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  1 / 165 MEDLINE  
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[PMID]:28099023
[Au] Autor:Birru WA; Warren DB; Headey SJ; Benameur H; Porter CJ; Pouton CW; Chalmers DK
[Ti] Título:Computational Models of the Gastrointestinal Environment. 1. The Effect of Digestion on the Phase Behavior of Intestinal Fluids.
[So] Source:Mol Pharm;14(3):566-579, 2017 Mar 06.
[Is] ISSN:1543-8392
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Improved models of the gastrointestinal environment have great potential to assist the complex process of drug formulation. Molecular dynamics (MD) is a powerful method for investigating phase behavior at a molecular level. In this study we use multiple MD simulations to calculate phase diagrams for bile before and after digestion. In these computational models, undigested bile is represented by mixtures of palmitoyl-oleoylphosphatidylcholine (POPC), sodium glycodeoxycholate (GDX), and water. Digested bile is modeled using a 1:1 mixture of oleic acid and palmitoylphosphatidylcholine (lysophosphatidylcholine, LPC), GDX, and water. The computational phase diagrams of undigested and digested bile are compared, and we describe the typical intermolecular interactions that occur between phospholipids and bile salts. The diffusion coefficients measured from MD simulation are compared to experimental diffusion data measured by DOSY-NMR, where we observe good qualitative agreement. In an additional set of simulations, the effect of different ionization states of oleic acid on micelle formation is investigated.
[Mh] Termos MeSH primário: Líquidos Corporais/química
Digestão/fisiologia
Trato Gastrointestinal/química
[Mh] Termos MeSH secundário: Bile/química
Ácidos e Sais Biliares/química
Química Farmacêutica/métodos
Simulação por Computador
Ácido Glicodesoxicólico/química
Espectroscopia de Ressonância Magnética/métodos
Micelas
Simulação de Dinâmica Molecular
Ácido Oleico/química
Fosfatidilcolinas/química
Fosfolipídeos/química
Água/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bile Acids and Salts); 0 (Micelles); 0 (Phosphatidylcholines); 0 (Phospholipids); 059QF0KO0R (Water); 2UMI9U37CP (Oleic Acid); 360-65-6 (Glycodeoxycholic Acid); TE895536Y5 (1-palmitoyl-2-oleoylphosphatidylcholine)
[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:170119
[St] Status:MEDLINE
[do] DOI:10.1021/acs.molpharmaceut.6b00888


  2 / 165 MEDLINE  
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[PMID]:26646271
[Au] Autor:Tomkötter L; Erbes J; Trepte C; Hinsch A; Dupree A; Bockhorn M; Mann O; Izbicki JR; Bachmann K
[Ad] Endereço:From the Departments of *General, Visceral and Thoracic Surgery, †Anesthesiology, and ‡Pathology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
[Ti] Título:The Effects of Pancreatic Microcirculatory Disturbances on Histopathologic Tissue Damage and the Outcome in Severe Acute Pancreatitis.
[So] Source:Pancreas;45(2):248-53, 2016 Feb.
[Is] ISSN:1536-4828
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: Severe acute pancreatitis is an inflammatory disease of the pancreas with a high morbidity and mortality. To date, no causal treatment is known. The aim of the present study was to analyze the impact of pancreatic microcirculatory disturbances in severe acute pancreatitis and to correlate the effects with histopathologic tissue damage and outcome. METHODS: Severe acute pancreatitis was induced in 129 pigs by injection of glycodeoxycholic acid into the pancreatic duct. Pancreatic microcirculation, pancreatic tissue oxygenation, histopathologic tissue damage, and survival were measured and analyzed. RESULTS: Our study demonstrates a strong correlation between pancreatic microcirculatory disturbances and histopathologic tissue damage (r = 0.728; P < 0.001). Furthermore, we showed a strong correlation between tissue oxygenation and the severity of the pancreatitis according to an established porcine pancreatitis score (r = 0.694; P < 0.001). In addition, disturbances of the pancreatic microcirculation were shown to be associated with an increased mortality rate in severe acute pancreatitis. CONCLUSIONS: We found that pancreatic microcirculatory disturbances have significant effects on histopathologic tissue damage and the outcome of severe acute pancreatitis. For a better survival of severe acute pancreatitis, the treatment should focus on an improvement of pancreatic microcirculation.
[Mh] Termos MeSH primário: Microcirculação/fisiologia
Pâncreas/irrigação sanguínea
Pâncreas/patologia
Pancreatite/fisiopatologia
[Mh] Termos MeSH secundário: Doença Aguda
Animais
Ácido Glicodesoxicólico/toxicidade
Microcirculação/efeitos dos fármacos
Oxigênio/metabolismo
Pâncreas/efeitos dos fármacos
Pancreatite/induzido quimicamente
Índice de Gravidade de Doença
Análise de Sobrevida
Suínos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
360-65-6 (Glycodeoxycholic Acid); S88TT14065 (Oxygen)
[Em] Mês de entrada:1610
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151210
[St] Status:MEDLINE
[do] DOI:10.1097/MPA.0000000000000440


  3 / 165 MEDLINE  
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[PMID]:26418907
[Au] Autor:Schneider L; Jabrailova B; Salem M; Kilk K; Hofer S; Brenner T; Strobel O; Hackert T; Werner J
[Ad] Endereço:From the Departments for *General, Visceral, and Transplantation Surgery and †Anaesthesiology, University of Heidelberg, Heidelberg; and ‡Department for General, Visceral, Transplantation, Thoracic, and Vascular Surgery, University of Munich, Munich, Germany.
[Ti] Título:Stimulation of Central α2 Receptors Attenuates Experimental Necrotizing Pancreatitis.
[So] Source:Pancreas;45(2):260-4, 2016 Feb.
[Is] ISSN:1536-4828
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: Severe necrotizing pancreatitis (SNP) is a disease with relevant morbidity and mortality until today. No specific therapy is in sight. Central α2 agonists such as clonidine and dexmedetomidine are known to have anti-inflammatory effects though the cholinergic anti-inflammatory pathway and are implemented in the clinical routine as adjunct sedative drugs. Their potential effect on SNP has not yet been tested. METHODS: Severe necrotizing pancreatitis was induced in male Wistar rats. Four treatment groups received either clonidine or dexmedetomidine before (prophylactic) or after induction of SNP (therapeutic). After 12 hours, pancreatic morphologic injury, systemic proinflammatory high-mobility group box 1 protein, and pancreatic and pulmonary myeloperoxidase levels were evaluated. RESULTS: Severe necrotizing pancreatitis was fully established 12 hours after induction. "Prophylactic" and "therapeutic" administration of clonidine and dexmedetomidine reduced pancreatic morphologic injury (P < 0.05 vs SNP), serum proinflammatory high-mobility group box 1 protein (P < 0.0001 vs SNP), as well as pancreatic and pulmonary myeloperoxidase levels (P < 0.01 vs SNP). CONCLUSIONS: Prophylactic and therapeutic applications of the central α2 agonists clonidine and dexmedetomidine are effective to attenuate local and systemic injury in experimental SNP and should be evaluated in the clinical setting.
[Mh] Termos MeSH primário: Agonistas de Receptores Adrenérgicos alfa 2/farmacologia
Pâncreas/efeitos dos fármacos
Pancreatite Necrosante Aguda/prevenção & controle
Receptores Adrenérgicos alfa 2/metabolismo
[Mh] Termos MeSH secundário: Animais
Clonidina/farmacologia
Dexmedetomidina/farmacologia
Ácido Glicodesoxicólico
Proteína HMGB1/sangue
Seres Humanos
Mediadores da Inflamação/sangue
Masculino
Pâncreas/metabolismo
Pâncreas/patologia
Pancreatite Necrosante Aguda/sangue
Pancreatite Necrosante Aguda/induzido quimicamente
Peroxidase/metabolismo
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenergic alpha-2 Receptor Agonists); 0 (HMGB1 Protein); 0 (Hbp1 protein, rat); 0 (Inflammation Mediators); 0 (Receptors, Adrenergic, alpha-2); 360-65-6 (Glycodeoxycholic Acid); 67VB76HONO (Dexmedetomidine); EC 1.11.1.7 (Peroxidase); MN3L5RMN02 (Clonidine)
[Em] Mês de entrada:1610
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150930
[St] Status:MEDLINE
[do] DOI:10.1097/MPA.0000000000000474


  4 / 165 MEDLINE  
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[PMID]:26958021
[Au] Autor:Wang CS; Liu SH; Peng J; Tang C; Zhu WG
[Ad] Endereço:Department of Radiotherapy, Lianshui People's Hospital, Huai'an, Jiangsu, 223400, China.
[Ti] Título:Bile acids cycle disruption in patients with nasopharyngeal carcinoma promotes the elevation of interleukin-10 secretion.
[So] Source:Afr Health Sci;15(4):1200-3, 2015 Dec.
[Is] ISSN:1729-0503
[Cp] País de publicação:Uganda
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Unclear pathogenesis existed for nasopharyngeal carcinoma. AIMS: to analyze the role of bile acids in the pathogenesis of nasopharyngeal carcinoma. METHODS: 20 healthy volunteers and 20 patients with nasopharyngeal carcinoma were enrolled between January 1(st), 2013 and December 31(st), 2014. ESI-QTOF-MS analysis of serum was performed to find altered bile acids components. The biological function of changed bile acids was investigated using in vitro experiment. RESULTS: Compared with healthy volunteers, the level of DCA and GDCA exhibited higher abundance in patients with nasopharyngeal carcinoma (p<0.01). Furthermore, the biological function was investigated for the inhibition of DCA and GDCA towards the secretion of IL-10 by CD4+CD25- T cells. Both DCA and GDCA significantly inhibited the secretion of IL-10 by CD4+CD25- T cells. Furthermore, DCA+GDCA can show stronger inhibition towards the secretion of IL-10 than DCA and GDCA. CONCLUSION: The inhibition of IL-10 secretion by elevated DCA and GDCA components in nasopharyngeal carcinoma patients is the inducer for nasopharyngeal carcinoma.
[Mh] Termos MeSH primário: Ácidos e Sais Biliares/sangue
Interleucina-10/sangue
Interleucina-10/secreção
Neoplasias Nasofaríngeas/patologia
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Linfócitos T CD4-Positivos/metabolismo
Carcinoma
Estudos de Casos e Controles
Ácido Desoxicólico/sangue
Feminino
Ácido Glicodesoxicólico/sangue
Seres Humanos
Interleucina-10/imunologia
Interleucina-10/metabolismo
Masculino
Meia-Idade
Neoplasias Nasofaríngeas/sangue
Neoplasias Nasofaríngeas/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bile Acids and Salts); 0 (IL10 protein, human); 005990WHZZ (Deoxycholic Acid); 130068-27-8 (Interleukin-10); 360-65-6 (Glycodeoxycholic Acid)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160310
[St] Status:MEDLINE
[do] DOI:10.4314/ahs.v15i4.19


  5 / 165 MEDLINE  
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[PMID]:26616587
[Au] Autor:Bayati S; Galantini L; Knudsen KD; Schillén K
[Ad] Endereço:Division of Physical Chemistry, Department of Chemistry, Lund University , P.O. Box 124, SE-221 00 Lund, Sweden.
[Ti] Título:Effects of Bile Salt Sodium Glycodeoxycholate on the Self-Assembly of PEO-PPO-PEO Triblock Copolymer P123 in Aqueous Solution.
[So] Source:Langmuir;31(50):13519-27, 2015 Dec 22.
[Is] ISSN:1520-5827
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A comprehensive experimental study on the interaction between the PEO-PPO-PEO block copolymer P123 (EO20PO68EO20) and the anionic bile salt sodium glycodeoxycholate (NaGDC) in water has been performed. The work was aimed at investigating the suitability of using P123 as bile salt sequestrant beside the fundamental aspects of PEO-PPO-PEO block copolymer-bile salt interactions. Various experimental techniques including dynamic and static light scattering, small-angle X-ray scattering, and differential scanning calorimetry (DSC) were employed in combination with electrophoretic mobility measurements. The system was investigated at a constant P123 concentration of 1.74 mM and with varying bile salt concentrations up to approximately 250 mM NaGDC (or a molar ratio n(NaGDC)/n(P123) = 144). In the mixed P123-NaGDC solutions, the endothermic process related to the self-assembly of P123 was observed to gradually decrease in enthalpy and shift to higher temperatures upon progressive addition of NaGDC. To explain this effect, the formation of NaGDC micelles carrying partly dehydrated P123 unimers was proposed and translated into a stoichiometric model, which was able to fit the experimental DSC data. In the mixtures at low molar ratios, NaGDC monomers associated with the P123 micelle forming a charged "P123 micelle-NaGDC" complex with a dehydrated PPO core. These complexes disintegrated upon increasing NaGDC concentration to form small "NaGDC-P123" complexes visualized as bile salt micelles including one or a few P123 copolymer chains.
[Mh] Termos MeSH primário: Ácidos e Sais Biliares/química
Ácido Glicodesoxicólico/química
Poloxaleno/química
Poloxaleno/síntese química
Água/química
[Mh] Termos MeSH secundário: Estrutura Molecular
Soluções
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Bile Acids and Salts); 0 (Solutions); 0 (pluronic block copolymer P123); 059QF0KO0R (Water); 360-65-6 (Glycodeoxycholic Acid); 9003-11-6 (Poloxalene)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:151222
[Lr] Data última revisão:
151222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151201
[St] Status:MEDLINE
[do] DOI:10.1021/acs.langmuir.5b03828


  6 / 165 MEDLINE  
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[PMID]:26208104
[Au] Autor:James L; Yan K; Pence L; Simpson P; Bhattacharyya S; Gill P; Letzig L; Kearns G; Beger R
[Ad] Endereço:Department of Pediatrics, University of Arkansas for Medical Sciences, Little Rock, AR 72202, United States of America; Arkansas Children's Hospital Research Institute, Little Rock, AR 72202, United States of America.
[Ti] Título:Comparison of Bile Acids and Acetaminophen Protein Adducts in Children and Adolescents with Acetaminophen Toxicity.
[So] Source:PLoS One;10(7):e0131010, 2015.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Metabolomics approaches have enabled the study of new mechanisms of liver injury in experimental models of drug toxicity. Disruption of bile acid homeostasis is a known mechanism of drug induced liver injury. The relationship of individual bile acids to indicators of oxidative drug metabolism (acetaminophen protein adducts) and liver injury was examined in children with acetaminophen overdose, hospitalized children with low dose exposure to acetaminophen, and children with no recent exposure to acetaminophen. Nine bile acids were quantified through targeted metabolomic analysis in the serum samples of the three groups. Bile acids were compared to serum levels of acetaminophen protein adducts and alanine aminotransferase. Glycodeoxycholic acid, taurodeoxycholic acid, and glycochenodeoxycholic acid were significantly increased in children with acetaminophen overdose compared to healthy controls. Among patients with acetaminophen overdose, bile acids were higher in subjects with acetaminophen protein adduct values > 1.0 nmol/mL and modest correlations were noted for three bile acids and acetaminophen protein adducts as follows: taurodeoxycholic acid (R=0.604; p<0.001), glycodeoxycholic acid (R=0.581; p<0.001), and glycochenodeoxycholic acid (R=0.571; p<0.001). Variability in bile acids was greater among hospitalized children receiving low doses of acetaminophen than in healthy children with no recent acetaminophen exposure. Compared to bile acids, acetaminophen protein adducts more accurately discriminated among children with acetaminophen overdose, children with low dose exposure to acetaminophen, and healthy control subjects. In children with acetaminophen overdose, elevations of conjugated bile acids were associated with specific indicators of acetaminophen metabolism and non-specific indicators of liver injury.
[Mh] Termos MeSH primário: Acetaminofen/envenenamento
Ácidos e Sais Biliares/sangue
Doença Hepática Induzida por Substâncias e Drogas/sangue
Overdose de Drogas/sangue
[Mh] Termos MeSH secundário: Acetaminofen/metabolismo
Adolescente
Alanina Transaminase/metabolismo
Biomarcadores/sangue
Doença Hepática Induzida por Substâncias e Drogas/diagnóstico
Criança
Pré-Escolar
Diagnóstico Diferencial
Overdose de Drogas/diagnóstico
Feminino
Ácido Glicoquenodesoxicólico/sangue
Ácido Glicodesoxicólico/sangue
Homeostase
Seres Humanos
Masculino
Metabolômica/métodos
Ligação Proteica
Sensibilidade e Especificidade
Ácido Taurodesoxicólico/sangue
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Bile Acids and Salts); 0 (Biomarkers); 360-65-6 (Glycodeoxycholic Acid); 362O9ITL9D (Acetaminophen); 516-50-7 (Taurodeoxycholic Acid); 640-79-9 (Glycochenodeoxycholic Acid); EC 2.6.1.2 (Alanine Transaminase)
[Em] Mês de entrada:1605
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150725
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0131010


  7 / 165 MEDLINE  
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[PMID]:26048149
[Au] Autor:Comhair SA; McDunn J; Bennett C; Fettig J; Erzurum SC; Kalhan SC
[Ad] Endereço:Department of Pathobiology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44195; Cleveland Clinic, Lerner College of Medicine, Case Western Reserve University, Cleveland, OH 44195;
[Ti] Título:Metabolomic Endotype of Asthma.
[So] Source:J Immunol;195(2):643-50, 2015 Jul 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Metabolomics, the quantification of small biochemicals in plasma and tissues, can provide insight into complex biochemical processes and enable the identification of biomarkers that may serve as therapeutic targets. We hypothesized that the plasma metabolome of asthma would reveal metabolic consequences of the specific immune and inflammatory responses unique to endotypes of asthma. The plasma metabolomic profiles of 20 asthmatic subjects and 10 healthy controls were examined using an untargeted global and focused metabolomic analysis. Individuals were classified based on clinical definitions of asthma severity or by levels of fraction of exhaled NO (FENO), a biomarker of airway inflammation. Of the 293 biochemicals identified in the plasma, 25 were significantly different among asthma and healthy controls (p < 0.05). Plasma levels of taurine, lathosterol, bile acids (taurocholate and glycodeoxycholate), nicotinamide, and adenosine-5-phosphate were significantly higher in asthmatics compared with healthy controls. Severe asthmatics had biochemical changes related to steroid and amino acid/protein metabolism. Asthmatics with high FENO, compared with those with low FENO, had higher levels of plasma branched-chain amino acids and bile acids. Asthmatics have a unique plasma metabolome that distinguishes them from healthy controls and points to activation of inflammatory and immune pathways. The severe asthmatic and high FENO asthmatic have unique endotypes that suggest changes in NO-associated taurine transport and bile acid metabolism.
[Mh] Termos MeSH primário: Asma/sangue
Asma/diagnóstico
Metaboloma
Óxido Nítrico/metabolismo
[Mh] Termos MeSH secundário: Monofosfato de Adenosina/sangue
Corticosteroides/uso terapêutico
Adulto
Anti-Inflamatórios/uso terapêutico
Asma/tratamento farmacológico
Asma/patologia
Ácidos e Sais Biliares/sangue
Biomarcadores/sangue
Estudos de Casos e Controles
Colesterol/sangue
Expiração
Feminino
Ácido Glicodesoxicólico/sangue
Seres Humanos
Pulmão/efeitos dos fármacos
Pulmão/metabolismo
Pulmão/patologia
Masculino
Metabolômica
Niacinamida/sangue
Testes de Função Respiratória
Índice de Gravidade de Doença
Taurina/sangue
Ácido Taurocólico/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Adrenal Cortex Hormones); 0 (Anti-Inflammatory Agents); 0 (Bile Acids and Salts); 0 (Biomarkers); 1EQV5MLY3D (Taurine); 25X51I8RD4 (Niacinamide); 31C4KY9ESH (Nitric Oxide); 360-65-6 (Glycodeoxycholic Acid); 415SHH325A (Adenosine Monophosphate); 5E090O0G3Z (Taurocholic Acid); 80-99-9 (lathosterol); 97C5T2UQ7J (Cholesterol)
[Em] Mês de entrada:1509
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:150607
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1500736


  8 / 165 MEDLINE  
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[PMID]:25145902
[Au] Autor:Alhan E; Usta A; Türkyilmaz S; Kural BV; Erçin C
[Ad] Endereço:Department of Surgery, Karadeniz Technical University, Trabzon, Turkey. Electronic address: alhanea@gmail.com.
[Ti] Título:Effects of glutamine alone on the acute necrotizing pancreatitis in rats.
[So] Source:J Surg Res;193(1):161-7, 2015 Jan.
[Is] ISSN:1095-8673
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The effects of the glutamine on the acute pancreatitis are controversial in the clinical and experimental studies. The aim of this study was to investigate the influence of glutamine alone on acute necrotizing pancreatitis (ANP) induced by glycodeoxycholic acid in rats. MATERIAL AND METHODS: Fifty-two male Sprague-Dawley rats weighing 300-350 g were used. Rats were divided into four groups as sham + saline, sham + glutamine, ANP + saline and ANP + glutamine. ANP in rats was induced by glycodeoxycholic acid. The extent of acinar cell injury, mortality, systemic cardiorespiratory variables, functional capillary density, renal/hepatic functions, and changes in some enzyme markers for pancreatic and lung tissue were investigated during ANP in rats. RESULTS: The induction of ANP resulted in a significant increase in the mortality rate, pancreatic necrosis, and serum activity of amylase, alanine aminotransferase, interleukin-6, lactate dehydrogenase in bronchoalveolar lavage fluid, serum concentration of urea, and tissue activity of myeloperoxidase and malondialdehyde in the pancreas and lung, and a significant decrease in concentrations of calcium, blood pressure, urine output, pO2, and functional capillary density. The use of glutamine alone improved these changes. CONCLUSIONS: Glutamine demonstrated beneficial effect on the course of ANP in rats. Therefore, it may be used by itself in the treatment of acute pancreatitis.
[Mh] Termos MeSH primário: Glutamina/farmacologia
Ácido Glicodesoxicólico/toxicidade
Microcirculação/efeitos dos fármacos
Pancreatite Necrosante Aguda/induzido quimicamente
Pancreatite Necrosante Aguda/tratamento farmacológico
[Mh] Termos MeSH secundário: Alanina Transaminase/sangue
Amilases/sangue
Animais
Detergentes/toxicidade
Modelos Animais de Doenças
Interleucina-6/sangue
L-Lactato Desidrogenase/sangue
Masculino
Pâncreas/irrigação sanguínea
Pâncreas/efeitos dos fármacos
Pancreatite Necrosante Aguda/mortalidade
Ratos Sprague-Dawley
Cloreto de Sódio/farmacologia
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Detergents); 0 (Interleukin-6); 0RH81L854J (Glutamine); 360-65-6 (Glycodeoxycholic Acid); 451W47IQ8X (Sodium Chloride); EC 1.1.1.27 (L-Lactate Dehydrogenase); EC 2.6.1.2 (Alanine Transaminase); EC 3.2.1.- (Amylases)
[Em] Mês de entrada:1503
[Cu] Atualização por classe:151119
[Lr] Data última revisão:
151119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140823
[St] Status:MEDLINE


  9 / 165 MEDLINE  
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[PMID]:25239633
[Au] Autor:Woolbright BL; McGill MR; Staggs VS; Winefield RD; Gholami P; Olyaee M; Sharpe MR; Curry SC; Lee WM; Jaeschke H; Acute Liver Failure Study Group
[Ad] Endereço:*Department of Pharmacology, Toxicology and Therapeutics, Department of Biostatistics, Department of Internal Medicine, University of Kansas Medical Center, Kansas City, Kansas 66160, Department of Medical Toxicology, Banner Good Samaritan Medical Center, Phoenix, Arizona 85006, Department of Medici
[Ti] Título:Glycodeoxycholic acid levels as prognostic biomarker in acetaminophen-induced acute liver failure patients.
[So] Source:Toxicol Sci;142(2):436-44, 2014 Dec.
[Is] ISSN:1096-0929
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Acetaminophen (APAP)-induced acute liver failure (ALF) remains a major clinical problem. Although a majority of patients recovers after severe liver injury, a subpopulation of patients proceeds to ALF. Bile acids are generated in the liver and accumulate in blood during liver injury, and as such, have been proposed as biomarkers for liver injury and dysfunction. The goal of this study was to determine whether individual bile acid levels could determine outcome in patients with APAP-induced ALF (AALF). Serum bile acid levels were measured in AALF patients using mass spectrometry. Bile acid levels were elevated 5-80-fold above control values in injured patients on day 1 after the overdose and decreased over the course of hospital stay. Interestingly, glycodeoxycholic acid (GDCA) was significantly increased in non-surviving AALF patients compared with survivors. GDCA values obtained at peak alanine aminotransferase (ALT) and from day 1 of admission indicated GDCA could predict survival in these patients by receiver-operating characteristic analysis (AUC = 0.70 for day 1, AUC = 0.68 for peak ALT). Of note, AALF patients also had significantly higher levels of serum bile acids than patients with active cholestatic liver injury. These data suggest measurements of GDCA in this patient cohort modestly predicted outcome and may serve as a prognostic biomarker. Furthermore, accumulation of bile acids in serum or plasma may be a result of liver cell dysfunction and not cholestasis, suggesting elevation of circulating bile acid levels may be a consequence and not a cause of liver injury.
[Mh] Termos MeSH primário: Acetaminofen/toxicidade
Doença Hepática Induzida por Substâncias e Drogas/sangue
Colestase/sangue
Overdose de Drogas
Ácido Glicodesoxicólico/sangue
[Mh] Termos MeSH secundário: Adulto
Biomarcadores/sangue
Estudos de Casos e Controles
Doença Hepática Induzida por Substâncias e Drogas/etiologia
Feminino
Seres Humanos
Testes de Função Hepática
Masculino
Meia-Idade
Valor Preditivo dos Testes
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Biomarkers); 360-65-6 (Glycodeoxycholic Acid); 362O9ITL9D (Acetaminophen)
[Em] Mês de entrada:1508
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140921
[St] Status:MEDLINE
[do] DOI:10.1093/toxsci/kfu195


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[PMID]:24994853
[Au] Autor:Shang Q; Guo GL; Honda A; Shi D; Saumoy M; Salen G; Xu G
[Ad] Endereço:Department of Medicine, Rutgers, New Jersey Medical School, Newark, New Jersey; Medical Research Service, Veterans Affairs Medical Center, East Orange, New Jersey;
[Ti] Título:Bile acid flux through portal but not peripheral veins inhibits CYP7A1 expression without involvement of ileal FGF19 in rabbits.
[So] Source:Am J Physiol Gastrointest Liver Physiol;307(4):G479-86, 2014 Aug 15.
[Is] ISSN:1522-1547
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:It was proposed that CYP7A1 expression is suppressed through the gut-hepatic signaling pathway fibroblast growth factor (FGF) 15/19-fibroblast growth factor receptor 4, which is initiated by activation of farnesoid X receptor in the intestine rather than in the liver. The present study tested whether portal bile acid flux alone without ileal FGF19 could downregulate CYP7A1 expression in rabbits. A rabbit model was developed by infusing glycodeoxycholic acid (GDCA) through the splenic vein to bypass ileal FGF19. Study was conducted in four groups of rabbits: control; bile fistula + bovine serum albumin solution perfusion (BF); BF + GDCA (by portal perfusion); and BF + GDCA-f (by femoral perfusion). Compared with only BF, BF + GDCA (6 h portal perfusion) suppressed CYP7A1 mRNA, whereas BF + GDCA-f (via femoral vein) with the same perfusion rate of GDCA did not show inhibitory effects. Meanwhile, there was a decrease in ileal FGF19 expression and portal FGF19 protein levels, but an equivalent increase in biliary bile acid outputs in both GDCA perfusion groups. This study demonstrated that portal bile acid flux alone downregulated CYP7A1 expression with diminished FGF19 expression and protein levels, whereas the same bile acid flux reaching the liver through the hepatic artery via femoral vein had no inhibitory effect on CYP7A1. We propose that bile acid flux through the portal venous system may be a kind of "intestinal factor" that suppresses CYP7A1 expression.
[Mh] Termos MeSH primário: Colesterol 7-alfa-Hidroxilase/biossíntese
Ácido Glicodesoxicólico/farmacologia
Íleo/metabolismo
[Mh] Termos MeSH secundário: Animais
Fístula Biliar
Regulação para Baixo
Fatores de Crescimento de Fibroblastos/metabolismo
Veia Porta
Coelhos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
360-65-6 (Glycodeoxycholic Acid); 62031-54-3 (Fibroblast Growth Factors); EC 1.14.14.23 (Cholesterol 7-alpha-Hydroxylase)
[Em] Mês de entrada:1410
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140705
[St] Status:MEDLINE
[do] DOI:10.1152/ajpgi.00062.2014



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