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  1 / 1982 MEDLINE  
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[PMID]:28166419
[Au] Autor:Durak MA; Parlakpinar H; Polat A; Vardi N; Ekici K; Ucar M; Ozhan O; Yildiz A; Pasahan R
[Ad] Endereço:a Departments of Neurosurgery.
[Ti] Título:Protective and therapeutic effects of molsidomine on radiation induced neural injury in rats.
[So] Source:Biotech Histochem;92(1):68-77, 2017.
[Is] ISSN:1473-7760
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:We investigated the protective and therapeutic effects of molsidomine (MOL) in a rat model of whole brain radiotherapy (RT). Forty female rats were divided into five groups of eight: group 1, control; group 2, 15 Gy single dose RT (RT); group 3, 4 mg/kg MOL treated for 5 days (MOL); group 4, 4 mg/kg MOL for 5 days, 10 days after RT treatment (RT + MOL); group 5, 4 mg/kg MOL treatment for 5 days before RT treatment and for 5 days after RT treatment (MOL + RT). All rats were sacrificed on day 16. Neurodegenerative changes in the brain and tissue levels of oxidants and antioxidants were evaluated. The oxidative parameters were increased and antioxidant status was decreased in group RT compared to groups MOL + RT and RT + MOL. Histopathological examination showed that treatment with MOL after RT application and treatment with MOL before RT treatment decreased neuronal degeneration. No difference in neuronal appearance was found between groups RT + MOL and MOL + RT. MOL treatment protected the nervous system of rats and may be a treatment option for preventing RT induced neural injury.
[Mh] Termos MeSH primário: Encéfalo/efeitos da radiação
Molsidomina/uso terapêutico
Lesões Experimentais por Radiação/prevenção & controle
[Mh] Termos MeSH secundário: Animais
Encéfalo/metabolismo
Feminino
Glutationa
Malondialdeído
Molsidomina/administração & dosagem
Radiação Ionizante
Protetores contra Radiação/administração & dosagem
Protetores contra Radiação/uso terapêutico
Ratos
Superóxido Dismutase
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Radiation-Protective Agents); 4Y8F71G49Q (Malondialdehyde); D46583G77X (Molsidomine); EC 1.15.1.1 (Superoxide Dismutase); GAN16C9B8O (Glutathione)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170323
[Lr] Data última revisão:
170323
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170207
[St] Status:MEDLINE
[do] DOI:10.1080/10520295.2016.1271454


  2 / 1982 MEDLINE  
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[PMID]:28098791
[Au] Autor:Abd El-Hay SS; Colyer CL
[Ad] Endereço:Faculty of Pharmacy, Pharmaceutical Chemistry Department, King Abdulaziz University, Jeddah 21589, Saudi Arabia. sabdulhai@kau.edu.sa.
[Ti] Título:Development of High-Throughput Method for Measurement of Vascular Nitric Oxide Generation in Microplate Reader.
[So] Source:Molecules;22(1), 2017 Jan 13.
[Is] ISSN:1420-3049
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Despite the importance of nitric oxide (NO) in vascular physiology and pathology, a high-throughput method for the quantification of its vascular generation is lacking. OBJECTIVE: By using the fluorescent probe 4-amino-5-methylamino-2',7'-difluorofluorescein (DAF-FM), we have optimized a simple method for the determination of the generation of endothelial nitric oxide in a microplate format. METHODS: A nitric oxide donor was used (3-morpholinosydnonimine hydrochloride, SIN-1). Different factors affecting the method were studied, such as the effects of dye concentration, different buffers, time of reaction, gain, and number of flashes. RESULTS: Beer's law was linear over a nanomolar range (1-10 nM) of SIN-1 with wavelengths of maximum excitation and emission at 495 and 525 nm; the limit of detection reached 0.897 nM. Under the optimized conditions, the generation of rat aortic endothelial NO was measured by incubating DAF-FM with serial concentrations (10-1000 µM) of acetylcholine (ACh) for 3 min. To confirm specificity, -Nitro-l-arginine methyl ester (l-NAME)-the standard inhibitor of endothelial NO synthase-was found to inhibit the ACh-stimulated generation of NO. In addition, vessels pre-exposed for 1 h to 400 µM of the endothelial damaging agent methyl glyoxal showed inhibited NO generation when compared to the control stimulated by ACh. CONCLUSIONS: The capability of the method to measure micro-volume samples makes it convenient for the simultaneous handling of a very large number of samples. Additionally, it allows samples to be run simultaneously with their replicates to ensure identical experimental conditions, thus minimizing the effect of biological variability.
[Mh] Termos MeSH primário: Ensaios de Triagem em Larga Escala/normas
Molsidomina/análogos & derivados
Doadores de Óxido Nítrico/química
Óxido Nítrico Sintase Tipo III/metabolismo
Óxido Nítrico/análise
[Mh] Termos MeSH secundário: Acetilcolina/farmacologia
Animais
Aorta/efeitos dos fármacos
Aorta/metabolismo
Tampões (Química)
Endotélio Vascular/efeitos dos fármacos
Endotélio Vascular/metabolismo
Fluoresceínas/química
Corantes Fluorescentes/química
Limite de Detecção
Masculino
Molsidomina/química
Molsidomina/metabolismo
NG-Nitroarginina Metil Éster/farmacologia
Óxido Nítrico/biossíntese
Doadores de Óxido Nítrico/metabolismo
Óxido Nítrico Sintase Tipo III/antagonistas & inibidores
Aldeído Pirúvico/farmacologia
Ratos
Ratos Wistar
Reprodutibilidade dos Testes
Técnicas de Cultura de Tecidos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (4-amino-5-methylamino-2',7'-difluorofluorescein diacetate); 0 (Buffers); 0 (Fluoresceins); 0 (Fluorescent Dyes); 0 (Nitric Oxide Donors); 31C4KY9ESH (Nitric Oxide); 5O5U71P6VQ (linsidomine); 722KLD7415 (Pyruvaldehyde); D46583G77X (Molsidomine); EC 1.14.13.39 (Nitric Oxide Synthase Type III); EC 1.14.13.39 (Nos3 protein, rat); N9YNS0M02X (Acetylcholine); V55S2QJN2X (NG-Nitroarginine Methyl Ester)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170515
[Lr] Data última revisão:
170515
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170119
[St] Status:MEDLINE


  3 / 1982 MEDLINE  
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[PMID]:27918857
[Au] Autor:Zorniak M; Mitrega KA; Porc M; Krzeminski TF
[Ad] Endereço:a Chair and Department of Pharmacology, Medical University of Silesia, ul. Jordana 38, 41-808, Zabrze, Poland.
[Ti] Título:New approach to molsidomine active metabolites coming from the results of 2 models of experimental cardiology.
[So] Source:Can J Physiol Pharmacol;95(2):111-121, 2017 Feb.
[Is] ISSN:1205-7541
[Cp] País de publicação:Canada
[La] Idioma:eng
[Ab] Resumo:Molsidomine is a well-known vasodilatating, antianginal drug. Despite earlier studies with its metabolites (3-morpholino-syndnonimine (SIN-1) and N-nitroso-N-morpholino-amino-acetonitrile (SIN-1A)), which indicated a potential favorable cardioprotective activity, a lot of controversy remains. The aim of our research was to compare molsidomine, SIN-1, SIN-1A, and lidocaine influence on arrhythmias and hemodynamic parameters in 2 experimental models in rats. In the Langendorff heart study, SIN-1A markedly elevated left ventricular systolic pressure, maximum rise and fall of the first pressure derivative, coronary flow, and myocardial oxygen consumption. In addition, SIN-1A more so than SIN-1 significantly lowered creatine kinase release. The antiarrhythmic action of SIN-1 was observed, while lidocaine significantly diminished ventricular arrhythmias duration in comparison with the control. In the ischemia-reperfusion-induced arrhythmias model, hypotensive action of molsidomine was observed as well as the reduction in pressure rate product. Molsidomine also prolonged ventricular tachycardia duration. On the other hand, no significant effects on hemodynamic parameters as well as on ventricular arrhythmias were found in any of the SIN-1 and SIN-1A groups. In conclusion, our research suggests a possible direct, cardioprotective action of SIN-1A. It seems worthwhile to further investigate molsidomine derivatives, especially SIN-1A, because of its potential use in invasive cardiology procedures such as percutaneous transluminal coronary angioplasty.
[Mh] Termos MeSH primário: Arritmias Cardíacas/tratamento farmacológico
Hemodinâmica/efeitos dos fármacos
Molsidomina/análogos & derivados
Molsidomina/farmacologia
Nitrosaminas/farmacologia
[Mh] Termos MeSH secundário: Animais
Antiasmáticos/farmacologia
Arritmias Cardíacas/complicações
Arritmias Cardíacas/metabolismo
Creatina Quinase/metabolismo
Modelos Animais de Doenças
Preparação de Coração Isolado
Lidocaína/farmacologia
Lidocaína/uso terapêutico
Masculino
Molsidomina/uso terapêutico
Nitrosaminas/uso terapêutico
Ratos
Traumatismo por Reperfusão/complicações
Traumatismo por Reperfusão/tratamento farmacológico
Traumatismo por Reperfusão/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Asthmatic Agents); 0 (Nitrosamines); 26687-79-6 (N-nitrosomorpholinoaminoacetonitrile); 5O5U71P6VQ (linsidomine); 98PI200987 (Lidocaine); D46583G77X (Molsidomine); EC 2.7.3.2 (Creatine Kinase)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170503
[Lr] Data última revisão:
170503
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161206
[St] Status:MEDLINE
[do] DOI:10.1139/cjpp-2016-0251


  4 / 1982 MEDLINE  
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[PMID]:27764702
[Au] Autor:Lorenc-Koci E; Czarnecka A; Kaminska K; Knutelska J; Zygmunt M; Dudek M
[Ad] Endereço:Institute of Pharmacology, Polish Academy of Sciences, Department of Neuro-Psychopharmacology, 31-343 Kraków, Smetna street 12, Poland. Electronic address: lorenc@if-pan.krakow.pl.
[Ti] Título:Contribution of the nitric oxide donor molsidomine and the antiparkinsonian drug l-DOPA to the modulation of the blood pressure in unilaterally 6-OHDA-lesioned rats.
[So] Source:Pharmacol Rep;69(1):29-35, 2017 Feb.
[Is] ISSN:1734-1140
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Interaction between dopaminergic and nitrergic neurotransmission in the brain plays a crucial role in the control of motor function and in the regulation of blood pressure (BP). In Parkinson's disease (PD), dopaminergic denervation of the striatum leads to disturbances in the nitrergic system in the basal ganglia. Recently, it has been demonstrated that addition of a low dose of the nitric oxide donor molsidomine to l-DOPA therapy improves dopaminergic neurotransmission in the denervated nigrostriatal system and weakens dyskinesias in rodent models of the disease. METHODS: The aim of the present study was to examine the impact of chronic administration of molsidomine (2mg/kg) and l-DOPA (25mg/kg), alone and in combination, on systolic (SBP) and diastolic (DBP) blood pressure in the anesthetized, unilaterally 6-OHDA-lesioned rats. The measurement of SBP and DBP was performed 24h after the penultimate and immediately after the last drug doses. RESULTS: In 6-OHDA-lesioned rats receiving saline, spontaneous, small decreases in SBP and DBP were observed during the measurements lasting 60min. Administration of molsidomine alone or in combination with l-DOPA distinctly decreased the BP in 6-OHDA-lesioned rats already after 10min compared to those treated with saline or l-DOPA alone, respectively. In both groups, the molsidomine-mediated declines in BP persisted till the end of measurement but they disappeared after 24h. CONCLUSIONS: Our results indicate that in this PD model molsidomine evokes a short-lasting decrease in BP in contrast to conventional antihypertensive drugs that maintain long-term effect and worsen orthostatic hypotension in parkinsonian patients.
[Mh] Termos MeSH primário: Antiparkinsonianos/administração & dosagem
Pressão Sanguínea/efeitos dos fármacos
Levodopa/administração & dosagem
Molsidomina/administração & dosagem
Doadores de Óxido Nítrico/administração & dosagem
Oxidopamina/toxicidade
[Mh] Termos MeSH secundário: Animais
Pressão Sanguínea/fisiologia
Masculino
Transtornos Parkinsonianos/induzido quimicamente
Transtornos Parkinsonianos/tratamento farmacológico
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antiparkinson Agents); 0 (Nitric Oxide Donors); 46627O600J (Levodopa); 8HW4YBZ748 (Oxidopamine); D46583G77X (Molsidomine)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170323
[Lr] Data última revisão:
170323
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161021
[St] Status:MEDLINE


  5 / 1982 MEDLINE  
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[PMID]:27135897
[Au] Autor:Uribe P; Treulen F; Boguen R; Sánchez R; Villegas JV
[Ad] Endereço:Center of Reproductive Biotechnology - Scientific and Technological Bioresource Nucleus (CEBIOR - BIOREN), Universidad de La Frontera, Temuco, Chile.
[Ti] Título:Nitrosative stress by peroxynitrite impairs ATP production in human spermatozoa.
[So] Source:Andrologia;49(3), 2017 Apr.
[Is] ISSN:1439-0272
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:The most toxic species in live systems include reactive nitrogen species such as peroxynitrite, which at high levels induces nitrosative stress. In human spermatozoa, the negative effect of peroxynitrite on motility and mitochondrial membrane potential was recently demonstrated, and the hypothesis of this work is that impairment of ATP production could be one cause of the effect on motility. Therefore, the aim here was to evaluate ATP production by both glycolysis and oxidative phosphorylation (OXPHOS) in spermatozoa exposed to peroxynitrite in vitro. Human spermatozoa were incubated with SIN-1, a molecule which generates peroxynitrite, and the ATP level was evaluated. Then, to inactivate glycolysis or OXPHOS, spermatozoa were incubated with pharmacological inhibitors of these pathways. Spermatozoa treated for inactivating one or the other pathway were exposed to SIN-1, and the ATP level was compared to the control without SIN-1 in each condition. The ATP level fell after peroxynitrite exposure. The ATP in spermatozoa treated for inactivating one or the other metabolic pathway and subsequently exposed to peroxynitrite was reduced compared with the control. These results show for the first time that an important mechanism by which peroxynitrite reduces sperm function is the inhibition of ATP production, affecting both glycolysis and OXPHOS.
[Mh] Termos MeSH primário: Trifosfato de Adenosina/metabolismo
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Ácido Peroxinitroso/toxicidade
Motilidade Espermática/efeitos dos fármacos
Espermatozoides/efeitos dos fármacos
[Mh] Termos MeSH secundário: Antimetabólitos/toxicidade
Desoxiglucose/toxicidade
Glicólise/efeitos dos fármacos
Seres Humanos
Masculino
Mitocôndrias/efeitos dos fármacos
Molsidomina/análogos & derivados
Molsidomina/metabolismo
Fosforilação Oxidativa/efeitos dos fármacos
Estresse Oxidativo
Rotenona/toxicidade
Espermatozoides/metabolismo
Desacopladores/toxicidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antimetabolites); 0 (Uncoupling Agents); 03L9OT429T (Rotenone); 14691-52-2 (Peroxynitrous Acid); 5O5U71P6VQ (linsidomine); 8L70Q75FXE (Adenosine Triphosphate); 9G2MP84A8W (Deoxyglucose); D46583G77X (Molsidomine)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170505
[Lr] Data última revisão:
170505
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160503
[St] Status:MEDLINE
[do] DOI:10.1111/and.12615


  6 / 1982 MEDLINE  
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[PMID]:27816693
[Au] Autor:Lencová-Popelová O; Jansová H; Jirkovský E; Bures J; Jirkovská-Vávrová A; Mazurová Y; Reimerová P; Vostatková L; Adamcová M; Hroch M; Pokorná Z; Kovaríková P; Simunek T; Sterba M
[Ad] Endereço:Department of Pharmacology, Faculty of Medicine in Hradec Králové, Charles University, Hradec Králové, Czech Republic.
[Ti] Título:Are cardioprotective effects of NO-releasing drug molsidomine translatable to chronic anthracycline cardiotoxicity settings?
[So] Source:Toxicology;372:52-63, 2016 Nov 30.
[Is] ISSN:1879-3185
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Chronic anthracycline (ANT) cardiotoxicity is a serious complication of cancer chemotherapy. Molsidomine, a NO-releasing drug, has been found cardioprotective in different models of I/R injury and recently in acute high-dose ANT cardiotoxicity. Hence, we examined whether its cardioprotective effects are translatable to chronic ANT cardiotoxicity settings without induction of nitrosative stress and interference with antiproliferative action of ANTs. The effects of molsidomine (0.025 and 0.5mg/kg, i.v.) were studied on the well-established model of chronic ANT cardiotoxicity in rabbits (daunorubicin/DAU/3mg/kg/week for 10 weeks). Molsidomine was unable to significantly attenuate mortality, development of heart failure and morphological damage induced by DAU. Molsidomine did not alter DAU-induced myocardial lipoperoxidation, MnSOD down-regulation, up-regulation of HO-1, IL-6, and molecular markers of cardiac remodeling. Although molsidomine increased 3-nitrotyrosine in the myocardium, this event had no impact on cardiotoxicity development. Using H9c2 myoblasts and isolated cardiomyocytes, it was found that SIN-1 (an active metabolite of molsidomine) induces significant protection against ANT toxicity, but only at high concentrations. In leukemic HL-60 cells, SIN-1 initially augmented ANT cytotoxicity (in low and clinically achievable concentrations), but it protected these cells against ANT in the high concentrations. UHPLC-MS/MS investigation demonstrated that the loss of ANT cytotoxicity after co-incubation of the cells in vitro with high concentrations of SIN-1 is caused by unexpected chemical depletion of DAU molecule. The present study demonstrates that cardioprotective effects of molsidomine are not translatable to clinically relevant chronic form of ANT cardiotoxicity. The augmentation of antineoplastic effects of ANT in low (nM) concentrations may deserve further study.
[Mh] Termos MeSH primário: Antraciclinas/toxicidade
Antibióticos Antineoplásicos/toxicidade
Cardiotônicos/farmacologia
Cardiopatias/induzido quimicamente
Cardiopatias/prevenção & controle
Molsidomina/farmacologia
Doadores de Óxido Nítrico/farmacologia
[Mh] Termos MeSH secundário: Animais
Cardiotoxicidade
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Doença Crônica
Daunorrubicina/toxicidade
Doxorrubicina/toxicidade
Insuficiência Cardíaca/prevenção & controle
Peroxidação de Lipídeos/efeitos dos fármacos
Estresse Oxidativo/efeitos dos fármacos
Coelhos
Espécies Reativas de Oxigênio/metabolismo
Remodelação Ventricular/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anthracyclines); 0 (Antibiotics, Antineoplastic); 0 (Cardiotonic Agents); 0 (Nitric Oxide Donors); 0 (Reactive Oxygen Species); 80168379AG (Doxorubicin); D46583G77X (Molsidomine); ZS7284E0ZP (Daunorubicin)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170505
[Lr] Data última revisão:
170505
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161107
[St] Status:MEDLINE


  7 / 1982 MEDLINE  
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[PMID]:27760216
[Au] Autor:Tirone M; Conti V; Manenti F; Nicolosi PA; D'Orlando C; Azzoni E; Brunelli S
[Ad] Endereço:School of Medicine and Surgery, University of Milano-Bicocca, Monza, Italy.
[Ti] Título:Nitric Oxide Donor Molsidomine Positively Modulates Myogenic Differentiation of Embryonic Endothelial Progenitors.
[So] Source:PLoS One;11(10):e0164893, 2016.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Embryonic VE-Cadherin-expressing progenitors (eVE-Cad+), including hemogenic endothelium, have been shown to generate hematopoietic stem cells and a variety of other progenitors, including mesoangioblasts, or MABs. MABs are vessel-associated progenitors with multilineage mesodermal differentiation potential that can physiologically contribute to skeletal muscle development and regeneration, and have been used in an ex vivo cell therapy setting for the treatment of muscular dystrophy. There is currently a therapeutic need for molecules that could improve the efficacy of cell therapy protocols; one such good candidate is nitric oxide. Several studies in animal models of muscle dystrophy have demonstrated that nitric oxide donors provide several beneficial effects, including modulation of the activity of endogenous cell populations involved in muscle repair and the delay of muscle degeneration. Here we used a genetic lineage tracing approach to investigate whether the therapeutic effect of nitric oxide in muscle repair could derive from an improvement in the myogenic differentiation of eVE-Cad+ progenitors during embryogenesis. We show that early in vivo treatment with the nitric oxide donor molsidomine enhances eVE-Cad+ contribution to embryonic and fetal myogenesis, and that this effect could originate from a modulation of the properties of yolk sac hemogenic endothelium.
[Mh] Termos MeSH primário: Hemangioblastos/citologia
Molsidomina/administração & dosagem
Desenvolvimento Muscular/efeitos dos fármacos
Doadores de Óxido Nítrico/administração & dosagem
[Mh] Termos MeSH secundário: Animais
Antígenos CD/metabolismo
Caderinas/metabolismo
Diferenciação Celular/efeitos dos fármacos
Embrião de Mamíferos/citologia
Embrião de Mamíferos/efeitos dos fármacos
Embrião de Mamíferos/metabolismo
Hemangioblastos/efeitos dos fármacos
Hemangioblastos/metabolismo
Camundongos
Molsidomina/farmacologia
Distrofia Muscular Animal/tratamento farmacológico
Distrofia Muscular Animal/patologia
Doadores de Óxido Nítrico/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Cadherins); 0 (Nitric Oxide Donors); 0 (cadherin 5); D46583G77X (Molsidomine)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170605
[Lr] Data última revisão:
170605
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161021
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0164893


  8 / 1982 MEDLINE  
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[PMID]:27721541
[Au] Autor:Minaz N; Razdan R
[Ad] Endereço:Department of Pharmacology, Al-Ameen College of Pharmacy, Bengaluru - 560 027, Karnataka, India.
[Ti] Título:Therapeutic insight into molsidomine, a nitric oxide donor in streptozotocin-induced diabetic nephropathy in rats.
[So] Source:Indian J Pharmacol;48(5):544-549, 2016 Sep-Oct.
[Is] ISSN:1998-3751
[Cp] País de publicação:India
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Diabetes-induced oxidative stress and hypertension play a major role in the development of nephropathy. Hence, the present study was undertaken to evaluate the protective effects of molsidomine, a nitric oxide donor in streptozotocin (STZ)-induced diabetic nephropathy (DN) in rats. MATERIALS AND METHODS: Type 1 diabetes was induced through a single dose of STZ (52 mg/kg, i.p.) in male Wistar rats and then treated with molsidomine (5 and 10 mg/kg; p.o.) for 8 weeks. Physical parameters, vital and renal function test including blood glucose, albuminuria, blood urine nitrogen, serum creatinine, and kidney index were determined. Oxidative stress and lipid peroxidation were assessed in the kidney homogenate by means of antioxidant enzymes and malondialdehyde levels. RESULTS: DN rats exhibited a significant renal dysfunction with a reduction in body weight, excessive oxidative stress, and pathological changes. Molsidomine treatment significantly improved vital sign, renal functions, and oxidative stress in DN rats in a dose-dependent manner. The protective effect of molsidomine was also substantiated by pathological changes in the architect of the kidney. CONCLUSION: Molsidomine shows a significant beneficial effect in Type 1 DN in rats.
[Mh] Termos MeSH primário: Diabetes Mellitus Experimental/tratamento farmacológico
Diabetes Mellitus Tipo 1/tratamento farmacológico
Nefropatias Diabéticas/tratamento farmacológico
Molsidomina/uso terapêutico
Doadores de Óxido Nítrico/uso terapêutico
[Mh] Termos MeSH secundário: Albuminúria/tratamento farmacológico
Animais
Anti-Hipertensivos/uso terapêutico
Antioxidantes/uso terapêutico
Glicemia/análise
Diabetes Mellitus Experimental/sangue
Diabetes Mellitus Experimental/patologia
Diabetes Mellitus Experimental/urina
Diabetes Mellitus Tipo 1/sangue
Diabetes Mellitus Tipo 1/patologia
Diabetes Mellitus Tipo 1/urina
Nefropatias Diabéticas/sangue
Nefropatias Diabéticas/patologia
Nefropatias Diabéticas/urina
Hipoglicemiantes/uso terapêutico
Rim/efeitos dos fármacos
Rim/patologia
Testes de Função Renal
Peroxidação de Lipídeos/efeitos dos fármacos
Masculino
Estresse Oxidativo/efeitos dos fármacos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antihypertensive Agents); 0 (Antioxidants); 0 (Blood Glucose); 0 (Hypoglycemic Agents); 0 (Nitric Oxide Donors); D46583G77X (Molsidomine)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161011
[St] Status:MEDLINE


  9 / 1982 MEDLINE  
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[PMID]:27644683
[Au] Autor:Loren P; Cheuquemán C; Sánchez E; Risopatrón J; Arias ME; Felmer R; Sánchez R
[Ad] Endereço:Student of Doctoral Program in Sciences major in Applied Cellular and Molecular Biology, Universidad de la Frontera, Temuco, Chile.
[Ti] Título:Effect of short-term exposure of cumulus-oocyte complex to 3-morpholinosydnonimine on in vitro embryo development and gene expression in cattle.
[So] Source:Reprod Domest Anim;51(6):1010-1019, 2016 Dec.
[Is] ISSN:1439-0531
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Short-term exposure of gametes to different types of stress might induce stress tolerance in mammalian embryos. The aim of this study was to evaluate the effect of short-term exposure of bovine mature cumulus-oocyte complex (COC) to 3-morpholinosydnonimine (SIN-1) on subsequent in vitro embryo development, embryo quality and relative gene expression. Matured COCs were incubated with SIN-1 (0, 0.1, 1, 10 and 100 µM SIN-1) for 1 hr before in vitro fertilization and zygotes were cultured until Day 7. The cleavage rate at 72 hr did not show any differences among groups. However, the blastocyst rate on Day 7 decreased with all treatments evaluated, with the embryos generated with 10 µM SIN-1 showing the lowest embryo production rate. Embryo quality analysis did not show any differences in total cell number (TCN) or inner cell mass (ICM) among groups. Relative gene expression analysis showed a downregulation of eNOS expression and an upregulation of nNOS expression in all treatments evaluated compared to the control group. Also, a downregulation was observed in some treatments: SOD2 at 0.1 µM; SOD1 at 0.1 and 100 µM; PRDX5 at 0.1, 10 and 100 µM; and NANOG at 10 and 100 µM; and an upregulation of CDX2 expression was observed at 100 µM. The other genes (OCT4, HIF1A, HSPA1A, BCL2A and iNOS) did not show any differences in the relative gene expression. These results suggest that the short-term exposure of mature bovine COCs to SIN-1 does not induce stress tolerance and has no beneficial effect on bovine in vitro embryo production.
[Mh] Termos MeSH primário: Bovinos/embriologia
Células do Cúmulo/fisiologia
Técnicas de Cultura Embrionária/veterinária
Regulação da Expressão Gênica no Desenvolvimento/efeitos dos fármacos
Molsidomina/análogos & derivados
Oócitos/fisiologia
[Mh] Termos MeSH secundário: Animais
Feminino
Regulação da Expressão Gênica no Desenvolvimento/fisiologia
Molsidomina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
5O5U71P6VQ (linsidomine); D46583G77X (Molsidomine)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170406
[Lr] Data última revisão:
170406
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160921
[St] Status:MEDLINE
[do] DOI:10.1111/rda.12788


  10 / 1982 MEDLINE  
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[PMID]:27496065
[Au] Autor:Chung E; Ohgami Y; Quock RM
[Ad] Endereço:Department of Pharmaceutical Sciences, College of Pharmacy, Washington State University, Pullman, WA 99164, United States.
[Ti] Título:Increasing the availability of l-arginine and nitric oxide increases sensitivity of nitrous oxide (N2O)-insensitive inbred mice to N2O-induced antinociception.
[So] Source:Brain Res Bull;125:218-21, 2016 Jul.
[Is] ISSN:1873-2747
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Nitrous oxide (N2O)-induced antinociception in mice is dependent on the neuromodulator nitric oxide (NO). In contrast to C57BL/6J (B6) mice, DBA/2J (D2) mice fail to respond to N2O with a robust antinociceptive response or with an increase in brain nitric oxide synthase (NOS) enzyme activity, suggesting that failure of D2 mice to respond to N2O might result from a deficit of NO function. Therefore, it was of interest to determine whether increasing the availability of NO might increase sensitivity of D2 mice to N2O. Male D2 mice were pretreated with sub-antinociceptive intracerebroventricular doses of the NO donor 3-morpholinosydnoimine or the NO precursor l-arginine then assessed for responsiveness to N2O-induced antinociception using the acetic acid abdominal constriction test. Both pretreatments increased the antinociceptive responsiveness of D2 mice to N2O. These results indicate that the NOS enzyme in D2 mice is functional and that the deficit in NO function that obstructs sensitivity to N2O-induced antinociception may lie in availability or utilization of l-arginine.
[Mh] Termos MeSH primário: Dor Abdominal/tratamento farmacológico
Analgésicos/uso terapêutico
Arginina/uso terapêutico
Óxido Nítrico/uso terapêutico
Óxido Nitroso/uso terapêutico
Limiar da Dor/efeitos dos fármacos
[Mh] Termos MeSH secundário: Dor Abdominal/complicações
Análise de Variância
Animais
Modelos Animais de Doenças
Relação Dose-Resposta a Droga
Sinergismo Farmacológico
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Endogâmicos DBA
Molsidomina/análogos & derivados
Molsidomina/farmacologia
Doadores de Óxido Nítrico/farmacologia
Especificidade da Espécie
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Analgesics); 0 (Nitric Oxide Donors); 31C4KY9ESH (Nitric Oxide); 5O5U71P6VQ (linsidomine); 94ZLA3W45F (Arginine); D46583G77X (Molsidomine); K50XQU1029 (Nitrous Oxide)
[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:160807
[St] Status:MEDLINE



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