Base de dados : MEDLINE
Pesquisa : D02.522.120 [Categoria DeCS]
Referências encontradas : 3816 [refinar]
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[PMID]:28473297
[Au] Autor:Pochapsky TC; Wong N; Zhuang Y; Futcher J; Pandelia ME; Teitz DR; Colthart AM
[Ad] Endereço:Department of Chemistry, Brandeis University, 415 South St., Waltham, MA 02454-9110, USA. Electronic address: pochapsk@brandeis.edu.
[Ti] Título:NADH reduction of nitroaromatics as a probe for residual ferric form high-spin in a cytochrome P450.
[So] Source:Biochim Biophys Acta;1866(1):126-133, 2018 01.
[Is] ISSN:0006-3002
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The existence of a substrate-sensitive equilibrium between high spin (S=5/2) and low spin (S=1/2) ferric iron is a well-established phenomenon in the cytochrome P450 (CYP) superfamily, although its origins are still a subject of discussion. A series of mutations that strongly perturb the spin state equilibrium in the camphor hydroxylase CYP101A1 were recently described (Colthart et al., Sci. Rep. 6, 22035 (2016)). Wild type CYP101A1 as well as some CYP101A1 mutants are herein shown to be capable of catalyzing the reduction of nitroacetophenones by NADH to the corresponding anilino compounds (nitroreductase or NRase activity). The distinguishing characteristic between those mutants that catalyze the reduction and those that cannot appears to be the extent to which residual high spin form exists in the absence of the native substrate d-camphor, with those showing the largest spin state shifts upon camphor binding also exhibiting NRase activity. Optical and EPR spectroscopy was used to further examine these phenomena. These results suggest that reduction of nitroaromatics may provide a useful probe of residual high spin states in the CYP superfamily. This article is part of a Special Issue entitled: Cytochrome P450 biodiversity and biotechnology, edited by Erika Plettner, Gianfranco Gilardi, Luet Wong, Vlada Urlacher, Jared Goldstone.
[Mh] Termos MeSH primário: Acetofenonas/química
Proteínas de Bactérias/química
Cânfora 5-Mono-Oxigenase/química
Cânfora/química
Compostos Férricos/química
Heme/química
NAD/química
[Mh] Termos MeSH secundário: Acetofenonas/metabolismo
Motivos de Aminoácidos
Proteínas de Bactérias/genética
Proteínas de Bactérias/metabolismo
Sítios de Ligação
Biocatálise
Cânfora/metabolismo
Cânfora 5-Mono-Oxigenase/genética
Cânfora 5-Mono-Oxigenase/metabolismo
Clonagem Molecular
Espectroscopia de Ressonância de Spin Eletrônica
Escherichia coli/genética
Escherichia coli/metabolismo
Expressão Gênica
Heme/metabolismo
Cinética
Modelos Moleculares
NAD/metabolismo
Oxirredução
Ligação Proteica
Conformação Proteica em alfa-Hélice
Conformação Proteica em Folha beta
Domínios e Motivos de Interação entre Proteínas
Proteínas Recombinantes/química
Proteínas Recombinantes/genética
Proteínas Recombinantes/metabolismo
Especificidade por Substrato
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Acetophenones); 0 (Bacterial Proteins); 0 (Ferric Compounds); 0 (Recombinant Proteins); 0U46U6E8UK (NAD); 100-19-6 (4-nitroacetophenone); 42VZT0U6YR (Heme); 76-22-2 (Camphor); EC 1.14.15.1 (Camphor 5-Monooxygenase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180208
[Lr] Data última revisão:
180208
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170506
[St] Status:MEDLINE


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[PMID]:27771430
[Au] Autor:Brenza TM; Ghaisas S; Ramirez JEV; Harischandra D; Anantharam V; Kalyanaraman B; Kanthasamy AG; Narasimhan B
[Ad] Endereço:Department of Chemical and Biological Engineering, Iowa State University, Ames, IA, USA.
[Ti] Título:Neuronal protection against oxidative insult by polyanhydride nanoparticle-based mitochondria-targeted antioxidant therapy.
[So] Source:Nanomedicine;13(3):809-820, 2017 04.
[Is] ISSN:1549-9642
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A progressive loss of neuronal structure and function is a signature of many neurodegenerative conditions including chronic traumatic encephalopathy, Parkinson's, Huntington's and Alzheimer's diseases. Mitochondrial dysfunction and oxidative and nitrative stress have been implicated as key pathological mechanisms underlying the neurodegenerative processes. However, current therapeutic approaches targeting oxidative damage are ineffective in preventing the progression of neurodegeneration. Mitochondria-targeted antioxidants were recently shown to alleviate oxidative damage. In this work, we investigated the delivery of biodegradable polyanhydride nanoparticles containing the mitochondria-targeted antioxidant apocynin to neuronal cells and the ability of the nano-formulation to protect cells against oxidative stress. The nano-formulated mitochondria-targeted apocynin provided excellent protection against oxidative stress-induced mitochondrial dysfunction and neuronal damage in a dopaminergic neuronal cell line, mouse primary cortical neurons, and a human mesencephalic cell line. Collectively, our results demonstrate that nano-formulated mitochondria-targeted apocynin may offer improved efficacy of mitochondria-targeted antioxidants to treat neurodegenerative disease.
[Mh] Termos MeSH primário: Acetofenonas/administração & dosagem
Antioxidantes/administração & dosagem
Portadores de Fármacos/química
Nanopartículas/química
Neuroproteção/efeitos dos fármacos
Estresse Oxidativo/efeitos dos fármacos
Polianidridos/química
[Mh] Termos MeSH secundário: Acetofenonas/farmacologia
Animais
Antioxidantes/farmacologia
Linhagem Celular
Células Cultivadas
Sistemas de Liberação de Medicamentos
Seres Humanos
Camundongos
Mitocôndrias/efeitos dos fármacos
Mitocôndrias/metabolismo
Nanopartículas/ultraestrutura
Neurônios/efeitos dos fármacos
Neurônios/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Acetophenones); 0 (Antioxidants); 0 (Drug Carriers); 0 (Polyanhydrides); B6J7B9UDTR (acetovanillone)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:180209
[Lr] Data última revisão:
180209
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


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[PMID]:29272319
[Au] Autor:Min M; Yan BX; Wang P; Landeck L; Chen JQ; Li W; Cai SQ; Zheng M; Man XY
[Ad] Endereço:Department of Dermatology, Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
[Ti] Título:Rottlerin as a therapeutic approach in psoriasis: Evidence from in vitro and in vivo studies.
[So] Source:PLoS One;12(12):e0190051, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Rottlerin is a natural polyphenolic compound that was initially indicated as a PKCδ inhibitor. However, it was recently revealed that it may target a number of molecules and have biological effects on various cell types and is considered as a possible agent for tumor and cell proliferative diseases. Psoriasis is a chronic inflammatory cutaneous disorder with undefined etiology and is characterized by abnormal cellular proliferation, angiogenesis, and inflammation. Therefore, this paper investigates the regulatory effects of rottlerin on normal human epidermal keratinocytes (NHEKs) and imiquimod (IMQ)-induced psoriasiform (IPI) lesions. In vitro results showed that rottlerin inhibited cell proliferation in NHEKs through growth arrest and NFκB inhibition. It may also induce apoptosis in an autophagy-dependent pathway. We found that rottlerin inhibited human microvascular endothelial cells tube formation on matrigel. Rottlerin also decreased the cell senescence of keratinocytes and intracellular ROS generation, which indicated its antioxidant effect. We also showed that rottlerin affects the expression of keratinocyte proliferation biomarkers. In 12-O-tetradecanoylphorbol13-acetate (TPA)-induced keratinocytes, rottlerin significantly inhibited the expression of the induced pro-inflammatory cytokines in keratinocytes. An animal experiment provided the corresponding evidence based on this evidence in vitro, by using IPI model, we found that rottlerin could relieve the psoriasiform of BALB/c mice by inhibiting keratinocyte proliferation, inflammatory cell infiltration, and vascular proliferation. In conclusion, our results suggest that rottlerin may prove useful in the development of therapeutic agents against psoriasis. However, the deep mechanism still requires further study.
[Mh] Termos MeSH primário: Acetofenonas/uso terapêutico
Benzopiranos/uso terapêutico
Psoríase/tratamento farmacológico
[Mh] Termos MeSH secundário: Adjuvantes Imunológicos/uso terapêutico
Adolescente
Adulto
Aminoquinolinas/uso terapêutico
Animais
Apoptose/efeitos dos fármacos
Autofagia/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Células Cultivadas
Feminino
Seres Humanos
Técnicas In Vitro
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Meia-Idade
NF-kappa B/metabolismo
Psoríase/metabolismo
Psoríase/patologia
Espécies Reativas de Oxigênio/metabolismo
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Acetophenones); 0 (Adjuvants, Immunologic); 0 (Aminoquinolines); 0 (Benzopyrans); 0 (NF-kappa B); 0 (Reactive Oxygen Species); E29LP3ZMUH (rottlerin); P1QW714R7M (imiquimod)
[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:171223
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190051


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[PMID]:29199217
[Au] Autor:Park KS; Yoo K; Kim MK; Jung W; Choi YK; Chong Y
[Ad] Endereço:Department of Bioscience and Biotechnology, Bio/Molecular Informatics Center, Konkuk University.
[Ti] Título:A Novel Probe with a Chlorinated α-Cyanoacetophenone Acceptor Moiety Shows Near-Infrared Fluorescence Specific for Tau Fibrils.
[So] Source:Chem Pharm Bull (Tokyo);65(12):1113-1116, 2017.
[Is] ISSN:1347-5223
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Development of a novel, tau-selective near-infrared fluorescence (NIRF) probe was attempted by combining the 3,5-dimethoxy-N,N-dimethylaniline-4-yl moiety with an α-cyanoacetophenone via hexatrienyl π-linker. In particular, for structure-activity relationship study of the α-cyanoacetophenones, a chlorine substituent was introduced to the aromatic ring to give a series of compounds (2a-2d). Among those, compound 2c with meta-chloro aryl substituent was identified as a tau-selective NIRF probe: selectivity for tau over amyloid ß (Aß) and bovine serum albumin (BSA) was estimated to be 10.3 and 19.5 fold, respectively. The mechanism for tau-selectivity of 2c was found to be based on the specific recognition of the microenviroment of tau fibrils, which was endowed by its molecular rotor-like properties. The tau-selective NIRF probe 2c was also able to stain tau fibrils in tau-green fluorescent protein (GFP)-transgenic human neuroblastoma cells (SH-SY5Y cells).
[Mh] Termos MeSH primário: Acetofenonas/química
Corantes Fluorescentes/química
Espectroscopia de Luz Próxima ao Infravermelho
Proteínas tau/química
[Mh] Termos MeSH secundário: Amiloide/química
Compostos de Anilina/química
Linhagem Celular Tumoral
Proteínas de Fluorescência Verde/genética
Proteínas de Fluorescência Verde/metabolismo
Halogenação
Seres Humanos
Proteínas Recombinantes de Fusão/genética
Proteínas Recombinantes de Fusão/metabolismo
Soroalbumina Bovina/química
Proteínas tau/genética
Proteínas tau/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Acetophenones); 0 (Amyloid); 0 (Aniline Compounds); 0 (Fluorescent Dyes); 0 (Recombinant Fusion Proteins); 0 (tau Proteins); 147336-22-9 (Green Fluorescent Proteins); 27432CM55Q (Serum Albumin, Bovine); 7426719369 (N,N-dimethylaniline)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180110
[Lr] Data última revisão:
180110
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171205
[St] Status:MEDLINE
[do] DOI:10.1248/cpb.c17-00559


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[PMID]:29203243
[Au] Autor:Wang Z; Shen GH; Xie JM; Li B; Gao QG
[Ad] Endereço:Department of General Surgery, The First People's Hospital of Wu Jiang, Suzhou, Jiangsu, 215200, China; Department of General Surgery, The Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu, 215006, China.
[Ti] Título:Rottlerin upregulates DDX3 expression in hepatocellular carcinoma.
[So] Source:Biochem Biophys Res Commun;495(1):1503-1509, 2018 01 01.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Rottlerin has been reported to exert its anti-tumor activity in various types of human cancers. However, the underlying molecular mechanism has not been fully elucidated. In the current study, we explored whether rottlerin exhibits its tumor suppressive function in hepatocellular carcinoma cells. Our MTT assay results showed that rottlerin inhibited cell growth in hepatocellular carcinoma cells. Moreover, we found that rottlerin induced cell apoptosis and caused cell cycle arrest at G1 phase. Furthermore, our wound healing assay result demonstrated that rottlerin retarded cell migration in hepatocellular carcinoma cells. Additionally, rottlerin suppressed cell migration and invasion. Notably, we found that rottlerin upregulated DDX3 expression and subsequently downregulated Cyclin D1 expression and increased p21 level. Importantly, down-regulation of DDX3 abrogated the rottlerin-mediated tumor suppressive function, whereas overexpression of DDX3 promoted the anti-tumor activity of rottlerin. Our study suggests that rottlerin exhibits its anti-cancer activity partly due to upregulation of DDX3 in hepatocellular carcinoma cells.
[Mh] Termos MeSH primário: Acetofenonas/administração & dosagem
Apoptose/efeitos dos fármacos
Benzopiranos/administração & dosagem
Carcinoma Hepatocelular/tratamento farmacológico
Carcinoma Hepatocelular/metabolismo
RNA Helicases DEAD-box/metabolismo
Neoplasias Hepáticas/tratamento farmacológico
Neoplasias Hepáticas/metabolismo
[Mh] Termos MeSH secundário: Antineoplásicos/administração & dosagem
Carcinoma Hepatocelular/patologia
Pontos de Checagem do Ciclo Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Movimento Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Relação Dose-Resposta a Droga
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Neoplasias Hepáticas/patologia
Regulação para Cima/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Acetophenones); 0 (Antineoplastic Agents); 0 (Benzopyrans); E29LP3ZMUH (rottlerin); EC 3.6.1.- (DDX3X protein, human); EC 3.6.4.13 (DEAD-box RNA Helicases)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180105
[Lr] Data última revisão:
180105
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171206
[St] Status:MEDLINE


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[PMID]:28946128
[Au] Autor:Ding LQ; Qiu TY; Liu ZX; Chen LX; Oppong MB; Zhang DQ; Zhang BL; Bai G; Qiu F
[Ad] Endereço:Tianjin Key Laboratory of TCM Chemistry and Analysis, Institute of Traditional Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin, China.
[Ti] Título:Systematic characterization of the metabolites of paeonol in rats using ultra performance liquid chromatography coupled with electrospray ionization quadrupole time-of-flight tandem mass spectrometry with an integrative strategy.
[So] Source:J Chromatogr B Analyt Technol Biomed Life Sci;1065-1066:70-78, 2017 Oct 15.
[Is] ISSN:1873-376X
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Paeonol, an active constituent in the root bark of Paeonia suffruticosa Andrews, is used to treat inflammation, headache and other diseases in clinic. Though the data on pharmacological researches of paeonol abounds, its metabolic profile is not so clear. It is essential to systematically characterize the in vivo metabolites in order to better understand its mechanism of action. In this study, ultra performance liquid chromatography coupled with electrospray ionization quadrupole time-of-flight tandem mass spectrometry (UPLC-ESI-Q/TOF-MS) with an integrative strategy was developed for analysis of paeonol metabolites. As a result, based on seven reference substances isolated or synthesized, twenty-five metabolites were detected and identified in urine, feces, bile and plasma of rats after oral administration of paeonol. To the best of our knowledge, 14 of these metabolites have not been reported previously. In addition, the dominating metabolic fates were oxidation, demethylation, hydrogenation, glucuronic acid and sulfate conjugations, and hydrogenation of paeonol was reported for the first time. This research provides scientific and reliable support for full understanding of the metabolic profiling of paeonol.
[Mh] Termos MeSH primário: Acetofenonas/análise
Acetofenonas/química
Cromatografia Líquida de Alta Pressão/métodos
Espectrometria de Massas por Ionização por Electrospray/métodos
Espectrometria de Massas em Tandem/métodos
[Mh] Termos MeSH secundário: Acetofenonas/metabolismo
Animais
Bile/química
Fezes/química
Masculino
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Acetophenones); 3R834EPI82 (paeonol)
[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:170926
[St] Status:MEDLINE


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[PMID]:28934273
[Au] Autor:Han F; Zhuang TT; Chen JJ; Zhu XL; Cai YF; Lu YP
[Ad] Endereço:College of Life Science, Anhui Normal University, Wuhu, China.
[Ti] Título:Novel derivative of Paeonol, Paeononlsilatie sodium, alleviates behavioral damage and hippocampal dendritic injury in Alzheimer's disease concurrent with cofilin1/phosphorylated-cofilin1 and RAC1/CDC42 alterations in rats.
[So] Source:PLoS One;12(9):e0185102, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Alzheimer's disease (AD) is a typical hippocampal amnesia and the most common senile dementia. Many studies suggest that cognitive impairments are more closely correlated with synaptic loss than the burden of amyloid deposits in AD progression. To date, there is no effective treatment for this disease. Paeonol has been widely employed in traditional Chinese medicine. This compound improves learning behavior in an animal model; however, the mechanism remains unclear. In this study, Paeononlsilatie sodium (Pa), a derivative of Paeonol, attenuated D-galactose (D-gal) and AlCl3-induced behavioral damages in rats based on evaluations of the open field test (OFT), elevated plus maze test (EPMT), and Morris water maze test (MWMT). Pa increased the dendritic complexity and the density of dendritic spines. Correlation analysis indicated that morphological changes in neuronal dendrites are closely correlated with behavioral changes. Pa treatment reduced the production of Aß, affected the phosphorylation and redistribution of cofilin1 and inhibited rod-like formation in hippocampal neurons. The induction of D-gal and AlCl3 promoted the expression of RAC1/CDC42 expression; however, the tendency of gene expression was inhibited by pretreatment with Pa. Taken together, our results suggest that Pa may represent a novel therapeutic agent for the improvement of cognitive and emotional behaviors and dendritic morphology in an AD animal model.
[Mh] Termos MeSH primário: Acetofenonas/farmacologia
Doença de Alzheimer/tratamento farmacológico
Dendritos/efeitos dos fármacos
Hipocampo/efeitos dos fármacos
Aprendizagem em Labirinto/efeitos dos fármacos
Fármacos Neuroprotetores/farmacologia
[Mh] Termos MeSH secundário: Doença de Alzheimer/metabolismo
Doença de Alzheimer/patologia
Doença de Alzheimer/psicologia
Peptídeos beta-Amiloides/metabolismo
Animais
Atrofia/tratamento farmacológico
Atrofia/metabolismo
Atrofia/patologia
Cofilina 1/metabolismo
Dendritos/metabolismo
Dendritos/patologia
Modelos Animais de Doenças
Avaliação Pré-Clínica de Medicamentos
Galactose
Hipocampo/metabolismo
Hipocampo/patologia
Masculino
Fragmentos de Peptídeos/metabolismo
Fosforilação
Distribuição Aleatória
Ratos Sprague-Dawley
Proteína cdc42 de Ligação ao GTP/metabolismo
Proteínas rac1 de Ligação ao GTP/metabolismo
Proteínas tau/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Acetophenones); 0 (Amyloid beta-Peptides); 0 (Cfl1 protein, rat); 0 (Cofilin 1); 0 (Mapt protein, rat); 0 (Neuroprotective Agents); 0 (Peptide Fragments); 0 (amyloid beta-protein (1-42)); 0 (tau Proteins); 88678-17-5 (sodium paeonol sulfate); EC 3.6.1.- (Rac1 protein, rat); EC 3.6.5.2 (cdc42 GTP-Binding Protein); EC 3.6.5.2 (rac1 GTP-Binding Protein); X2RN3Q8DNE (Galactose)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170922
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0185102


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[PMID]:28838645
[Au] Autor:Zhang Y; Cheng Y; Liu Z; Ding L; Qiu T; Chai L; Qiu F; Wang Z; Xiao W; Zhao L; Chen X
[Ad] Endereço:School of Pharmacy, Shenyang Pharmaceutical University, Shenyang Pharmaceutical University, 103 Wenhua Road, Shenyang 110016, PR China.
[Ti] Título:Systematic screening and characterization of multiple constituents in Guizhi Fuling capsule and metabolic profiling of bioactive components in rats using ultra-high-performance liquid chromatography/quadrupole-time-of-flight mass spectrometry.
[So] Source:J Chromatogr B Analyt Technol Biomed Life Sci;1061-1062:474-486, 2017 Sep 01.
[Is] ISSN:1873-376X
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Guizhi Fuling capsule (GFC), a prestigious traditional Chinese medicinal (TCM) prescription, is efficiently used to treat primary dysmenorrhea in the clinical practice. It's significant to explore the metabolic fate of multiple components in vivo which are responsible for the pharmacological effects but not fully investigated. A rapid and high-throughput method using ultra performance liquid chromatography/quadrupole time-of-flight tandem mass spectrometry (UPLC/Q-TOF-MS/MS) was established for systematic investigation on GFC, including GFC chemical compositions, and their absorption and metabolism in rat plasma, urine, uterus and brain after oral administration of GFC. A total of 102 nonvolatile GFC phytochemistry components were identified based on the accurately measured mass value, fragmentation pattern and retention behavior. Compared to the previous GFC study, additional 47 different GFC components were detected. Furthermore 21, 9, 4 and 3 prototype compounds were separately observed in plasma, urine, uterus and brain samples with the support of in vitro GFC study. While 29, 33, 10 and 8 metabolites were also identified with the assistance of the MetaboLynx tool in these biological samples. The result indicated that the developed method was suitable for the components identification even in the complex matrix. The chemical and metabolic profiling of GFC provided an abundant substance foundation for the extensive GFC research, especially for the pharmacodynamic mechanisms research.
[Mh] Termos MeSH primário: Cromatografia Líquida de Alta Pressão/métodos
Medicamentos de Ervas Chinesas
Metabolômica/métodos
Espectrometria de Massas em Tandem/métodos
[Mh] Termos MeSH secundário: Acetofenonas/análise
Acetofenonas/química
Acetofenonas/metabolismo
Animais
Encéfalo/metabolismo
Química Encefálica
Cápsulas
Medicamentos de Ervas Chinesas/análise
Medicamentos de Ervas Chinesas/metabolismo
Medicamentos de Ervas Chinesas/farmacocinética
Feminino
Ácido Gálico/análise
Ácido Gálico/química
Ácido Gálico/metabolismo
Glicosídeos/análise
Glicosídeos/química
Glicosídeos/metabolismo
Monoterpenos/análise
Monoterpenos/química
Monoterpenos/metabolismo
Ratos
Ratos Sprague-Dawley
Espectrometria de Massas por Ionização e Dessorção a Laser Assistida por Matriz
Distribuição Tecidual
Útero/química
Útero/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Acetophenones); 0 (Capsules); 0 (Drugs, Chinese Herbal); 0 (Glycosides); 0 (Monoterpenes); 0 (guizhi-fuling); 632XD903SP (Gallic Acid)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170826
[St] Status:MEDLINE


  9 / 3816 MEDLINE  
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[PMID]:28822840
[Au] Autor:Chakraborti S; Sarkar J; Chowdhury A; Chakraborti T
[Ad] Endereço:Department of Biochemistry and Biophysics, University of Kalyani, Kalyani 741235, West Bengal, India. Electronic address: sajal_chakraborti@yahoo.com.
[Ti] Título:Role of ADP ribosylation factor6- Cytohesin1-PhospholipaseD signaling axis in U46619 induced activation of NADPH oxidase in pulmonary artery smooth muscle cell membrane.
[So] Source:Arch Biochem Biophys;633:1-14, 2017 Nov 01.
[Is] ISSN:1096-0384
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Treatment of human pulmonary artery smooth muscle cells (HPASMCs) with the thromboxane A2 receptor antagonist, SQ29548 inhibited U46619 stimulation of phospholipase D (PLD) and NADPH oxidase activities in the cell membrane. Pretreatment with apocynin inhibited U46619 induced increase in NADPH oxidase activity. The cell membrane contains predominantly PLD2 along with PLD1 isoforms of PLD. Pretreatment with pharmacological and genetic inhibitors of PLD2, but not PLD1, attenuated U46619 stimulation of NADPH oxidase activity. U46619 stimulation of PLD and NADPH oxidase activities were insensitive to BFA and Clostridium botulinum C3 toxin; however, pretreatment with secinH3 inhibited U46619 induced increase in PLD and NADPH oxidase activities suggesting a major role of cytohesin in U46619-induced increase in PLD and NADPH oxidase activities. Arf-1, Arf-6, cytohesin-1 and cytohesin-2 were observed in the cytosolic fraction, but only Arf-6 and cytohesin-1 were translocated to the cell membrane upon treatment with U46619. Coimmunoprecipitation study showed association of Arf-6 with cytohesin-1 in the cell membrane fraction. In vitro binding of GTPγS with Arf-6 required the presence of cytohesin-1 and that occurs in BFA insensitive manner. Overall, BFA insensitive Arf6-cytohesin1 signaling axis plays a pivotal role in U46619-mediated activation of PLD leading to stimulation of NADPH oxidase activity in HPASMCs.
[Mh] Termos MeSH primário: Ácido 15-Hidroxi-11 alfa,9 alfa-(epoximetano)prosta-5,13-dienoico/farmacologia
Fatores de Ribosilação do ADP/genética
Fatores de Troca do Nucleotídeo Guanina/genética
NADPH Oxidases/genética
Fosfolipase D/genética
Vasoconstritores/farmacologia
[Mh] Termos MeSH secundário: ADP Ribose Transferases/farmacologia
Fatores de Ribosilação do ADP/metabolismo
Acetofenonas/farmacologia
Antioxidantes/farmacologia
Toxinas Botulínicas/farmacologia
Brefeldina A/farmacologia
Membrana Celular/efeitos dos fármacos
Membrana Celular/metabolismo
Proteínas Ativadoras de GTPase/antagonistas & inibidores
Proteínas Ativadoras de GTPase/genética
Proteínas Ativadoras de GTPase/metabolismo
Regulação da Expressão Gênica
Fatores de Troca do Nucleotídeo Guanina/antagonistas & inibidores
Fatores de Troca do Nucleotídeo Guanina/metabolismo
Guanosina 5'-O-(3-Tiotrifosfato)/farmacologia
Seres Humanos
Hidrazinas/farmacologia
Miócitos de Músculo Liso/citologia
Miócitos de Músculo Liso/efeitos dos fármacos
Miócitos de Músculo Liso/metabolismo
NADPH Oxidases/metabolismo
Fosfolipase D/antagonistas & inibidores
Fosfolipase D/metabolismo
Cultura Primária de Células
Inibidores da Síntese de Proteínas/farmacologia
Artéria Pulmonar/citologia
Artéria Pulmonar/efeitos dos fármacos
Artéria Pulmonar/metabolismo
Receptores de Tromboxano A2 e Prostaglandina H2/antagonistas & inibidores
Receptores de Tromboxano A2 e Prostaglandina H2/genética
Receptores de Tromboxano A2 e Prostaglandina H2/metabolismo
Transdução de Sinais
Triazóis/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Acetophenones); 0 (Antioxidants); 0 (GTPase-Activating Proteins); 0 (Guanine Nucleotide Exchange Factors); 0 (Hydrazines); 0 (Protein Synthesis Inhibitors); 0 (Receptors, Thromboxane A2, Prostaglandin H2); 0 (SecinH3); 0 (Triazoles); 0 (Vasoconstrictor Agents); 0 (cytohesin-1); 0 (cytohesin-2); 20350-15-6 (Brefeldin A); 37589-80-3 (Guanosine 5'-O-(3-Thiotriphosphate)); 76898-47-0 (15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid); 98299-61-7 (SQ 29548); B6J7B9UDTR (acetovanillone); EC 1.6.3.- (NADPH Oxidases); EC 2.4.2.- (ADP Ribose Transferases); EC 2.4.2.- (exoenzyme C3, Clostridium botulinum); EC 3.1.4.- (phospholipase D2); EC 3.1.4.4 (Phospholipase D); EC 3.1.4.4 (phospholipase D1); EC 3.4.24.69 (Botulinum Toxins); EC 3.6.5.2 (ADP-Ribosylation Factors); EC 3.6.5.2 (ADP-ribosylation factor 6)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170821
[St] Status:MEDLINE


  10 / 3816 MEDLINE  
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[PMID]:28734998
[Au] Autor:Kang SW; Kim SJ; Kim MS
[Ad] Endereço:College of Pharmacy and Research Institute of Life Pharmaceutical Sciences, Sunchon National University, 255 Jungangro, Suncheon, Jeonnam 57922, Republic of Korea.
[Ti] Título:Oxidative stress with tau hyperphosphorylation in memory impaired 1,2-diacetylbenzene-treated mice.
[So] Source:Toxicol Lett;279:53-59, 2017 Sep 05.
[Is] ISSN:1879-3169
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Long-term exposure to organic solvent may be related to the incidence of neuronal diseases, such as, Alzheimer's disease, depression, multiple sclerosis, dementia, Parkinson's disease. Previously, the authors reported 1,2-diacetylbenzene (DAB; a neurotoxic metabolite of 1,2-diethylbenzene) causes central and peripheral neuropathies that lead to motor neuronal deficits. Furthermore, it is known DAB increases oxidative stress and protein adduct levels and impairs hippocampal neurogenesis in mice. The authors examined the relevance of oxidative stress and tau hyperphosphorylation in the hippocampus. Five-week-old male C57BL/6 mice were treated with 1 or 5mg/kg/day DAB for 2weeks. Neither overall body weight increases nor behavioral differences were observed after treatment, but kidney and liver weights decreased. Increased ROS production, activated glycogen synthase kinase-3ß (GSK-3ß) and tau hyperphosphorylation were observed in hippocampal homogenates. To assess memory impairment, the Morris Water Maze was used. Animals in the DAB-treated groups took longer to reach the platform. Movement patterns of DAB treated mice were more complicated and their swimming speeds were lower than those of controls. When SHSY5Y neuroblastoma cells were pretreated with NAC (an antioxidant) or a GSK-3ß inhibitor, the expression of active GSK-3ß and tau hyperphosphorylation were reduced. These results suggest ROS produced by DAB causes tau hyperphosphorylation via GSK-3ß phosphorylation and it might be related to impaired memory deficit.
[Mh] Termos MeSH primário: Comportamento Animal
Hipocampo/metabolismo
Transtornos da Memória/metabolismo
Memória
Estresse Oxidativo
Proteínas tau/metabolismo
[Mh] Termos MeSH secundário: Acetofenonas
Animais
Antioxidantes/farmacologia
Comportamento Animal/efeitos dos fármacos
Linhagem Celular Tumoral
Modelos Animais de Doenças
Produtos Finais de Glicação Avançada/metabolismo
Glicogênio Sintase Quinase 3 beta/antagonistas & inibidores
Glicogênio Sintase Quinase 3 beta/metabolismo
Hipocampo/efeitos dos fármacos
Hipocampo/patologia
Hipocampo/fisiopatologia
Masculino
Aprendizagem em Labirinto
Memória/efeitos dos fármacos
Transtornos da Memória/induzido quimicamente
Transtornos da Memória/patologia
Transtornos da Memória/psicologia
Camundongos Endogâmicos C57BL
Atividade Motora
Neurogênese
Estresse Oxidativo/efeitos dos fármacos
Fosforilação
Inibidores de Proteínas Quinases/farmacologia
Espécies Reativas de Oxigênio/metabolismo
Transdução de Sinais
Natação
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Acetophenones); 0 (Antioxidants); 0 (Glycation End Products, Advanced); 0 (MAPT protein, human); 0 (Mapt protein, mouse); 0 (Protein Kinase Inhibitors); 0 (Reactive Oxygen Species); 0 (tau Proteins); 704-00-7 (1,2-diacetylbenzene); EC 2.7.11.1 (Glycogen Synthase Kinase 3 beta); EC 2.7.11.1 (Gsk3b protein, mouse)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170724
[St] Status:MEDLINE



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