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[PMID]:28806604
[Au] Autor:Berger A; Tanuhadi E; Brecker L; Schinnerl J; Valant-Vetschera K
[Ad] Endereço:Chemodiversity Research Group, Department of Botany and Biodiversity Research, University of Vienna, Rennweg 14, A-1030, Vienna, Austria. Electronic address: andi.berger@univie.ac.at.
[Ti] Título:Chemodiversity of tryptamine-derived alkaloids in six Costa Rican Palicourea species (Rubiaceae-Palicoureeae).
[So] Source:Phytochemistry;143:124-131, 2017 Nov.
[Is] ISSN:1873-3700
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:We report 14 harmala and tryptamine-iridoid alkaloids with various tri-, tetra- and pentacyclic cores from leaves and stem bark of six species of the large and complex neotropical genus Palicourea. Among them is the previously undescribed compound deoxostrictosamide which is related to strictosamide, a key intermediate in camptothecin biosynthesis. In addition, we describe the occurrence of 1,2,3,4-tetrahydronorharman-1-one for the first time within Rubiaceae and ophiorine A and B, two alkaloids with an unusual core bearing a betaine function and a zwitterion as new for the genus. Although the other compounds are already known from other species, their degree of structural diversity highlights the remarkable biosynthetic capabilities of the genus Palicourea. Furthermore, the present paper provides additional support for the hypothesis that tryptamine-iridoid alkaloids represent a distinct chemosystematic feature for the genus Palicourea.
[Mh] Termos MeSH primário: Rubiaceae/química
Triptaminas/química
[Mh] Termos MeSH secundário: Alcaloides/análise
Alcaloides/química
Biodiversidade
Camptotecina
Costa Rica
Iridoides/análise
Estrutura Molecular
Ressonância Magnética Nuclear Biomolecular
Extratos Vegetais/química
Folhas de Planta/química
Alcaloides de Vinca/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Alkaloids); 0 (Iridoids); 0 (Plant Extracts); 0 (Tryptamines); 0 (Vinca Alkaloids); 0 (strictosamide); 422ZU9N5TV (tryptamine); XT3Z54Z28A (Camptothecin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171002
[Lr] Data última revisão:
171002
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170815
[St] Status:MEDLINE


  2 / 1767 MEDLINE  
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[PMID]:28787019
[Au] Autor:Wang RC; Chen X; Parissenti AM; Joy AA; Tuszynski J; Brindley DN; Wang Z
[Ad] Endereço:Department of Medical Genetics and Signal Transduction Research Group, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, Alberta, Canada.
[Ti] Título:Sensitivity of docetaxel-resistant MCF-7 breast cancer cells to microtubule-destabilizing agents including vinca alkaloids and colchicine-site binding agents.
[So] Source:PLoS One;12(8):e0182400, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: One of the main reasons for disease recurrence in the curative breast cancer treatment setting is the development of drug resistance. Microtubule targeted agents (MTAs) are among the most commonly used drugs for the treatment of breaset cancer and therefore overcoming taxane resistance is of primary clinical importance. Our group has previously demonstrated that the microtubule dynamics of docetaxel-resistant MCF-7TXT cells are insensitivity to docetaxel due to the distinct expression profiles of ß-tubulin isotypes in addition to the high expression of p-glycoprotein (ABCB1). In the present investigation we examined whether taxane-resistant breast cancer cells are more sensitive to microtubule destabilizing agents including vinca alkaloids and colchicine-site binding agents (CSBAs) than the non-resistant cells. METHODS: Two isogenic MCF-7 breast cancer cell lines were selected for resistance to docetaxel (MCF-7TXT) and the wild type parental cell line (MCF-7CC) to examine if taxane-resistant breast cancer cells are sensitive to microtubule-destabilizing agents including vinca alkaloids and CSBAs. Cytotoxicity assays, immunoblotting, indirect immunofluorescence and live imaging were used to study drug resistance, apoptosis, mitotic arrest, microtubule formation, and microtubule dynamics. RESULTS: MCF-7TXT cells were demonstrated to be cross resistant to vinca alkaloids, but were more sensitive to treatment with colchicine compared to parental non-resistant MCF-7CC cells. Cytotoxicity assays indicated that the IC50 of MCF-7TXT cell to vinorelbine and vinblastine was more than 6 and 3 times higher, respectively, than that of MCF-7CC cells. By contrast, the IC50 of MCF-7TXT cell for colchincine was 4 times lower than that of MCF-7CC cells. Indirect immunofluorescence showed that all MTAs induced the disorganization of microtubules and the chromatin morphology and interestingly each with a unique pattern. In terms of microtubule and chromain morphology, MCF-7TXT cells were more resistant to vinorelbine and vinblastine, but more sensitive to colchicine compared to MCF-7CC cells. PARP cleavage assay further demonstrated that all of the MTAs induced apoptosis of the MCF-7 cells. However, again, MCF-7TXT cells were more resistant to vinorelbine and vinblastine, and more sensitive to colchicine compared to MCF-7CC cells. Live imaging demonstrated that the microtubule dynamics of MCF-7TXT cells were less sensitive to vinca alkaloids, and more sensitive to colchicine. MCF-7TXT cells were also noted to be more sensitive to other CSBAs including 2MeOE2, ABT-751 and phosphorylated combretastatin A-4 (CA-4P). CONCLUSION: Docetaxel-resistant MCF-7TXT cells have demonstrated cross-resistance to vinca alkaloids, but appear to be more sensitive to CSBAs (colchicine, 2MeOE2, ABT-751 and CA-4P) compared to non-resistant MCF-7CC cells. Taken together these results suggest that CSBAs should be evaluated further in the treatment of taxane resistant breast cancer.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Neoplasias da Mama/patologia
Colchicina/farmacologia
Resistência a Medicamentos Antineoplásicos/efeitos dos fármacos
Microtúbulos/efeitos dos fármacos
Taxoides/farmacologia
Alcaloides de Vinca/farmacologia
[Mh] Termos MeSH secundário: Apoptose/efeitos dos fármacos
Hidrocarbonetos Aromáticos com Pontes/farmacologia
Cromatina/efeitos dos fármacos
Cromatina/metabolismo
Seres Humanos
Células MCF-7
Microtúbulos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Bridged-Ring Compounds); 0 (Chromatin); 0 (Taxoids); 0 (Vinca Alkaloids); 15H5577CQD (docetaxel); 1605-68-1 (taxane); SML2Y3J35T (Colchicine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171004
[Lr] Data última revisão:
171004
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170809
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0182400


  3 / 1767 MEDLINE  
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[PMID]:28594915
[Au] Autor:Nakade Y; Sakamoto K; Yamauchi T; Inoue T; Kobayashi Y; Yamamoto T; Ishii N; Ohashi T; Sumida Y; Ito K; Nakao H; Fukuzawa Y; Umezawa K; Yoneda M
[Ad] Endereço:Division of Gastroenterology and Hepatology, Department of Internal Medicine, Aichi Medical University, Nagakute, Aichi, Japan.
[Ti] Título:Conophylline inhibits non-alcoholic steatohepatitis in mice.
[So] Source:PLoS One;12(6):e0178436, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Conophylline (CnP), a vinca alkaloid extracted from the leaves of the tropical plant Ervatamia microphylla, attenuates hepatic fibrosis in mice. However, little is known about whether CnP inhibits steatosis, inflammation, and fibrosis in non-alcoholic steatohepatitis (NASH) in mice. A methionine-choline-deficient (MCD) diet was administered to male db/db mice as a NASH model, and CnP (1 µg/kg/d) was co-administered. Eight weeks after the commencement of the MCD diet, hepatic steatosis, inflammation, and fibrosis, and hepatic fat metabolism-, inflammation-, and fibrosis-related markers were examined. Feeding on an MCD for 8 weeks induced hepatic steatosis, inflammation, and fibrosis. CnP significantly attenuated the MCD-induced increases in hepatic steatosis, as well as hepatic inflammation and fibrosis. The MCD diet increased hepatic transforming growth factor-ß (TGF-ß) mRNA levels, which are correlated with hepatic steatosis, inflammation, and fibrosis. The diet also attenuated acyl-coenzyme A oxidase 1 (ACOX1) and carnitine palmitoyltransferase 1 (CPT1) mRNA levels, which are involved in ß-oxidation. The putative mechanism of the CnP effect involves reduced hepatic TGF-ß mRNA levels, and increased mRNA levels of hepatic peroxisome proliferator-activated receptor (PPAR) α and its target genes ACOX1 and CPT1. The results of this study indicate that CnP inhibits steatohepatitis, possibly through the inhibition of hepatic TGF-ß mRNA levels, and induces an increase in PPARα mRNA levels, resulting in the attenuation of hepatic steatosis, inflammation, and fibrosis in mice. CnP might accordingly be a suitable therapeutic option for NASH.
[Mh] Termos MeSH primário: Hepatopatia Gordurosa não Alcoólica/tratamento farmacológico
Alcaloides de Vinca/uso terapêutico
[Mh] Termos MeSH secundário: Alanina Transaminase/sangue
Animais
Ácidos Graxos não Esterificados/sangue
Fígado Gorduroso/sangue
Fígado Gorduroso/tratamento farmacológico
Fígado Gorduroso/metabolismo
Imuno-Histoquímica
Inflamação/sangue
Inflamação/tratamento farmacológico
Inflamação/metabolismo
Metabolismo dos Lipídeos/fisiologia
Fígado/efeitos dos fármacos
Fígado/metabolismo
Masculino
Malondialdeído/sangue
Camundongos
Hepatopatia Gordurosa não Alcoólica/sangue
Hepatopatia Gordurosa não Alcoólica/metabolismo
RNA/genética
Reação em Cadeia da Polimerase em Tempo Real
Triglicerídeos/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fatty Acids, Nonesterified); 0 (Triglycerides); 0 (Vinca Alkaloids); 0 (conophylline); 4Y8F71G49Q (Malondialdehyde); 63231-63-0 (RNA); EC 2.6.1.2 (Alanine Transaminase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170919
[Lr] Data última revisão:
170919
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170609
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0178436


  4 / 1767 MEDLINE  
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[PMID]:28579361
[Au] Autor:Sáez-Calvo G; Sharma A; Balaguer FA; Barasoain I; Rodríguez-Salarichs J; Olieric N; Muñoz-Hernández H; Berbís MÁ; Wendeborn S; Peñalva MA; Matesanz R; Canales Á; Prota AE; Jímenez-Barbero J; Andreu JM; Lamberth C; Steinmetz MO; Díaz JF
[Ad] Endereço:Department of Physical and Chemical Biology, Centro de Investigaciones Biológicas, Consejo Superior de Investigaciones Científicas, Ramiro de Maeztu 9, 28040 Madrid, Spain.
[Ti] Título:Triazolopyrimidines Are Microtubule-Stabilizing Agents that Bind the Vinca Inhibitor Site of Tubulin.
[So] Source:Cell Chem Biol;24(6):737-750.e6, 2017 Jun 22.
[Is] ISSN:2451-9456
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Microtubule-targeting agents (MTAs) are some of the clinically most successful anti-cancer drugs. Unfortunately, instances of multidrug resistances to MTA have been reported, which highlights the need for developing MTAs with different mechanistic properties. One less explored class of MTAs are [1,2,4]triazolo[1,5-a]pyrimidines (TPs). These cytotoxic compounds are microtubule-stabilizing agents that inexplicably bind to vinblastine binding site on tubulin, which is typically targeted by microtubule-destabilizing agents. Here we used cellular, biochemical, and structural biology approaches to address this apparent discrepancy. Our results establish TPs as vinca-site microtubule-stabilizing agents that promote longitudinal tubulin contacts in microtubules, in contrast to classical microtubule-stabilizing agents that primarily promote lateral contacts. Additionally we observe that TPs studied here are not affected by p-glycoprotein overexpression, and suggest that TPs are promising ligands against multidrug-resistant cancer cells.
[Mh] Termos MeSH primário: Microtúbulos/efeitos dos fármacos
Microtúbulos/metabolismo
Pirimidinas/farmacologia
Triazóis/farmacologia
Tubulina (Proteína)/metabolismo
Alcaloides de Vinca/metabolismo
[Mh] Termos MeSH secundário: Sítios de Ligação
Linhagem Celular Tumoral
Seres Humanos
Ligantes
Modelos Moleculares
Multimerização Proteica/efeitos dos fármacos
Estrutura Quaternária de Proteína
Tubulina (Proteína)/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (1,2,4-triazole(1,5a)pyrimidine); 0 (Ligands); 0 (Pyrimidines); 0 (Triazoles); 0 (Tubulin); 0 (Vinca Alkaloids)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170719
[Lr] Data última revisão:
170719
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170606
[St] Status:MEDLINE


  5 / 1767 MEDLINE  
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[PMID]:28353359
[Au] Autor:Pérez-Pitarch A; Guglieri-López B; Nacher A; Merino V; Merino-Sanjuán M
[Ad] Endereço:a Pharmaceutical and Pharmaceutical Technology Department , University of Valencia , Valencia , Spain.
[Ti] Título:Impact of Undernutrition on the Pharmacokinetics and Pharmacodynamics of Anticancer Drugs: A Literature Review.
[So] Source:Nutr Cancer;69(4):555-563, 2017 May-Jun.
[Is] ISSN:1532-7914
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The etiology of undernourishment in cancer patients is multifactorial: tumor-related mechanisms (such as obstruction, metabolic abnormalities, and functionality changes) in addition to the influence of anticancer therapies, which can induce or worsen undernutrition. The evident role of undernutrition in cancer treatment outcomes suggests the need of considering nutritional status when evaluating anticancer drugs. In order to merge the available data and offer researchers and clinicians a global view of this phenomenon, the present manuscript reviews on a drug-by-drug basis the undernutrition-related pharmacokinetic and pharmacodynamic aspects of anticancer treatments. This review notes interesting trends in the relationship between undernourishment and pharmacokinetics across studies, and indicates that dosing modifications of these drugs may be necessary to optimize chemotherapeutic treatments. Furthermore, this review has compiled evidence regarding undernourishment's capacity of enhancing treatment-related myelosuppression, cardiotoxicity, ototoxicity, neurotoxicity, and malignancies.
[Mh] Termos MeSH primário: Antineoplásicos/farmacocinética
Desnutrição/fisiopatologia
[Mh] Termos MeSH secundário: Antraciclinas/farmacocinética
Etoposídeo/farmacocinética
Fluoruracila/farmacocinética
Seres Humanos
Metotrexato/farmacocinética
Alcaloides de Vinca/farmacocinética
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anthracyclines); 0 (Antineoplastic Agents); 0 (Vinca Alkaloids); 6PLQ3CP4P3 (Etoposide); U3P01618RT (Fluorouracil); YL5FZ2Y5U1 (Methotrexate)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171109
[Lr] Data última revisão:
171109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170330
[St] Status:MEDLINE
[do] DOI:10.1080/01635581.2017.1299878


  6 / 1767 MEDLINE  
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[PMID]:28296551
[Au] Autor:Sönmez MF; Ozdemir S; Guzel M; Kaymak E
[Ad] Endereço:a Departments of Histology and Embryology.
[Ti] Título:The ameliorative effects of vinpocetine on apoptosis and HSP-70 expression in testicular torsion in rats.
[So] Source:Biotech Histochem;92(2):92-99, 2017.
[Is] ISSN:1473-7760
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Vinpocetine is a potent antioxidant and free radical scavenger. We investigated the effects of vinpocetine on torsion/detorsion (T/D) induced testicular damage, HSP-70 expression and germ cell apoptosis in rats. Sixty Wistar albino adult male rats were divided into five groups of 12. The groups comprised a control group, a sham treated group, a T/D group, a vinpocetine treated group, and a T/D plus vinpocetine treated group. The left testis of each rat was subjected to unilateral torsion followed by detorsion after 2 h. Vinpocetine was administered intraperitoneally immediately and for 10 days following detorsion. At the end of the study, the rats were sacrificed and their testes removed and processed. HSP-70 expression, apoptosis and histopathological damage scores were determined for each group. Testicular T/D caused significant increases in apoptosis and HSP-70 expression, and a significant decrease in Johnsen's testicular biopsy scores and mean seminiferous tubule diameter. Vinpocetine ameliorated testicular histopathology and HSP-70 expression in the T/D + vinpocetine group. Consequently, vinpocetine may prevent testicular injury following testicular torsion owing to its antioxidant effects.
[Mh] Termos MeSH primário: Antioxidantes/farmacologia
Apoptose/efeitos dos fármacos
Proteínas de Choque Térmico HSP70/metabolismo
Torção do Cordão Espermático/tratamento farmacológico
Testículo/efeitos dos fármacos
Alcaloides de Vinca/farmacologia
[Mh] Termos MeSH secundário: Animais
Células Germinativas/efeitos dos fármacos
Células Germinativas/metabolismo
Masculino
Ratos Wistar
Traumatismo por Reperfusão/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (HSP70 Heat-Shock Proteins); 0 (Vinca Alkaloids); 543512OBTC (vinpocetine)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170330
[Lr] Data última revisão:
170330
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170316
[St] Status:MEDLINE
[do] DOI:10.1080/10520295.2016.1259499


  7 / 1767 MEDLINE  
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[PMID]:28101929
[Au] Autor:Ponticelli E; Clari M; Frigerio S; De Clemente A; Bergese I; Scavino E; Bernardini A; Sacerdote C
[Ad] Endereço:Città della Salute e della Scienza University Hospital, Turin, Italy.
[Ti] Título:Dysgeusia and health-related quality of life of cancer patients receiving chemotherapy: A cross-sectional study.
[So] Source:Eur J Cancer Care (Engl);26(2), 2017 Mar.
[Is] ISSN:1365-2354
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The aim of the study was to evaluate taste disorders in patients receiving chemotherapy and to assess the impact of dysgeusia on patients' health-related quality of life (HRQOL). A total of 289 patients with a diagnosis of malignant solid or haematological cancer undergoing chemotherapy completed a questionnaire assessing dysgeusia and HRQOL. Sixty-four per cent of patients developed dysgeusia after and during chemotherapy. A statistically significant correlation was found between type of cancer and dysgeusia (p = .012), moreover a statistically significant association was found between type of chemotherapy and occurrence of dysgeusia (p = .031). Patients with dysgeusia had a worse overall HRQOL than those who did not have dysgeusia, and the association between HRQOL and dysgeusia was also statistically significant (p = .003). Patients with dysgeusia had a higher probability of having a worse HRQOL (p = .002). In line with previous studies, we observed a significant correlation between chemotherapy and dysgeusia. Furthermore, this study found that cancer patients with dysgeusia have a lower quality of life. In particular the domains "role," "social aspect," "nausea-vomiting" and "appetite" are most influenced by dysgeusia. Improving the communication and information to patients considered at higher risk of developing dysgeusia can have a positive impact on patients' quality of life.
[Mh] Termos MeSH primário: Antineoplásicos/efeitos adversos
Disgeusia/induzido quimicamente
Neoplasias/tratamento farmacológico
Qualidade de Vida
[Mh] Termos MeSH secundário: Idoso
Anorexia/induzido quimicamente
Antraciclinas/efeitos adversos
Antibióticos Antineoplásicos/efeitos adversos
Antineoplásicos Alquilantes/efeitos adversos
Bortezomib/efeitos adversos
Neoplasias da Mama/tratamento farmacológico
Neoplasias Colorretais/diagnóstico por imagem
Estudos Transversais
Feminino
Nível de Saúde
Seres Humanos
Neoplasias Pulmonares/tratamento farmacológico
Linfoma/tratamento farmacológico
Masculino
Meia-Idade
Náusea/induzido quimicamente
Compostos de Platina/efeitos adversos
Reprodutibilidade dos Testes
Papel (Figurativo)
Inquéritos e Questionários
Taxoides/efeitos adversos
Alcaloides de Vinca/efeitos adversos
Vômito/induzido quimicamente
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anthracyclines); 0 (Antibiotics, Antineoplastic); 0 (Antineoplastic Agents); 0 (Antineoplastic Agents, Alkylating); 0 (Platinum Compounds); 0 (Taxoids); 0 (Vinca Alkaloids); 69G8BD63PP (Bortezomib)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171004
[Lr] Data última revisão:
171004
[Sb] Subgrupo de revista:N
[Da] Data de entrada para processamento:170120
[St] Status:MEDLINE
[do] DOI:10.1111/ecc.12633


  8 / 1767 MEDLINE  
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[PMID]:28052870
[Au] Autor:Thieme M; Sivritas SH; Mergia E; Potthoff SA; Yang G; Hering L; Grave K; Hoch H; Rump LC; Stegbauer J
[Ad] Endereço:Department of Nephrology, Medical Faculty, University Hospital Düsseldorf, Heinrich-Heine-University Düsseldorf, Düsseldorf, Germany; and.
[Ti] Título:Phosphodiesterase 5 inhibition ameliorates angiotensin II-dependent hypertension and renal vascular dysfunction.
[So] Source:Am J Physiol Renal Physiol;312(3):F474-F481, 2017 Mar 01.
[Is] ISSN:1522-1466
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Changes in renal hemodynamics have a major impact on blood pressure (BP). Angiotensin (Ang) II has been shown to induce vascular dysfunction by interacting with phosphodiesterase (PDE)1 and PDE5. The predominant PDE isoform responsible for renal vascular dysfunction in hypertension is unknown. Here, we measured the effects of PDE5 (sildenafil) or PDE1 (vinpocetine) inhibition on renal blood flow (RBF), BP, and renal vascular function in normotensive and hypertensive mice. During acute short-term Ang II infusion, sildenafil decreased BP and increased RBF in C57BL/6 (WT) mice. In contrast, vinpocetine showed no effect on RBF and BP. Additionally, renal cGMP levels were significantly increased after acute sildenafil but not after vinpocetine infusion, indicating a predominant role of PDE5 in renal vasculature. Furthermore, chronic Ang II infusion (500 ng·kg ·min ) increased BP and led to impaired NO-dependent vasodilation in kidneys of WT mice. Additional treatment with sildenafil (100 mg·kg ·day ) attenuated Ang II-dependent hypertension and improved NO-mediated vasodilation. During chronic Ang II infusion, urinary nitrite excretion, a marker for renal NO generation, was increased in WT mice, whereas renal cGMP generation was decreased and restored after sildenafil treatment, suggesting a preserved cGMP signaling after PDE5 inhibition. To investigate the dependency of PDE5 effects on NO/cGMP signaling, we next analyzed eNOS-KO mice, a mouse model characterized by low vascular NO/cGMP levels. In eNOS-KO mice, chronic Ang II infusion increased BP but did not impair NO-mediated vasodilation. Moreover, sildenafil did not influence BP or vascular function in eNOS-KO mice. These results highlight PDE5 as a key regulator of renal hemodynamics in hypertension.
[Mh] Termos MeSH primário: Angiotensina II
Anti-Hipertensivos/farmacologia
Pressão Sanguínea/efeitos dos fármacos
Hipertensão/prevenção & controle
Inibidores da Fosfodiesterase 5/farmacologia
Artéria Renal/efeitos dos fármacos
Circulação Renal/efeitos dos fármacos
Citrato de Sildenafila/farmacologia
Vasodilatadores/farmacologia
[Mh] Termos MeSH secundário: Animais
GMP Cíclico/metabolismo
Modelos Animais de Doenças
Relação Dose-Resposta a Droga
Hipertensão/induzido quimicamente
Hipertensão/enzimologia
Hipertensão/fisiopatologia
Masculino
Camundongos Endogâmicos C57BL
Camundongos Knockout
Óxido Nítrico/metabolismo
Óxido Nítrico Sintase Tipo III/deficiência
Óxido Nítrico Sintase Tipo III/genética
Artéria Renal/enzimologia
Artéria Renal/fisiopatologia
Vasodilatação/efeitos dos fármacos
Alcaloides de Vinca/farmacologia
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antihypertensive Agents); 0 (Phosphodiesterase 5 Inhibitors); 0 (Vasodilator Agents); 0 (Vinca Alkaloids); 11128-99-7 (Angiotensin II); 31C4KY9ESH (Nitric Oxide); 543512OBTC (vinpocetine); BW9B0ZE037 (Sildenafil Citrate); EC 1.14.13.39 (Nitric Oxide Synthase Type III); EC 1.14.13.39 (Nos3 protein, mouse); H2D2X058MU (Cyclic GMP)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170713
[Lr] Data última revisão:
170713
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170106
[St] Status:MEDLINE
[do] DOI:10.1152/ajprenal.00376.2016


  9 / 1767 MEDLINE  
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[PMID]:27989509
[Au] Autor:Li D; Chen J; Ye J; Zhai X; Song J; Jiang C; Wang J; Zhang H; Jia X; Zhu F
[Ad] Endereço:Affiliated Hospital of Integrated Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine, Nanjing 210028, PR China; Jiangsu Province Academy of Traditional Chinese Medicine, Nanjing 210028, PR China; Department of Analytical Chemistry, China Pharmaceutical University, Nanji
[Ti] Título:Anti-inflammatory effect of the six compounds isolated from Nauclea officinalis Pierrc ex Pitard, and molecular mechanism of strictosamide via suppressing the NF-κB and MAPK signaling pathway in LPS-induced RAW 264.7 macrophages.
[So] Source:J Ethnopharmacol;196:66-74, 2017 Jan 20.
[Is] ISSN:1872-7573
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:ETHNOPHARMACOLOGICAL RELEVANCE: Nauclea officinalis Pierrc ex Pitard. is a Chinese medicinal herb that contains high level of alkaloids which is the most abundant and active constituent. Strictosamide isolated from Nauclea officinalis Pierrc ex Pitard. showed significant effects on inflammatory response, compared with pumiloside, 3-epi-pumiloside, vincosamide, 3α,5α-tetrahydrodeoxycordifoline lactam and naucleamide A-10-O-ß-D-glucopyranoside of this plant. AIM OF STUDY: we investigated the biological activities of the six compounds mentioned-above, and the underlying molecular mechanism exerted by the most potent one, strictosamide. MATERIALS AND METHODS: The effects of strictosamide and other five compounds on the inhibitory activity of nitric oxide (NO) were screened by Griess test. The contents of tumor necrosis factor-α (TNF-α) and interleukin-1ß (IL-1ß) in media were detected by using Enzyme-linked immunosorbent (ELISA) kits. The effects on the mRNA expression of nitric oxide synthase (iNOS), TNF-α and IL-1ß of strictosamide were further investigated by RT-qPCR. Western blot assay was conducted to illustrate the effects of strictosamide on iNOS and phosphorylation of p65, inhibitor of NF-κB (IκB)-α, IκB-kinase (IKK)-α as well as p-extracellular signal-regulated kinase (ERK), p-c-jun N-terminal kinase (JNK) and p-p38 in the protein levels. RESULTS: Strictosamide potently suppressed the productions of NO, TNF-α and IL-1ß in LPS-induced RAW 264.7 macrophages, and it dose-dependently alleviated the LPS-simulated protein level of iNOS as well as the mRNA expressions of iNOS, TNF-α and IL-1ß. In addition, molecular data revealed that strictosamide markedly decreased the expressions of p-p65, p-IκBα and p-IKKα. Furthermore, strictosamide significantly attenuated LPS-induced the phosphorylation of p38, ERK and JNK. CONCLUSIONS: At present study, the results indicated that the anti-inflammatory activity of strictosamide was associated with the restraint of NO, TNF-α and IL-1ß via negative regulation of both NF-κB and mitogen-activated protein kinases (MAPKs) in LPS-induced RAW 264.7 cells.
[Mh] Termos MeSH primário: Alcaloides/farmacologia
Anti-Inflamatórios/farmacologia
Macrófagos/efeitos dos fármacos
Proteínas Quinases Ativadas por Mitógeno/metabolismo
NF-kappa B/metabolismo
Rubiaceae
[Mh] Termos MeSH secundário: Animais
Sobrevivência Celular/efeitos dos fármacos
Interleucina-1beta/genética
Interleucina-1beta/metabolismo
Lipopolissacarídeos
Macrófagos/metabolismo
Camundongos
Óxido Nítrico/metabolismo
Óxido Nítrico Sintase Tipo II/genética
Óxido Nítrico Sintase Tipo II/metabolismo
Fosforilação/efeitos dos fármacos
Células RAW 264.7
RNA Mensageiro/metabolismo
Transdução de Sinais/efeitos dos fármacos
Fator de Necrose Tumoral alfa/genética
Fator de Necrose Tumoral alfa/metabolismo
Alcaloides de Vinca
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Alkaloids); 0 (Anti-Inflammatory Agents); 0 (Interleukin-1beta); 0 (Lipopolysaccharides); 0 (NF-kappa B); 0 (RNA, Messenger); 0 (Tumor Necrosis Factor-alpha); 0 (Vinca Alkaloids); 0 (strictosamide); 31C4KY9ESH (Nitric Oxide); EC 1.14.13.39 (Nitric Oxide Synthase Type II); EC 1.14.13.39 (Nos2 protein, mouse); EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170713
[Lr] Data última revisão:
170713
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161220
[St] Status:MEDLINE


  10 / 1767 MEDLINE  
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[PMID]:27967259
[Au] Autor:Feng X; Wang Y; Hao Y; Ma Q; Dai J; Liang Z; Liu Y; Li X; Song Y; Si C
[Ad] Endereço:a Department of Neurology , Affiliated Hospital of Jining Medical University , Jining , Shandong Province , People's Republic of China.
[Ti] Título:Vinpocetine Inhibited the CpG Oligodeoxynucleotide-induced Immune Response in Plasmacytoid Dendritic Cells.
[So] Source:Immunol Invest;46(3):263-273, 2017 Apr.
[Is] ISSN:1532-4311
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Plasmacytoid dendritic cells (pDCs) exert dual roles in immune responses through inducing inflammation and maintaining immune tolerance. A switch of pDC phenotype from pro-inflammation to tolerance has therapeutic promise in the treatment of autoimmune diseases. Vinpocetine, a vasoactive vinca alkaloid extracted from the periwinkle plant, has recently emerged as an immunomodulatory agent. In this study, we evaluated the effect of vinpocetine on phenotype of pDCs isolated from C57BL/6 mice and explored its possible mechanism. Our data showed that vinpocetine significantly downregulated the expression of CD40, CD80, and CD86 on pDCs and increased the expression of translocator protein (TSPO), the specific receptor of vinpocetine, in pDCs. Vinpocetine significantly inhibited the Toll-like receptor 9 signaling pathway and reduced the secretion of related cytokines in pDCs through TSPO. Furthermore, viability of pDCs was significantly promoted by vinpocetine. These findings imply that vinpocetine serves as an immunomodulatory agent for pDCs and may be applied for the treatment of pDCs-related autoimmune diseases.
[Mh] Termos MeSH primário: Doenças Autoimunes/tratamento farmacológico
Células Dendríticas/efeitos dos fármacos
Fatores Imunológicos/farmacologia
Alcaloides de Vinca/farmacologia
Vinca/imunologia
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular/efeitos dos fármacos
Células Cultivadas
Ilhas de CpG/genética
Citocinas/metabolismo
Células Dendríticas/imunologia
Seres Humanos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Oligodesoxirribonucleotídeos/imunologia
Receptores de GABA/genética
Receptores de GABA/metabolismo
Transdução de Sinais/efeitos dos fármacos
Receptor Toll-Like 9/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bzrp protein, mouse); 0 (Cytokines); 0 (Immunologic Factors); 0 (Oligodeoxyribonucleotides); 0 (Receptors, GABA); 0 (Tlr9 protein, mouse); 0 (Toll-Like Receptor 9); 0 (Vinca Alkaloids); 543512OBTC (vinpocetine)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170407
[Lr] Data última revisão:
170407
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161215
[St] Status:MEDLINE
[do] DOI:10.1080/08820139.2016.1248561



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