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[PMID]:29318581
[Au] Autor:Vietto V; Franco JV; Saenz V; Cytryn D; Chas J; Ciapponi A
[Ad] Endereço:Family and Community Medicine Service, Hospital Italiano de Buenos Aires, Buenos Aires, Argentina.
[Ti] Título:Prostanoids for critical limb ischaemia.
[So] Source:Cochrane Database Syst Rev;1:CD006544, 2018 01 10.
[Is] ISSN:1469-493X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Peripheral arterial occlusive disease (PAOD) is a common cause of morbidity and mortality due to cardiovascular disease in the general population. Although numerous treatments have been adopted for patients at different disease stages, no option other than amputation is available for patients presenting with critical limb ischaemia (CLI) unsuitable for rescue or reconstructive intervention. In this regard, prostanoids have been proposed as a therapeutic alternative, with the aim of increasing blood supply to the limb with occluded arteries through their vasodilatory, antithrombotic, and anti-inflammatory effects. This is an update of a review first published in 2010. OBJECTIVES: To determine the effectiveness and safety of prostanoids in patients with CLI unsuitable for rescue or reconstructive intervention. SEARCH METHODS: For this update, the Cochrane Vascular Information Specialist searched the Specialised Register (January 2017) and the Cochrane Central Register of Controlled Trials (CENTRAL; 2017, Issue 1). In addition, we searched trials registries (January 2017) and contacted pharmaceutical manufacturers, in our efforts to identify unpublished data and ongoing trials. SELECTION CRITERIA: Randomised controlled trials describing the efficacy and safety of prostanoids compared with placebo or other pharmacological control treatments for patients presenting with CLI without chance of rescue or reconstructive intervention. DATA COLLECTION AND ANALYSIS: Two review authors independently selected trials, assessed trials for eligibility and methodological quality, and extracted data. We resolved disagreements by consensus or by consultation with a third review author. MAIN RESULTS: For this update, 15 additional studies fulfilled selection criteria. We included in this review 33 randomised controlled trials with 4477 participants; 21 compared different prostanoids versus placebo, seven compared prostanoids versus other agents, and five conducted head-to-head comparisons using two different prostanoids.We found low-quality evidence that suggests no clear difference in the incidence of cardiovascular mortality between patients receiving prostanoids and those given placebo (risk ratio (RR) 0.81, 95% confidence interval (CI) 0.41 to 1.58). We found high-quality evidence showing that prostanoids have no effect on the incidence of total amputations when compared with placebo (RR 0.97, 95% CI 0.86 to 1.09). Adverse events were more frequent with prostanoids than with placebo (RR 2.11, 95% CI 1.79 to 2.50; moderate-quality evidence). The most commonly reported adverse events were headache, nausea, vomiting, diarrhoea, flushing, and hypotension. We found moderate-quality evidence showing that prostanoids reduced rest-pain (RR 1.30, 95% CI 1.06 to 1.59) and promoted ulcer healing (RR 1.24, 95% CI 1.04 to 1.48) when compared with placebo, although these small beneficial effects were diluted when we performed a sensitivity analysis that excluded studies at high risk of bias. Additionally, we found evidence of low to very low quality suggesting the effects of prostanoids versus other active agents or versus other prostanoids because studies conducting these comparisons were few and we judged them to be at high risk of bias. None of the included studies assessed quality of life. AUTHORS' CONCLUSIONS: We found high-quality evidence showing that prostanoids have no effect on the incidence of total amputations when compared against placebo. Moderate-quality evidence showed small beneficial effects of prostanoids for rest-pain relief and ulcer healing when compared with placebo. Additionally, moderate-quality evidence showed a greater incidence of adverse effects with the use of prostanoids, and low-quality evidence suggests that prostanoids have no effect on cardiovascular mortality when compared with placebo. None of the included studies reported quality of life measurements. The balance between benefits and harms associated with use of prostanoids in patients with critical limb ischaemia with no chance of reconstructive intervention is uncertain; therefore careful assessment of therapeutic alternatives should be considered. Main reasons for downgrading the quality of evidence were high risk of attrition bias and imprecision of effect estimates.
[Mh] Termos MeSH primário: Isquemia/tratamento farmacológico
Perna (Membro)/irrigação sanguínea
Doenças Vasculares Periféricas/tratamento farmacológico
Prostaglandinas/uso terapêutico
[Mh] Termos MeSH secundário: Alprostadil/uso terapêutico
Amputação/estatística & dados numéricos
Epoprostenol/uso terapêutico
Seres Humanos
Iloprosta/uso terapêutico
Isquemia/mortalidade
Perna (Membro)/cirurgia
Úlcera da Perna/tratamento farmacológico
Nafronil/uso terapêutico
Ácidos Nicotínicos/uso terapêutico
Pentoxifilina/uso terapêutico
Prostaglandinas/efeitos adversos
Ensaios Clínicos Controlados Aleatórios como Assunto
Vasodilatadores/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (Nicotinic Acids); 0 (Prostaglandins); 0 (Vasodilator Agents); 42H8PQ0NMJ (Nafronyl); A99MK953KZ (Inositol Niacinate); DCR9Z582X0 (Epoprostenol); F5TD010360 (Alprostadil); JED5K35YGL (Iloprost); SD6QCT3TSU (Pentoxifylline)
[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:180111
[St] Status:MEDLINE
[do] DOI:10.1002/14651858.CD006544.pub3


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[PMID]:29261735
[Au] Autor:Boivin A; Burban M; Clere-Jehl R; Le Borgne P; Merdji H; Auger C; Schini-Kerth V; Meziani F; Helms J
[Ad] Endereço:Université de Strasbourg (UNISTRA), Faculté de Médecine, Hôpitaux universitaires de Strasbourg, service de réanimation, nouvel hôpital civil, Strasbourg, France.
[Ti] Título:Docosahexaenoic acid, but not eicosapentaenoic acid, improves septic shock-induced arterial dysfunction in rats.
[So] Source:PLoS One;12(12):e0189658, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Long chain n-3 fatty acid supplementation may modulate septic shock-induced host response to pathogen-induced sepsis. The composition of lipid emulsions for parenteral nutrition however remains a real challenge in intensive care, depending on their fatty acid content. Because they have not been assessed yet, we aimed at determining the respective effects of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) during septic shock-induced vascular dysfunction. METHODS: In a peritonitis-induced septic shock model, rats were infused with EPA, DHA, an EPA/DHA mixture or 5% dextrose (D5) during 22 hours. From H18, rats were resuscitated and monitored during 4 hours. At H22, plasma, aorta and mesenteric resistance arteries were collected to perform ex vivo experiments. RESULTS: We have shown that septic rats needed an active resuscitation with fluid challenge and norepinephrine treatment, while SHAM rats did not. In septic rats, norepinephrine requirements were significantly decreased in DHA and EPA/DHA groups (10.6±12.0 and 3.7±8.0 µg/kg/min respectively versus 17.4±19.3 µg/kg/min in D5 group, p<0.05) and DHA infusion significantly improved contractile response to phenylephrine through nitric oxide pathway inhibition. DHA moreover significantly reduced vascular oxidative stress and nitric oxide production, phosphorylated IκB expression and vasodilative prostaglandin production. DHA also significantly decreased polyunsaturated fatty acid pro-inflammatory mediators and significantly increased several anti-inflammatory metabolites. CONCLUSIONS: DHA infusion in septic rats improved hemodynamic dysfunction through decreased vascular oxidative stress and inflammation, while EPA infusion did not have beneficial effects.
[Mh] Termos MeSH primário: Artérias/patologia
Ácidos Docosa-Hexaenoicos/uso terapêutico
Ácido Eicosapentaenoico/uso terapêutico
Choque Séptico/complicações
Doenças Vasculares/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Epoprostenol/biossíntese
Masculino
Óxido Nítrico/biossíntese
Norepinefrina/administração & dosagem
Estresse Oxidativo
Ratos
Ratos Wistar
Doenças Vasculares/etiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
25167-62-8 (Docosahexaenoic Acids); 31C4KY9ESH (Nitric Oxide); AAN7QOV9EA (Eicosapentaenoic Acid); DCR9Z582X0 (Epoprostenol); X4W3ENH1CV (Norepinephrine)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180116
[Lr] Data última revisão:
180116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171221
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189658


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[PMID]:27771466
[Au] Autor:Marra AM; Benjamin N; Eichstaedt C; Salzano A; Arcopinto M; Gargani L; D Alto M; Argiento P; Falsetti L; Di Giosia P; Isidori AM; Ferrara F; Bossone E; Cittadini A; Grünig E
[Ad] Endereço:IRCCS SDN, Via Gianturco 113, 80143 Naples, Italy. Electronic address: alberto_marra@hotmail.it.
[Ti] Título:Gender-related differences in pulmonary arterial hypertension targeted drugs administration.
[So] Source:Pharmacol Res;114:103-109, 2016 Dec.
[Is] ISSN:1096-1186
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:During the last 15 years, a real "paradigm-shift" occurred, due to the development of PAH-targeted drugs, leading to crucial improvements in symptoms, exercise capacity, hemodynamics and outcome of PAH patients. In order to describe differences regarding epidemiology and therapy in PAH according to gender, we performed a review of the available literature in "PubMed" and "Web of Science" databases. In order to find relevant articles, we combined each of the following the keywords "pulmonary arterial hypertension", "gender", "sex", "men", "woman", "male", "female", "phosphodiesterase inhibitors", "endothelin receptor antagonists", "prostanoids". While there is a substantial agreement among epidemiological studies in reporting an increased prevalence of pulmonary arterial hypertension (PAH) among women, male PAH patients are affected by a higher impairment of the right ventricular function and consequently experience poorer outcomes. With regards to PAH-targeted drug administration, endothelin receptor antagonists (ERAs) and prostacyclin analogues (PC) show better treatment results in female PAH patients, while phosphodiesterase-5 inhibitors (PD5-I) seem to exert a more beneficial effect on male patients. However, to date no clear consensus could be formed by the available literature, which is constituted mainly by retrospective studies. Females with PAH are more prone to develop PAH, while males experience poorer outcomes. Females PAH might benefit more from ERAs and PC, while males seem to have more beneficial effects from PD5-I administration. However, more research is warranted in order to assess the most effective treatment for PAH patients according to gender.
[Mh] Termos MeSH primário: Anti-Hipertensivos/uso terapêutico
Antagonistas dos Receptores de Endotelina/uso terapêutico
Epoprostenol/uso terapêutico
Hipertensão Pulmonar/tratamento farmacológico
Hipertensão Pulmonar/epidemiologia
Inibidores da Fosfodiesterase 5/uso terapêutico
[Mh] Termos MeSH secundário: Anti-Hipertensivos/administração & dosagem
Antagonistas dos Receptores de Endotelina/administração & dosagem
Epoprostenol/administração & dosagem
Epoprostenol/análogos & derivados
Feminino
Seres Humanos
Hipertensão Pulmonar/fisiopatologia
Masculino
Inibidores da Fosfodiesterase 5/administração & dosagem
Fatores Sexuais
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antihypertensive Agents); 0 (Endothelin Receptor Antagonists); 0 (Phosphodiesterase 5 Inhibitors); DCR9Z582X0 (Epoprostenol)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171226
[Lr] Data última revisão:
171226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161107
[St] Status:MEDLINE


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[PMID]:28887131
[Au] Autor:Misawa H; Ohashi W; Tomita K; Hattori K; Shimada Y; Hattori Y
[Ad] Endereço:Department of Molecular and Medical Pharmacology, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, Toyama, Japan; Department of Japanese Oriental Medicine, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, Toyama, Japan.
[Ti] Título:Prostacyclin mimetics afford protection against lipopolysaccharide/d-galactosamine-induced acute liver injury in mice.
[So] Source:Toxicol Appl Pharmacol;334:55-65, 2017 Nov 01.
[Is] ISSN:1096-0333
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Prostacyclin (PGI ) serves as a protective, anti-inflammatory mediator and PGI mimetics may be useful as a hepatoprotective agent. We examined whether two PGI mimetics, ONO-1301 and beraprost, are beneficial in acute liver injury and attempted to delineate the possible mechanism underlying the hepatoprotective effect. Acute liver injury was induced by lipopolysaccharide/d-galactosamine (LPS/GalN) in mice. Mice were given an intraperitoneal injection of PGI mimetics 1h before LPS/GalN challenge. Both ONO-1301 and beraprost significantly declined the LPS/GalN-induced increase in serum aminotransferase activity. ONO-1301 and, to a lesser extent, beraprost inhibited hepatic gene expression levels of pro-inflammatory cytokines, which were sharply elevated by LPS/GalN. The hepatoprotective effects of ONO-1301, to a lesser extent, of beraprost were also supported by liver histopathological examinations. The PGI receptor antagonist CAY10441 abrogated their hepatoprotective effects. The mechanisms behind the benefit of PGI mimetics in reducing LPS/GalN-induced liver injury involved, in part, their suppressive effects on increased generation of reactive oxygen species (ROS), since their ability to prevent LPS/GalN-induced hepatic apoptosis was mimicked by the antioxidant N-acetyl-l-cysteine. They significantly diminished LPS/GalN-induced activation of signal transducers and activators of transcription 3 (STAT3) in liver tissues, an effect which was highly associated with their hepatoprotective effects. We indicate that IP receptor activation with PGI mimetics can rescue the damage in the liver induced by LPS/GalN by undermining activation of STAT3 and leading to a lower production of ROS. Our findings point to PGI mimetics, especially ONO-1301, as a potential novel therapeutic modality for the treatment of acute liver injury.
[Mh] Termos MeSH primário: Doença Hepática Induzida por Substâncias e Drogas/prevenção & controle
Epoprostenol/análogos & derivados
Galactosamina/toxicidade
Lipopolissacarídeos/toxicidade
Piridinas/farmacologia
[Mh] Termos MeSH secundário: Animais
Compostos de Benzil/farmacologia
Proteína de Ligação a CREB/genética
Proteína de Ligação a CREB/metabolismo
Epoprostenol/farmacologia
Galactosamina/administração & dosagem
Regulação da Expressão Gênica
Imidazóis/farmacologia
Lipopolissacarídeos/administração & dosagem
Camundongos
Quinases de Proteína Quinase Ativadas por Mitógeno/genética
Quinases de Proteína Quinase Ativadas por Mitógeno/metabolismo
Prostaglandinas I/química
Prostaglandinas I/farmacologia
Espécies Reativas de Oxigênio
Fator de Transcrição STAT3/genética
Fator de Transcrição STAT3/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 ((2-(4-(4-isopropoxybenzyl)-phenylamino) imidazoline)); 0 (Benzyl Compounds); 0 (Imidazoles); 0 (Lipopolysaccharides); 0 (Prostaglandins I); 0 (Pyridines); 0 (Reactive Oxygen Species); 0 (STAT3 Transcription Factor); 0 (Stat3 protein, mouse); 176391-41-6 (ONO 1301); 35E3NJJ4O6 (beraprost); 7535-00-4 (Galactosamine); DCR9Z582X0 (Epoprostenol); EC 2.3.1.48 (CREB-Binding Protein); EC 2.3.1.48 (Crebbp protein, mouse); EC 2.7.12.2 (Mitogen-Activated Protein Kinase Kinases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171017
[Lr] Data última revisão:
171017
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170910
[St] Status:MEDLINE


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[PMID]:28880908
[Au] Autor:Obilade OA; Akanmu AS; Broughton Pipkin F; Afolabi BB
[Ad] Endereço:Department of Obstetrics and Gynaecology, Lagos University Teaching Hospital, Idi-Araba, Lagos, Nigeria.
[Ti] Título:Prostacyclin, thromboxane and glomerular filtration rate are abnormal in sickle cell pregnancy.
[So] Source:PLoS One;12(9):e0184345, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Pregnancy increases the risk of morbidity and mortality in sickle cell disease. We previously showed pregnant women with sickle cell disease to have a relatively low plasma renin concentration in late pregnancy, associated with a lack of the expected plasma volume expansion. We hypothesized this to be due to increased systemic vascular resistance through an imbalance between the vasodilator prostacyclin and vasoconstrictor thromboxane, associated with decreased glomerular filtration rate (GFR). OBJECTIVE: To compare estimated prostacyclin, thromboxane and GFR in non-pregnant and pregnant women with hemoglobin SS (HbSS) and AA (HbAA). STUDY DESIGN: Four groups of 20 normotensive, nulliparous women were studied in Lagos, Nigeria: pregnant HbSS or HbAA women at 36-40 weeks gestation; non-pregnant HbSS and HbAA controls. We measured stable metabolites of prostacyclin and thromboxane A2 by enzyme-linked immunosorbent assay; GFR using the Cockcroft-Gault equation. Data analysis was by independent (Student's) t-test or Mann-Whitney U test for comparisons between any two groups of continuous variables, univariate ANOVA for multiple groups and Pearson's correlation coefficient for degree of association between variables. RESULTS: HbSS women had lower serum 6-keto-PGF1α concentrations than HbAA, whether pregnant or non-pregnant (P<0.001; P<0.004 respectively). Conversely, pregnant HbSS women had higher serum TxB2 (P<0.001); non-pregnant HbSS women had non-significantly higher TxB2 concentrations. The 6-keto-PGF1α:TxB2 ratio was markedly increased (pro-vasodilatory) in HbAA pregnancy (P<0.001) but reduced in HbSS pregnancy (P = 0.037). GFRs (mL/min) were higher in non-pregnant HbSS than HbAA (P<0.008) but only marginally raised in HbSS women in late pregnancy (P = 0.019) while markedly raised in HbAA pregnancy (P<0.001). CONCLUSION: The lower ratio of prostacyclin-thromboxane metabolites in HbSS pregnancy may indicate endothelial damage and an increased tendency to vasoconstriction and clotting. If confirmed by subsequent longitudinal studies, interventions to increase prostacyclin and reduce thromboxane, such as low dose aspirin, may be potentially useful in their management.
[Mh] Termos MeSH primário: Anemia Falciforme/sangue
Epoprostenol/sangue
Tromboxanos/sangue
[Mh] Termos MeSH secundário: 6-Cetoprostaglandina F1 alfa/sangue
Adulto
Pressão Sanguínea/fisiologia
Creatinina/sangue
Estudos Transversais
Eicosanoides/sangue
Feminino
Genótipo
Taxa de Filtração Glomerular/fisiologia
Seres Humanos
Estudos Longitudinais
Gravidez
Resultado da Gravidez
Tromboxano A2/sangue
Tromboxano B2/sangue
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Eicosanoids); 0 (Thromboxanes); 54397-85-2 (Thromboxane B2); 57576-52-0 (Thromboxane A2); 58962-34-8 (6-Ketoprostaglandin F1 alpha); AYI8EX34EU (Creatinine); DCR9Z582X0 (Epoprostenol)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170908
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184345


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[PMID]:28733316
[Au] Autor:Attaway AH; Myers C; Velani S; Schilz R
[Ad] Endereço:University Hospital Cleveland Department of Pulmonary and Critical Care Medicine Cleveland Ohio amyattaway25@gmail.com.
[Ti] Título:Inhaled Prostacyclin as Salvage Therapy for ARDS: Can We Find the Right Patient?
[So] Source:Respir Care;62(8):1113-1115, 2017 08.
[Is] ISSN:1943-3654
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Epoprostenol
Terapia de Salvação
[Mh] Termos MeSH secundário: Administração por Inalação
Hemodinâmica/efeitos dos fármacos
Seres Humanos
Hipertensão Pulmonar
Óxido Nítrico
Síndrome do Desconforto Respiratório do Adulto
Vasodilatadores
[Pt] Tipo de publicação:EDITORIAL; COMMENT
[Nm] Nome de substância:
0 (Vasodilator Agents); 31C4KY9ESH (Nitric Oxide); DCR9Z582X0 (Epoprostenol)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170814
[Lr] Data última revisão:
170814
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170723
[St] Status:MEDLINE
[do] DOI:10.4187/respcare.05708


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[PMID]:28732575
[Au] Autor:Zhang P; Xu L; Guan H; Liu L; Liu J; Huang Z; Cao X; Liao Z; Xiao H; Li Y
[Ad] Endereço:The First Affiliated Hospital, Sun Yat-sen University, Department of Endocrinology, Guangzhou, 510080, China.
[Ti] Título:Beraprost sodium, a prostacyclin analogue, reduces fructose-induced hepatocellular steatosis in mice and in vitro via the microRNA-200a and SIRT1 signaling pathway.
[So] Source:Metabolism;73:9-21, 2017 Aug.
[Is] ISSN:1532-8600
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: To determine whether beraprost sodium, a prostacyclin analogue, could reduce hepatic lipid accumulation induced by fructose in mice and cultured human hepatocytes, and to investigate the expression of microRNAs and the sirtuin 1 (SIRT1) pathway. METHODS: Male C57BL/6JNju mice were divided into three groups and fed one of the following diets: a normal diet, a high fructose diet, or a high fructose diet with beraprost sodium treatment. In addition, human-derived HepG2 cells were cultured and treated with fructose (25mmol/L) with or without beraprost sodium (10µmol/L) for 24h, and transfected with small interfering RNA (siRNA) against SIRT1, miR-200a mimic, or miR-200a inhibitor for 48h. The miRNA microarray analysis was performed on the HepG2 cells, and the expression profiles of miRNAs were analyzed using Gene Cluster 3.0 and verified using qPCR. RESULTS: Beraprost sodium treatment attenuated hepatic steatosis, induced the transcription of genes involved in lipid metabolism in C57BL/6 mice (P<0.05), and increased the expression of hepatic SIRT1 and peroxisome proliferator activated receptor α (PPARα) in the cells treated with fructose. These effects were blocked in HepG2 cells after transfection with siRNA against SIRT1. MiR-200a was highly expressed during fructose treatment and was down regulated by beraprost sodium (P<0.05). A luciferase assay showed that miR-200a regulated SIRT1 by binding to the 3' UTR. Overexpression of miR-200a inhibited expression of hepatic SIRT1. CONCLUSIONS: Our study demonstrated that SIRT1 pathway mediated the effects of beraprost sodium on attenuation of hepatic lipid disorders induced by fructose and revealed the primary role of miR-200a in the regulation of hepatic SIRT1 by beraprost sodium. Our findings suggested that SIRT1 might be a therapeutic target of fructose-related metabolism disorders.
[Mh] Termos MeSH primário: Epoprostenol/análogos & derivados
Fígado Gorduroso/tratamento farmacológico
Frutose/farmacologia
MicroRNAs/metabolismo
Sirtuína 1/metabolismo
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Epoprostenol/farmacologia
Fígado Gorduroso/induzido quimicamente
Regulação da Expressão Gênica/efeitos dos fármacos
Células Hep G2
Seres Humanos
Metabolismo dos Lipídeos/genética
Camundongos
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MicroRNAs); 0 (Mirn200 microRNA, mouse); 30237-26-4 (Fructose); 35E3NJJ4O6 (beraprost); DCR9Z582X0 (Epoprostenol); EC 3.5.1.- (Sirtuin 1)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171003
[Lr] Data última revisão:
171003
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170723
[St] Status:MEDLINE


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[PMID]:28690295
[Au] Autor:Akagi S; Oto T; Kobayashi M; Miyoshi K; Sugimoto S; Yamane M; Nakamura K; Sarashina T; Miyoshi S; Ito H
[Ad] Endereço:Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences.
[Ti] Título:High Frequency of Acute Adverse Cardiovascular Events After Lung Transplantation in Patients With Pulmonary Arterial Hypertension Receiving Preoperative Long-Term Intravenous Prostacyclin.
[So] Source:Int Heart J;58(4):557-561, 2017 Aug 03.
[Is] ISSN:1349-3299
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Adverse cardiovascular events after lung transplantation (LT) increase the mortality in patients with pulmonary arterial hypertension (PAH). Long-term intravenous prostacyclin is the usual treatment in severe patients with PAH, but it may increase the risk of hemorrhage due to its antiplatelet aggregation effect or thrombocytopenia. We investigated the impact of length of intravenous prostacyclin therapy on acute adverse cardiovascular events including hemorrhagic complication after LT. We retrospectively compared the incidence of adverse events (death, intrathoracic hematoma and bleeding, cardiac congestion or shock, cerebral infarction and pulmonary embolism) within 30 days after LT between no/short-term (median 0.6 years, n = 13) and long-term (median 3.7 years, n = 15) intravenous prostacyclin groups. There were no differences in the dose of intravenous prostacyclin and pulmonary artery pressure between the two groups. Among 22 adverse events (0.8 ± 1.1 events/patient), 4 events occurred in the no/short-term intravenous prostacyclin group and 18 occurred in the long-term intravenous prostacyclin group. The event rate per patient in the long-term intravenous prostacyclin group (1.2 ± 1.3 events/patient) was significantly higher than that in the no/short-term intravenous prostacyclin group (0.3 ± 0.5 events/patient) (P < 0.05). Intrathoracic hematoma and bleeding was the most frequent adverse event (9 events, 41%). Preoperative long-term intravenous prostacyclin therapy increases acute adverse cardiovascular events after LT in patients with PAH.
[Mh] Termos MeSH primário: Doenças Cardiovasculares/epidemiologia
Epoprostenol/administração & dosagem
Hipertensão Pulmonar/terapia
Transplante de Pulmão/efeitos adversos
Cuidados Pré-Operatórios/métodos
[Mh] Termos MeSH secundário: Doença Aguda
Adolescente
Adulto
Anti-Hipertensivos/administração & dosagem
Doenças Cardiovasculares/diagnóstico
Doenças Cardiovasculares/etiologia
Relação Dose-Resposta a Droga
Ecocardiografia
Feminino
Seguimentos
Seres Humanos
Hipertensão Pulmonar/fisiopatologia
Incidência
Injeções Intravenosas
Japão/epidemiologia
Masculino
Complicações Pós-Operatórias
Pressão Propulsora Pulmonar/fisiologia
Estudos Retrospectivos
Taxa de Sobrevida/tendências
Fatores de Tempo
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antihypertensive Agents); DCR9Z582X0 (Epoprostenol)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170810
[Lr] Data última revisão:
170810
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170711
[St] Status:MEDLINE
[do] DOI:10.1536/ihj.16-389


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[PMID]:28674339
[Au] Autor:Hazekawa M; Kojima H; Haraguchi T; Yoshida M; Uchida T
[Ad] Endereço:School of Pharmaceutical Science, Mukogawa Women's University.
[Ti] Título:Effect of Self-healing Encapsulation on the Initial Burst Release from PLGA Microspheres Containing a Long-Acting Prostacyclin Agonist, ONO-1301.
[So] Source:Chem Pharm Bull (Tokyo);65(7):653-659, 2017.
[Is] ISSN:1347-5223
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:The purpose of this study was to perform self-healing encapsulation of ONO-1301, a long-acting prostacyclin agonist, into poly(lactide-co-glycolide) (PLGA) microspheres using the oil-in-water (o/w) emulsion solvent evaporation method in order to try to limit the initial burst release of drug. Adequate self-healing of PLGA seemed to be achieved by stirring during the evaporation of solvent at 40°C close to the glass transition temperature (T ) of the polymer (40.1°C). The plasticizers dimethylphthalate (DEP) or tributyl O-acetylcitrate (TBAC), at concentrations of 0.1-1.0%, to the internal oleogeneous phase in the o/w emulsion system was effective in restricting the initial burst release of the prepared microspheres. The combination of a self-healing at T of the polymer and the addition of 1% of each plasticizer was ultimately found to be the most effective in restricting the initial burst release. It is suggested that this is due to the synergistic effect of smooth surface morphology promoted by self-healing at T of the polymer and a decrease of the T of PLGA caused by the addition of plasticizers.
[Mh] Termos MeSH primário: Epoprostenol/agonistas
Ácido Láctico/química
Microesferas
Ácido Poliglicólico/química
Piridinas/administração & dosagem
[Mh] Termos MeSH secundário: Varredura Diferencial de Calorimetria
Interações Hidrofóbicas e Hidrofílicas
Cinética
Microscopia Eletrônica de Varredura
Tamanho da Partícula
Solventes/química
Temperatura Ambiente
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Pyridines); 0 (Solvents); 0 (polylactic acid-polyglycolic acid copolymer); 176391-41-6 (ONO 1301); 26009-03-0 (Polyglycolic Acid); 33X04XA5AT (Lactic Acid); DCR9Z582X0 (Epoprostenol)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170814
[Lr] Data última revisão:
170814
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170705
[St] Status:MEDLINE
[do] DOI:10.1248/cpb.c17-00025


  10 / 12327 MEDLINE  
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[PMID]:28658134
[Au] Autor:Park BY; Chung SH
[Ad] Endereço:Department of Pediatrics, Kyung Hee University School of Medicine, Seoul, Korea.
[Ti] Título:Treprostinil for persistent pulmonary hypertension of the newborn, with early onset sepsis in preterm infant: 2 Case reports.
[So] Source:Medicine (Baltimore);96(26):e7303, 2017 Jun.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Persistent pulmonary hypertension of the newborn (PPHN) is a syndrome of failed circulatory adaptation at birth with persisting increased pulmonary vascular resistance that is associated with high mortality rates especially in preterm infants. PATIENT CONCERNS: We reported 2 cases of PPHN in preterm infants with respiratory distress syndrome and early onset sepsis refractory to therapy with vasopressors, inotropes, and inhaled nitric oxide (iNO), in whom treatment with treprostinil was successful. DIAGNOSES: Infants showed a difference of more than 10% between pre- and postductal saturation of peripheral oxygen by pulse oximetry. Echocardiogram showed flattened ventricular septum, right to left shunting through the patent ductus arteriosus, and tricuspid regurgitation velocity above 2.9 m/s. INTERVENTIONS: The patients received treprostinil through central venous line because iNO therapy was not effective. OUTCOMES: Within 6 to 12 hours after treatment with treprostinil, the patients showed dramatic clinical improvement, and no systemic side effects were observed, including intraventricular hemorrhage (≥grade II). LESSONS: IV treprostinil might be given to preterm infants with severe PPHN, who did not respond to conservative therapies, including iNO.
[Mh] Termos MeSH primário: Anti-Hipertensivos/administração & dosagem
Epoprostenol/análogos & derivados
Recém-Nascido Prematuro
Síndrome da Persistência do Padrão de Circulação Fetal/complicações
Síndrome da Persistência do Padrão de Circulação Fetal/tratamento farmacológico
Sepse/complicações
[Mh] Termos MeSH secundário: Administração Intravenosa
Resistência a Medicamentos
Epoprostenol/administração & dosagem
Seres Humanos
Recém-Nascido
Masculino
Sepse/tratamento farmacológico
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antihypertensive Agents); DCR9Z582X0 (Epoprostenol); RUM6K67ESG (treprostinil)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170629
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000007303



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