Base de dados : MEDLINE
Pesquisa : D04.210.500.105.225.261 [Categoria DeCS]
Referências encontradas : 321 [refinar]
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[PMID]:25945334
[Au] Autor:Martinez Mdel C; Ruspini SF; Afonso SG; Meiss R; Buzaleh AM; Batlle A
[Ad] Endereço:Departamento de Química Biológica, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Ciudad Universitaria, Intendente Güiraldes 2160, 1428 Buenos Aires, Argentina.
[Ti] Título:Experimental protoporphyria: effect of bile acids on liver damage induced by griseofulvin.
[So] Source:Biomed Res Int;2015:436319, 2015.
[Is] ISSN:2314-6141
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The effect of bile acids administration to an experimental mice model of Protoporphyria produced by griseofulvin (Gris) was investigated. The aim was to assess whether porphyrin excretion could be accelerated by bile acids treatment in an attempt to diminish liver damage induced by Gris. Liver damage markers, heme metabolism, and oxidative stress parameters were analyzed in mice treated with Gris and deoxycholic (DXA), dehydrocholic (DHA), chenodeoxycholic, or ursodeoxycholic (URSO). The administration of Gris alone increased the activities of glutathione reductase (GRed), superoxide dismutase (SOD), alkaline phosphatase (AP), gamma glutamyl transpeptidase (GGT), and glutathione-S-transferase (GST), as well as total porphyrins, glutathione (GSH), and cytochrome P450 (CYP) levels in liver. Among the bile acids studied, DXA and DHA increased PROTO IX excretion, DXA also abolished the action of Gris, reducing lipid peroxidation and hepatic GSH and CYP levels, and the activities of GGT, AP, SOD, and GST returned to control values. However, porphyrin accumulation was not prevented by URSO; instead this bile acid reduced ALA-S and the antioxidant defense enzymes system activities. In conclusion, we postulate that DXA acid would be more effective to prevent liver damage induced by Gris.
[Mh] Termos MeSH primário: Doença Hepática Induzida por Substâncias e Drogas/tratamento farmacológico
Estresse Oxidativo/efeitos dos fármacos
Protoporfiria Eritropoética/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Catalase/metabolismo
Doença Hepática Induzida por Substâncias e Drogas/metabolismo
Doença Hepática Induzida por Substâncias e Drogas/patologia
Ácido Quenodesoxicólico/administração & dosagem
Ácido Desidrocólico/administração & dosagem
Ácido Desoxicólico/administração & dosagem
Glutationa Peroxidase/metabolismo
Glutationa Redutase/metabolismo
Glutationa Transferase/metabolismo
Griseofulvina/toxicidade
Seres Humanos
Peroxidação de Lipídeos/efeitos dos fármacos
Camundongos
Porfirinas/metabolismo
Protoporfiria Eritropoética/induzido quimicamente
Protoporfiria Eritropoética/metabolismo
Superóxido Dismutase/metabolismo
Ácido Ursodesoxicólico/administração & dosagem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Porphyrins); 005990WHZZ (Deoxycholic Acid); 0GEI24LG0J (Chenodeoxycholic Acid); 32HRV3E3D5 (Griseofulvin); 724L30Y2QR (Ursodeoxycholic Acid); EC 1.11.1.6 (Catalase); EC 1.11.1.9 (Glutathione Peroxidase); EC 1.15.1.1 (Superoxide Dismutase); EC 1.8.1.7 (Glutathione Reductase); EC 2.5.1.18 (Glutathione Transferase); NH5000009I (Dehydrocholic Acid)
[Em] Mês de entrada:1602
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150507
[St] Status:MEDLINE
[do] DOI:10.1155/2015/436319


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[PMID]:25641915
[Au] Autor:Sun B; Hartl F; Castiglione K; Weuster-Botz D
[Ad] Endereço:Inst. of Biochemical Engineering, Dept. of Mechanical Engineering, Technische Universität München, Garching, 85748, Germany.
[Ti] Título:Dynamic mechanistic modeling of the multienzymatic one-pot reduction of dehydrocholic acid to 12-keto ursodeoxycholic acid with competing substrates and cofactors.
[So] Source:Biotechnol Prog;31(2):375-86, 2015 Mar-Apr.
[Is] ISSN:1520-6033
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Ursodeoxycholic acid (UDCA) is a bile acid which is used as pharmaceutical for the treatment of several diseases, such as cholesterol gallstones, primary sclerosing cholangitis or primary biliary cirrhosis. A potential chemoenzymatic synthesis route of UDCA comprises the two-step reduction of dehydrocholic acid to 12-keto-ursodeoxycholic acid (12-keto-UDCA), which can be conducted in a multienzymatic one-pot process using 3α-hydroxysteroid dehydrogenase (3α-HSDH), 7ß-hydroxysteroid dehydrogenase (7ß-HSDH), and glucose dehydrogenase (GDH) with glucose as cosubstrate for the regeneration of cofactor. Here, we present a dynamic mechanistic model of this one-pot reduction which involves three enzymes, four different bile acids, and two different cofactors, each with different oxidation states. In addition, every enzyme faces two competing substrates, whereas each bile acid and cofactor is formed or converted by two different enzymes. First, the kinetic mechanisms of both HSDH were identified to follow an ordered bi-bi mechanism with EBQ-type uncompetitive substrate inhibition. Rate equations were then derived for this mechanism and for mechanisms describing competing substrates. After the estimation of the model parameters of each enzyme independently by progress curve analyses, the full process model of a simple batch-process was established by coupling rate equations and mass balances. Validation experiments of the one-pot multienzymatic batch process revealed high prediction accuracy of the process model and a model analysis offered important insight to the identification of optimum reaction conditions.
[Mh] Termos MeSH primário: Ácido Desidrocólico/química
Ácido Desidrocólico/metabolismo
Engenharia Metabólica/métodos
Modelos Biológicos
Ácido Ursodesoxicólico/química
Ácido Ursodesoxicólico/metabolismo
[Mh] Termos MeSH secundário: Reatores Biológicos
Escherichia coli/genética
Escherichia coli/metabolismo
Glucose 1-Desidrogenase/genética
Glucose 1-Desidrogenase/metabolismo
Hidroxiesteroide Desidrogenases/genética
Hidroxiesteroide Desidrogenases/metabolismo
Cinética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
724L30Y2QR (Ursodeoxycholic Acid); EC 1.1.- (Hydroxysteroid Dehydrogenases); EC 1.1.1.47 (Glucose 1-Dehydrogenase); NH5000009I (Dehydrocholic Acid)
[Em] Mês de entrada:1601
[Cu] Atualização por classe:150423
[Lr] Data última revisão:
150423
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150203
[St] Status:MEDLINE
[do] DOI:10.1002/btpr.2036


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[PMID]:23352263
[Au] Autor:Rosenthal RL
[Ti] Título:What we counted.
[So] Source:Am J Cardiol;111(7):1073-5, 2013 Apr 01.
[Is] ISSN:1879-1913
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Cardiomegalia/sangue
Colagogos e Coleréticos
Ácido Desidrocólico
Insuficiência Cardíaca/diagnóstico
Peptídeo Natriurético Encefálico/sangue
Medição de Risco/métodos
Complexos Ventriculares Prematuros/fisiopatologia
[Mh] Termos MeSH secundário: Insuficiência Cardíaca/fisiopatologia
Seres Humanos
[Pt] Tipo de publicação:EDITORIAL
[Nm] Nome de substância:
0 (Cholagogues and Choleretics); 114471-18-0 (Natriuretic Peptide, Brain); NH5000009I (Dehydrocholic Acid)
[Em] Mês de entrada:1305
[Cu] Atualização por classe:151119
[Lr] Data última revisão:
151119
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:130129
[St] Status:MEDLINE


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[PMID]:22899496
[Au] Autor:Liu L; Braun M; Gebhardt G; Weuster-Botz D; Gross R; Schmid RD
[Ad] Endereço:Institute of Technical Biochemistry, University of Stuttgart, Allmandring 31, 70569 Stuttgart, Germany.
[Ti] Título:One-step synthesis of 12-ketoursodeoxycholic acid from dehydrocholic acid using a multienzymatic system.
[So] Source:Appl Microbiol Biotechnol;97(2):633-9, 2013 Jan.
[Is] ISSN:1432-0614
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:12-ketoursodeoxycholic acid (12-keto-UDCA) is a key intermediate for the synthesis of ursodeoxycholic acid (UDCA), an important therapeutic agent for non-surgical treatment of human cholesterol gallstones and various liver diseases. The goal of this study is to develop a new enzymatic route for the synthesis 12-keto-UDCA based on a combination of NADPH-dependent 7ß-hydroxysteroid dehydrogenase (7ß-HSDH, EC 1.1.1.201) and NADH-dependent 3α-hydroxysteroid dehydrogenase (3α-HSDH, EC 1.1.1.50). In the presence of NADPH and NADH, the combination of these enzymes has the capacity to reduce the 3-carbonyl- and 7-carbonyl-groups of dehydrocholic acid (DHCA), forming 12-keto-UDCA in a single step. For cofactor regeneration, an engineered formate dehydrogenase, which is able to regenerate NADPH and NADH simultaneously, was used. All three enzymes were overexpressed in an engineered expression host Escherichia coli BL21(DE3)Δ7α-HSDH devoid of 7α-hydroxysteroid dehydrogenase, an enzyme indigenous to E. coli, in order to avoid formation of the undesired by-product 12-chenodeoxycholic acid in the reaction mixture. The stability of enzymes and reaction conditions such as pH value and substrate concentration were evaluated. No significant loss of activity was observed after 5 days under reaction condition. Under the optimal condition (10 mM of DHCA and pH 6), 99 % formation of 12-keto-UDCA with 91 % yield was observed.
[Mh] Termos MeSH primário: Ácido Desidrocólico/química
Ácido Desidrocólico/metabolismo
Enzimas/metabolismo
Ácido Ursodesoxicólico/química
Ácido Ursodesoxicólico/metabolismo
[Mh] Termos MeSH secundário: Escherichia coli/enzimologia
Escherichia coli/genética
Formiato Desidrogenases/metabolismo
Hidroxiesteroide Desidrogenases/metabolismo
Estrutura Molecular
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Enzymes); 724L30Y2QR (Ursodeoxycholic Acid); EC 1.1.- (Hydroxysteroid Dehydrogenases); EC 1.1.1.- (7 beta-hydroxysteroid dehydrogenase); EC 1.2.1.2 (Formate Dehydrogenases); NH5000009I (Dehydrocholic Acid)
[Em] Mês de entrada:1306
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:120818
[St] Status:MEDLINE
[do] DOI:10.1007/s00253-012-4340-5


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[PMID]:22806613
[Au] Autor:Sun B; Kantzow C; Bresch S; Castiglione K; Weuster-Botz D
[Ad] Endereço:Institute of Biochemical Engineering, Technische Universität München, Boltzmannstr 15, 85748 Garching, Germany.
[Ti] Título:Multi-enzymatic one-pot reduction of dehydrocholic acid to 12-keto-ursodeoxycholic acid with whole-cell biocatalysts.
[So] Source:Biotechnol Bioeng;110(1):68-77, 2013 Jan.
[Is] ISSN:1097-0290
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Ursodeoxycholic acid (UDCA) is a bile acid of industrial interest as it is used as an agent for the treatment of primary sclerosing cholangitis and the medicamentous, non-surgical dissolution of gallstones. Currently, it is prepared industrially from cholic acid following a seven-step chemical procedure with an overall yield of <30%. In this study, we investigated the key enzymatic steps in the chemo-enzymatic preparation of UDCA-the two-step reduction of dehydrocholic acid (DHCA) to 12-keto-ursodeoxycholic acid using a mutant of 7ß-hydroxysteroid dehydrogenase (7ß-HSDH) from Collinsella aerofaciens and 3α-hydroxysteroid dehydrogenase (3α-HSDH) from Comamonas testosteroni. Three different one-pot reaction approaches were investigated using whole-cell biocatalysts in simple batch processes. We applied one-biocatalyst systems, where 3α-HSDH, 7ß-HSDH, and either a mutant of formate dehydrogenase (FDH) from Mycobacterium vaccae N10 or a glucose dehydrogenase (GDH) from Bacillus subtilis were expressed in a Escherichia coli BL21(DE3) based host strain. We also investigated two-biocatalyst systems, where 3α-HSDH and 7ß-HSDH were expressed separately together with FDH enzymes for cofactor regeneration in two distinct E. coli hosts that were simultaneously applied in the one-pot reaction. The best result was achieved by the one-biocatalyst system with GDH for cofactor regeneration, which was able to completely convert 100 mM DHCA to >99.5 mM 12-keto-UDCA within 4.5 h in a simple batch process on a liter scale.
[Mh] Termos MeSH primário: Reatores Biológicos/microbiologia
Biotecnologia/métodos
Ácido Desidrocólico/metabolismo
Hidroxiesteroide Desidrogenases/metabolismo
Ácido Ursodesoxicólico/metabolismo
[Mh] Termos MeSH secundário: Actinobacteria/enzimologia
Bacillus subtilis/genética
Bacillus subtilis/metabolismo
Proteínas de Bactérias/genética
Proteínas de Bactérias/metabolismo
Biocatálise
Clonagem Molecular
Comamonas/enzimologia
Ácido Desidrocólico/análise
Escherichia coli/genética
Escherichia coli/metabolismo
Hidroxiesteroide Desidrogenases/genética
Mycobacterium/genética
Mycobacterium/metabolismo
Oxirredução
Proteínas Recombinantes/genética
Proteínas Recombinantes/metabolismo
Ácido Ursodesoxicólico/análogos & derivados
Ácido Ursodesoxicólico/análise
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Bacterial Proteins); 0 (Recombinant Proteins); 724L30Y2QR (Ursodeoxycholic Acid); EC 1.1.- (Hydroxysteroid Dehydrogenases); NH5000009I (Dehydrocholic Acid)
[Em] Mês de entrada:1304
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:120719
[St] Status:MEDLINE
[do] DOI:10.1002/bit.24606


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[PMID]:22581067
[Au] Autor:Braun M; Sun B; Anselment B; Weuster-Botz D
[Ad] Endereço:Institute of Biochemical Engineering, Technische Universität München, Boltzmannstr. 15, 85748 Garching, Germany.
[Ti] Título:Novel whole-cell biocatalysts with recombinant hydroxysteroid dehydrogenases for the asymmetric reduction of dehydrocholic acid.
[So] Source:Appl Microbiol Biotechnol;95(6):1457-68, 2012 Sep.
[Is] ISSN:1432-0614
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Ursodeoxycholic acid is an important pharmaceutical so far chemically synthesized from cholic acid. Various biocatalytic alternatives have already been discussed with hydroxysteroid dehydrogenases (HSDH) playing a crucial role. Several whole-cell biocatalysts based on a 7α-HSDH-knockout strain of Escherichia coli overexpressing a recently identified 7ß-HSDH from Collinsella aerofaciens and a NAD(P)-bispecific formate dehydrogenase mutant from Mycobacterium vaccae for internal cofactor regeneration were designed and characterized. A strong pH dependence of the whole-cell bioreduction of dehydrocholic acid to 3,12-diketo-ursodeoxycholic acid was observed with the selected recombinant E. coli strain. In the optimal, slightly acidic pH range dehydrocholic acid is partly undissolved and forms a suspension in the aqueous solution. The batch process was optimized making use of a second-order polynomial to estimate conversion as function of initial pH, initial dehydrocholic acid concentration, and initial formate concentration. Complete conversion of 72 mM dehydrocholic acid was thus made possible at pH 6.4 in a whole-cell batch process within a process time of 1 h without cofactor addition. Finally, a NADH-dependent 3α-HSDH from Comamonas testosteroni was expressed additionally in the E. coli production strain overexpressing the 7ß-HSDH and the NAD(P)-bispecific formate dehydrogenase mutant. It was shown that this novel whole-cell biocatalyst was able to convert 50 mM dehydrocholic acid directly to 12-keto-ursodeoxycholic acid with the formation of only small amounts of intermediate products. This approach may be an efficient process alternative which avoids the costly chemical epimerization at C-7 in the production of ursodeoxycholic acid.
[Mh] Termos MeSH primário: Proteínas de Bactérias/metabolismo
Ácido Desidrocólico/metabolismo
Escherichia coli/metabolismo
Hidroxiesteroide Desidrogenases/metabolismo
Microbiologia Industrial/métodos
[Mh] Termos MeSH secundário: Actinobacteria/enzimologia
Proteínas de Bactérias/genética
Biocatálise
Ácido Desidrocólico/química
Escherichia coli/genética
Formiato Desidrogenases/genética
Formiato Desidrogenases/metabolismo
Expressão Gênica
Hidroxiesteroide Desidrogenases/genética
Cinética
Estrutura Molecular
Mycobacterium/enzimologia
Oxirredução
Ácido Ursodesoxicólico/química
Ácido Ursodesoxicólico/metabolismo
[Pt] Tipo de publicação:EVALUATION STUDIES; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Bacterial Proteins); 724L30Y2QR (Ursodeoxycholic Acid); EC 1.1.- (Hydroxysteroid Dehydrogenases); EC 1.2.1.2 (Formate Dehydrogenases); NH5000009I (Dehydrocholic Acid)
[Em] Mês de entrada:1301
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:120515
[St] Status:MEDLINE
[do] DOI:10.1007/s00253-012-4072-6


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[PMID]:22153852
[Au] Autor:Mohamed AA; Matijevic E
[Ad] Endereço:Center for Advanced Materials Processing, Clarkson University, Potsdam, NY 13699-5814, USA.
[Ti] Título:Preparation and characterization of uniform drug particles: dehydrocholic acid.
[So] Source:J Colloid Interface Sci;368(1):625-8, 2012 Feb 15.
[Is] ISSN:1095-7103
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Two methods for the preparation of uniform dispersions of dehydrocholic acid of different morphologies are described. In the first case, the drug was dissolved in acetone and then re-precipitated by adding a non-solvent (either water or an aqueous stabilizer solution), which yielded rod-like particles. In the second procedure, spheres, consisting of small elongated subunits, were obtained by acidification of basic aqueous solutions of the drug. The resulting particles were characterized in terms of their structure and surface charge characteristics.
[Mh] Termos MeSH primário: Acetona/química
Ácido Desidrocólico/química
Água/química
[Mh] Termos MeSH secundário: Tamanho da Partícula
Solubilidade
Soluções
Propriedades de Superfície
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Solutions); 059QF0KO0R (Water); 1364PS73AF (Acetone); NH5000009I (Dehydrocholic Acid)
[Em] Mês de entrada:1205
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:111214
[St] Status:MEDLINE
[do] DOI:10.1016/j.jcis.2011.11.005


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[PMID]:21954318
[Au] Autor:Fukuoka S; Richter W; Howe J; Andrä J; Rössle M; Alexander C; Gutsmann T; Brandenburg K
[Ad] Endereço:National Institute of Advanced Industrial Science and Technology (AIST), Takamatsu, Japan.
[Ti] Título:Biophysical investigations into the interactions of endotoxins with bile acids.
[So] Source:Innate Immun;18(2):307-17, 2012 Apr.
[Is] ISSN:1753-4267
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The interaction of selected endotoxin preparations (lipid A from Erwinia carotovora and LPS Re and Ra from Salmonella enterica sv. Minnesota strains R595 and R60, respectively) with selected bile acids was investigated biophysically. Endotoxin aggregates were analyzed for their gel-to-liquid crystalline phase behavior, the type of their aggregates, the conformation of particular functional groups, and their Zeta potential in the absence and presence of the bile acids by applying Fourier-transform infrared spectroscopy, differential scanning calorimetry, measurements of the electrophoretic mobility, and synchrotron radiation X-ray scattering. In addition, the ability of the endotoxins to induce cytokines in human mononuclear cells was tested in the absence and presence of varying concentrations of bile acids. The data show that the endotoxin:bile acid interaction is not governed by Coulomb forces, rather a hydrophobic interaction takes place. This leads to an enhanced formation of the inherent cubic aggregate structures of the endotoxins, concomitant with a slight disaggregation, as evidenced by freeze-fracture electron microscopy. Parallel to this, the addition of bile acids increased the bioactivity of lipid A and, to a lower degree, also that of the tested rough mutant LPS at lower concentrations of the endotoxin preparation, a finding similar as reported for the interaction of other agents such as hemoglobin. These data imply that there are general mechanisms that govern the expression of biological activities of endotoxins.
[Mh] Termos MeSH primário: Ácidos e Sais Biliares/química
Endotoxinas/química
[Mh] Termos MeSH secundário: Biofísica
Varredura Diferencial de Calorimetria
Ácido Quenodesoxicólico/química
Citocinas/biossíntese
Ácido Desidrocólico/química
Ácido Desoxicólico/química
Eletroquímica
Técnica de Fratura por Congelamento
Seres Humanos
Técnicas In Vitro
Lipídeo A/farmacologia
Ácido Litocólico/química
Monócitos/metabolismo
Pectobacterium carotovorum/química
Salmonella enterica/química
Colato de Sódio/química
Espectroscopia de Infravermelho com Transformada de Fourier
Difração de Raios X
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Bile Acids and Salts); 0 (Cytokines); 0 (Endotoxins); 0 (Lipid A); 005990WHZZ (Deoxycholic Acid); 0GEI24LG0J (Chenodeoxycholic Acid); 5QU0I8393U (Lithocholic Acid); NH5000009I (Dehydrocholic Acid); NU3Y4CCH8Z (Sodium Cholate)
[Em] Mês de entrada:1207
[Cu] Atualização por classe:141120
[Lr] Data última revisão:
141120
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:110929
[St] Status:MEDLINE
[do] DOI:10.1177/1753425911404093


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[PMID]:22194894
[Au] Autor:Úriz M; Sáez E; Prieto J; Medina JF; Banales JM
[Ad] Endereço:Division of Gene Therapy and Hepatology, CIMA Clinic and School of Medicine, University of Navarra, Centro de Investigación Biomédica en Red en el Área temática de Enfermedades Hepáticas y Digestivas, Pamplona, Spain.
[Ti] Título:Ursodeoxycholic acid is conjugated with taurine to promote secretin-stimulated biliary hydrocholeresis in the normal rat.
[So] Source:PLoS One;6(12):e28717, 2011.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND & AIMS: Secretin induces bicarbonate-rich hydrocholeresis in healthy individuals, but not in untreated patients with primary biliary cirrhosis (PBC). Ursodeoxycholic acid (UDCA)--the first choice treatment for PBC--restores the secretin response. Compared with humans, secretin has poor effect in experimental normal-rat models with biliary drainage, although it may elicit hydrocholeresis when the bile-acid pool is maintained. In view of the benefits of UDCA in PBC, we used normal-rat models to unravel the acute contribution of UDCA (and/or taurine-conjugated TUDCA) for eliciting the biliary secretin response. METHODS: Intravascular and/or intrabiliary administration of agonists and inhibitors was performed in normal rats with biliary monitoring. Secretin/bile-acid interplay was analyzed in 3D cultured rat cholangiocytes that formed expansive cystic structures with intralumenal hydroionic secretion. RESULTS: In vivo, secretin stimulates hydrocholeresis upon UDCA/TUDCA infusion, but does not modify the intrinsic hypercholeretic effect of dehydrocholic acid (DHCA). The former effect is dependent on microtubule polymerization, and involves PKCα, PI3K and MEK pathways, as shown by colchicine (i.p.) and retrograde biliary inhibitors. In vitro, while secretin alone accelerates the spontaneous expansion of 3D-cystic structures, this effect is enhanced in the presence of TUDCA, but not UDCA or DHCA. Experiments with inhibitors and Ca(2+)-chelator confirmed that the synergistic effect of secretin plus TUDCA involves microtubules, intracellular Ca(2+), PKCα, PI3K, PKA and MEK pathways. Gene silencing also demonstrated the involvement of the bicarbonate extruder Ae2. CONCLUSIONS: UDCA is conjugated in order to promote secretin-stimulated hydrocholeresis in rats through Ae2, microtubules, intracellular Ca(2+), PKCα, PI3K, PKA, and MEK.
[Mh] Termos MeSH primário: Cirrose Hepática Biliar/patologia
Secretina/farmacologia
Taurina/farmacologia
Ácido Tauroquenodesoxicólico/farmacologia
Ácido Ursodesoxicólico/farmacologia
[Mh] Termos MeSH secundário: Animais
Proteínas de Transporte de Ânions/metabolismo
Antiporters/metabolismo
Bile/efeitos dos fármacos
Bile/metabolismo
Células Cultivadas
Cisto do Colédoco/metabolismo
Cisto do Colédoco/patologia
Ácido Desidrocólico/farmacologia
Inativação Gênica/efeitos dos fármacos
Seres Humanos
Cirrose Hepática Biliar/enzimologia
Masculino
Microtúbulos/efeitos dos fármacos
Microtúbulos/metabolismo
Quinases de Proteína Quinase Ativadas por Mitógeno/metabolismo
Modelos Biológicos
Fosfatidilinositol 3-Quinases/metabolismo
Polimerização/efeitos dos fármacos
Proteína Quinase C/metabolismo
Ratos
Ratos Wistar
Proteínas SLC4A
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anion Transport Proteins); 0 (Antiporters); 0 (SLC4A Proteins); 1393-25-5 (Secretin); 1EQV5MLY3D (Taurine); 516-35-8 (Taurochenodeoxycholic Acid); 60EUX8MN5X (tauroursodeoxycholic acid); 724L30Y2QR (Ursodeoxycholic Acid); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.11.13 (Protein Kinase C); EC 2.7.12.2 (Mitogen-Activated Protein Kinase Kinases); NH5000009I (Dehydrocholic Acid)
[Em] Mês de entrada:1208
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:111224
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0028717


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[PMID]:21439375
[Au] Autor:Maestrelli F; Cirri M; Mennini N; Zerrouk N; Mura P
[Ad] Endereço:Department of Pharmaceutical Sciences, University of Florence, Sesto Fiorentino, Italy.
[Ti] Título:Improvement of oxaprozin solubility and permeability by the combined use of cyclodextrin, chitosan, and bile components.
[So] Source:Eur J Pharm Biopharm;78(3):385-93, 2011 Aug.
[Is] ISSN:1873-3441
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The effect of the combined use of randomly methylated ß-cyclodextrin (RAMEB), chitosan (CS), and bile components (dehydrocholic (DHCA) or ursodeoxycholic (UDCA) acids and their sodium salts) on solubility and permeability through Caco-2 cells of oxaprozin (a very poorly water-soluble non-steroidal anti-inflammatory drug) has been investigated. Addition of CS, bile acids, and their sodium salts increased the RAMEB solubilizing power of 4, 2, and 5 times, respectively. Drug-RAMEB-CS co-ground systems showed very higher dissolution rate than corresponding drug-RAMEB systems. Addition of bile components further improved drug dissolution rate. The CS presence enabled a significant increase in drug permeability through Caco-2 cells with respect to drug-RAMEB systems. Moreover, CS and NaDHC showed a synergistic enhancer effect, enabling a 1.4-fold permeability increase in comparison with systems without bile salt. However, unexpectedly, no significant differences were found between physical mixtures and co-ground products, indicating that drug permeation improvement was due to the intrinsic enhancer effect of the carriers and not to drug-carrier interactions brought about by co-grinding, as instead found in dissolution rate studies. The combined use of RAMEB, CS, and NaDHC could be exploited to develop effective oral dosage forms of oxaprozin, with increased drug solubility and permeability, and then improved bioavailability.
[Mh] Termos MeSH primário: Anti-Inflamatórios não Esteroides/química
Bile/química
Quitosana/química
Composição de Medicamentos/métodos
Propionatos/química
beta-Ciclodextrinas/química
[Mh] Termos MeSH secundário: Bile/metabolismo
Células CACO-2
Colagogos e Coleréticos/química
Ácido Desidrocólico/química
Portadores de Fármacos
Sistemas de Liberação de Medicamentos
Sinergismo Farmacológico
Excipientes/química
Seres Humanos
L-Lactato Desidrogenase/efeitos dos fármacos
Permeabilidade
Solubilidade
Ácido Ursodesoxicólico/química
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Cholagogues and Choleretics); 0 (Drug Carriers); 0 (Excipients); 0 (Propionates); 0 (beta-Cyclodextrins); 724L30Y2QR (Ursodeoxycholic Acid); 9012-76-4 (Chitosan); EC 1.1.1.27 (L-Lactate Dehydrogenase); MHJ80W9LRB (oxaprozin); NH5000009I (Dehydrocholic Acid)
[Em] Mês de entrada:1201
[Cu] Atualização por classe:151119
[Lr] Data última revisão:
151119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:110329
[St] Status:MEDLINE
[do] DOI:10.1016/j.ejpb.2011.03.012



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