidores
Receptores sigma/metabolismo
Transdução de Sinais/efeitos dos fármacos
Ácido Valproico/química
Ácido Valproico/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Histone Deacetylase Inhibitors); 0 (Phenylbutyrates); 0 (Prodrugs); 0 (Receptors, sigma); 614OI1Z5WI (Valproic Acid); J6292F8L3D (Haloperidol)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171025
[Lr] Data última revisão:
171025
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170905
[St] Status:MEDLINE
[do] DOI:10.4155/fmc-2017-0064


  8 / 1563 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28829799
[Au] Autor:Chen YJ; Wang WH; Wu WY; Hsu CC; Wei LR; Wang SF; Hsu YW; Liaw CC; Tsai WC
[Ad] Endereço:Department of Medical Laboratory Science and Biotechnology, Kaohsiung Medical University, Kaohsiung, Taiwan.
[Ti] Título:Novel histone deacetylase inhibitor AR-42 exhibits antitumor activity in pancreatic cancer cells by affecting multiple biochemical pathways.
[So] Source:PLoS One;12(8):e0183368, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Pancreatic cancer is one of the most lethal types of cancer with a 5-year survival rate of ~5%. Histone deacetylases (HDACs) participate in many cellular processes, including carcinogenesis, and pharmacological inhibition of HDACs has emerged as a potential therapeutic strategy. In this study, we explored antitumor activity of the novel HDAC inhibitor AR-42 in pancreatic cancer. METHODS: Human pancreatic cancer cell lines BxPC-3 and PANC-1 were used in this study. Real-time PCR, RT-PCR, and western blotting were employed to investigate expression of specific genes and proteins, respectively. Translocation of apoptosis-inducing factor was investigated by immunofluorescence and subcellular fractionation. The number of apoptotic cells, cell cycle stages, and reactive oxygen species (ROS) generation levels were determined by flow cytometry. Cell invasiveness was examined by the Matrigel invasion assay. Efficacy of AR-42 in vivo was evaluated by utilizing BxPC-3 xenograft mouse model. RESULTS: AR-42 inhibited pancreatic cancer cell proliferation by causing G2/M cell cycle arrest via regulating expression levels of genes and proteins involved in cell cycle. AR-42 also induced ROS generation and DNA damage, triggering apoptosis of pancreatic cancer cells via both caspase-3-dependent and caspase-3-independent pathways. In addition, AR-42 increased expression levels of negative regulators of p53 (miR-125b, miR-30d, and miR33), which could contribute to lower expression level of mutant p53 in pancreatic cancer cells. Cell invasion assay showed that AR-42 reduced cancer cell aggressiveness and significantly diminished BxPC-3 xenograft tumor growth in vivo. CONCLUSION: AR-42, a novel HDAC inhibitor, inhibited pancreatic cancer cells by regulating p53 expression, inducing cell cycle arrest, particularly at the G2/M stage, and activating multiple apoptosis pathways. Additionally, AR-42 inhibited cell invasiveness and potently suppressed pancreatic cancer tumors in vivo. We conclude that by virtue of its multiple mechanisms of action, AR-42 possesses a considerable potential as an antitumor agent in pancreatic cancer.
[Mh] Termos MeSH primário: Inibidores de Histona Desacetilases/farmacologia
Neoplasias Pancreáticas/patologia
Fenilbutiratos/farmacologia
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Ciclo Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Seres Humanos
Camundongos
Camundongos Endogâmicos BALB C
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Histone Deacetylase Inhibitors); 0 (OSU-HDAC42 compound); 0 (Phenylbutyrates)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170823
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0183368


  9 / 1563 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28728848
[Au] Autor:Liu Y; Zhu H; Yan X; Gu H; Gu Z; Liu F
[Ad] Endereço:Department of Orthopaedics, Affiliated Hospital of Nantong University, Nantong, Jiangsu Province, China.
[Ti] Título:Endoplasmic reticulum stress participates in the progress of senescence and apoptosis of osteoarthritis chondrocytes.
[So] Source:Biochem Biophys Res Commun;491(2):368-373, 2017 Sep 16.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Endoplasmic reticulum stress (ERS) has been shown to participate in many disease pathologies. Recent reports have reported that ERS exists in human osteoarthritis (OA) chondrocytes. During OA, chondrocytes exhibit increased level of some senescence marker, such as senescence-associated ß-galactosidase (SA ß-gal) activity. However, the persistence and accumulation of senescent cells in various tissues can also impair function and have been involved in the pathogenesis of many age-related diseases, including OA. In this present study, we used IL-1ß (10 ng/ml) to mimic OA chondrocytes and we found that IL-1ß stimulated chondrocytes caused the increasing expression of ADAMTS5 and MMP13, decreasing COL2A1 expression, which were in accord with OA chondrocytes changes. Our data also showed that ERS is involved in the OA chondrocytes, SA ß-gal activity significantly increases and inhibition of ERS can decrease the SA ß-gal activity, apoptosis of OA chondrocytes and increase cell viability. These results help us to open new perspectives for the development of molecular-targeted treatment approaches and thus present an effective novel therapeutic approach for OA.
[Mh] Termos MeSH primário: Condrócitos/efeitos dos fármacos
Estresse do Retículo Endoplasmático/efeitos dos fármacos
Interleucina-1beta/farmacologia
Osteoartrite/genética
Fenilbutiratos/farmacologia
[Mh] Termos MeSH secundário: Proteína ADAMTS5/genética
Proteína ADAMTS5/metabolismo
Apoptose/efeitos dos fármacos
Cartilagem Articular/citologia
Cartilagem Articular/efeitos dos fármacos
Cartilagem Articular/metabolismo
Sobrevivência Celular/efeitos dos fármacos
Senescência Celular/efeitos dos fármacos
Condrócitos/citologia
Condrócitos/metabolismo
Colágeno Tipo II/genética
Colágeno Tipo II/metabolismo
Estresse do Retículo Endoplasmático/genética
Regulação da Expressão Gênica
Seres Humanos
Interleucina-1beta/antagonistas & inibidores
Metaloproteinase 13 da Matriz/genética
Metaloproteinase 13 da Matriz/metabolismo
Modelos Biológicos
Osteoartrite/metabolismo
Osteoartrite/patologia
Cultura Primária de Células
Transdução de Sinais
beta-Galactosidase/antagonistas & inibidores
beta-Galactosidase/genética
beta-Galactosidase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (COL2A1 protein, human); 0 (Collagen Type II); 0 (IL1B protein, human); 0 (Interleukin-1beta); 0 (Phenylbutyrates); 7WY7YBI87E (4-phenylbutyric acid); EC 3.2.1.23 (beta-Galactosidase); EC 3.4.24.- (ADAMTS5 Protein); EC 3.4.24.- (ADAMTS5 protein, human); EC 3.4.24.- (MMP13 protein, human); EC 3.4.24.- (Matrix Metalloproteinase 13)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170722
[St] Status:MEDLINE


  10 / 1563 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28712870
[Au] Autor:Espada S; Stavik B; Holm S; Sagen EL; Bjerkeli V; Skjelland M; Dahl TB; Espevik T; Kanse S; Sandset PM; Skretting G; Halvorsen B
[Ad] Endereço:Department of Haematology, Oslo University Hospital, BOX 4950 Nydalen, 0424 Oslo, Norway; Research Institute of Internal Medicine, Oslo University Hospital, BOX 4950 Nydalen, 0424 Oslo, Norway; Institute of Basic Medical Sciences, University of Oslo, Box 1072 Blindern, 0316 Oslo, Norway.
[Ti] Título:Tissue factor pathway inhibitor attenuates ER stress-induced inflammation in human M2-polarized macrophages.
[So] Source:Biochem Biophys Res Commun;491(2):442-448, 2017 Sep 16.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Endoplasmic reticulum (ER) stress has been shown to play a key role during the initiation and clinical progression of the cardiovascular diseases, such as atherosclerosis. We have recently shown that expression of tissue factor pathway inhibitor (TFPI) in human monocyte-derived macrophages (MDMs) was induced by cholesterol crystals (CC). In the present study we aimed to determine the role of TFPI under ER stress conditions using human MDMs. qRT-PCR and immunohistochemistry analysis were performed to determine the presence of the ER stress marker CCAAT/enhancer binding protein homologous protein (CHOP) and TFPI in human carotid plaque material and also in human MDMs polarized into pro-inflammatory M1 or anti-inflammatory M2 populations. CHOP mRNA levels were upregulated in the plaques compared to healthy vessels, and CHOP protein was localized in the same area as TFPI in the plaques. Both CHOP and TFPI mRNA levels were upregulated after CC treatment, especially in the M2 phenotype, and the ER stress inhibitor 4-phenylbutyric acid (PBA) reversed this effect. Furthermore, CC treatment increased the levels of the pro-inflammatory cytokines TNF-α, IL-6, and IL-8, which for TNF-α and IL-8 was inhibited by PBA, and reduced the levels of the anti-inflammatory cytokine IL-10 in M2-polarized macrophages. Knockdown of TFPI prior to CC treatment exacerbated TNF-α and IL-6 levels, but reduced IL-8 and IL-10 levels. Our results show that CC induce TFPI and cytokine expression in M2-polarized macrophages through activation of the ER stress pathway and that TFPI has a protective effect against TNF-α and IL-6 mediated inflammation. These mechanisms may have implications for the pathogenesis of atherosclerosis.
[Mh] Termos MeSH primário: Aterosclerose/genética
Colesterol/farmacologia
Estresse do Retículo Endoplasmático/genética
Lipoproteínas/genética
Placa Aterosclerótica/genética
RNA Mensageiro/genética
[Mh] Termos MeSH secundário: Aterosclerose/imunologia
Aterosclerose/patologia
Aterosclerose/cirurgia
Artérias Carótidas/efeitos dos fármacos
Artérias Carótidas/imunologia
Artérias Carótidas/patologia
Artérias Carótidas/cirurgia
Cristalização
Endarterectomia das Carótidas
Retículo Endoplasmático/efeitos dos fármacos
Retículo Endoplasmático/genética
Retículo Endoplasmático/metabolismo
Estresse do Retículo Endoplasmático/efeitos dos fármacos
Regulação da Expressão Gênica
Seres Humanos
Interleucina-10/genética
Interleucina-10/imunologia
Interleucina-6/genética
Interleucina-6/imunologia
Interleucina-8/genética
Interleucina-8/imunologia
Lipoproteínas/antagonistas & inibidores
Lipoproteínas/imunologia
Macrófagos/efeitos dos fármacos
Macrófagos/imunologia
Macrófagos/patologia
Fenilbutiratos/farmacologia
Placa Aterosclerótica/imunologia
Placa Aterosclerótica/patologia
Placa Aterosclerótica/cirurgia
Cultura Primária de Células
RNA Mensageiro/imunologia
RNA Interferente Pequeno/genética
RNA Interferente Pequeno/metabolismo
Transdução de Sinais
Fator de Transcrição CHOP/genética
Fator de Transcrição CHOP/imunologia
Fator de Necrose Tumoral alfa/genética
Fator de Necrose Tumoral alfa/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DDIT3 protein, human); 0 (IL10 protein, human); 0 (IL6 protein, human); 0 (Interleukin-6); 0 (Interleukin-8); 0 (Lipoproteins); 0 (Phenylbutyrates); 0 (RNA, Messenger); 0 (RNA, Small Interfering); 0 (Tumor Necrosis Factor-alpha); 0 (lipoprotein-associated coagulation inhibitor); 130068-27-8 (Interleukin-10); 147336-12-7 (Transcription Factor CHOP); 7WY7YBI87E (4-phenylbutyric acid); 97C5T2UQ7J (Cholesterol)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170829
[Lr] Data última revisão:
170829
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170718
[St] Status:MEDLINE



página 1 de 157 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