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  1 / 3706 MEDLINE  
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[PMID]:29419378
[Au] Autor:Chappell LC; Chambers J; Thornton JG; Williamson C
[Ad] Endereço:Women's Health Academic Centre, King's College London, London, UK lucy.chappell@kcl.ac.uk.
[Ti] Título:Does ursodeoxycholic acid improve perinatal outcomes in women with intrahepatic cholestasis of pregnancy?
[So] Source:BMJ;360:k104, 2018 02 01.
[Is] ISSN:1756-1833
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Colagogos e Coleréticos/efeitos adversos
Colestase Intra-Hepática/tratamento farmacológico
Feto/efeitos dos fármacos
Complicações na Gravidez/tratamento farmacológico
Ácido Ursodesoxicólico/efeitos adversos
[Mh] Termos MeSH secundário: Colagogos e Coleréticos/administração & dosagem
Colagogos e Coleréticos/uso terapêutico
Colestase Intra-Hepática/epidemiologia
Feminino
Seres Humanos
Gravidez
Complicações na Gravidez/epidemiologia
Resultado da Gravidez/epidemiologia
Ácido Ursodesoxicólico/administração & dosagem
Ácido Ursodesoxicólico/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cholagogues and Choleretics); 724L30Y2QR (Ursodeoxycholic Acid)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180209
[St] Status:MEDLINE
[do] DOI:10.1136/bmj.k104


  2 / 3706 MEDLINE  
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[PMID]:29465536
[Au] Autor:Yan X; Jin J
[Ad] Endereço:Department of Hepatology, The First Hospital of Jilin University, Changchun, Jilin, China.
[Ti] Título:Primary cutaneous amyloidosis associated with autoimmune hepatitis-primary biliary cirrhosis overlap syndrome and Sjögren syndrome: A case report.
[So] Source:Medicine (Baltimore);97(8):e0004, 2018 Feb.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Primary cutaneous amyloidosis (PCA) is a localized skin disorder characterized by the abnormal deposition of amyloid in the extracellular matrix of the dermis. The association between PCA and other diseases, although rare, has been documented for various autoimmune diseases. PCA associated with autoimmune hepatitis-primary biliary cirrhosis (AIH-PBC) overlap syndrome and Sjögren syndrome (SS) has not been previously reported in the literature. PATIENT CONCERNS: A 50-year-old woman presented with progressive abnormal liver enzyme levels and was referred to our department. DIAGNOSES: Due to the patient's symptoms, laboratory test results, radiographic findings, and pathologic results, she was diagnosed with PCA associated with AIH-PBC overlap syndrome and SS. INTERVENTIONS: She was subsequently treated with a combination of ursodeoxycholic acid (UDCA), prednisone, and azathioprine. OUTCOMES: While this treatment can achieve therapeutic success, it cannot prevent complications from cirrhosis. This patient remains alive but experienced an emergent gastrointestinal hemorrhage. LESSONS: While we acknowledge that this is a single case, these findings extend our knowledge of immunological diseases associated with PCA and suggest a common, immune-mediated pathogenic pathway between PCA, AIH-PBC overlap syndrome, and SS. After 12 years of follow up, clinical manifestations have developed, and these autoimmune diseases have progressed. The combination of UDCA, prednisone, and azathioprine can achieve therapeutic success but cannot prevent disease progression. Routine follow up for this patient is necessary to document disease progression.
[Mh] Termos MeSH primário: Amiloidose Familiar/imunologia
Hepatite Autoimune/complicações
Cirrose Hepática Biliar/complicações
Síndrome de Sjogren/complicações
Dermatopatias Genéticas/imunologia
Doenças do Tecido Conjuntivo Indiferenciado/complicações
[Mh] Termos MeSH secundário: Amiloidose Familiar/tratamento farmacológico
Anti-Inflamatórios/administração & dosagem
Azatioprina/administração & dosagem
Colagogos e Coleréticos/administração & dosagem
Quimioterapia Combinada
Feminino
Hepatite Autoimune/tratamento farmacológico
Hepatite Autoimune/imunologia
Seres Humanos
Imunossupressores/administração & dosagem
Cirrose Hepática Biliar/tratamento farmacológico
Cirrose Hepática Biliar/imunologia
Meia-Idade
Prednisona/administração & dosagem
Síndrome de Sjogren/tratamento farmacológico
Síndrome de Sjogren/imunologia
Dermatopatias Genéticas/tratamento farmacológico
Resultado do Tratamento
Doenças do Tecido Conjuntivo Indiferenciado/tratamento farmacológico
Doenças do Tecido Conjuntivo Indiferenciado/imunologia
Ácido Ursodesoxicólico/administração & dosagem
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Cholagogues and Choleretics); 0 (Immunosuppressive Agents); 724L30Y2QR (Ursodeoxycholic Acid); MRK240IY2L (Azathioprine); VB0R961HZT (Prednisone)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180222
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000010004


  3 / 3706 MEDLINE  
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[PMID]:28471355
[Au] Autor:Wang R; Wu J; Jin DK; Chen Y; Lv Z; Chen Q; Miao Q; Huo X; Wang F
[Ad] Endereço:Wuxi Biortus Biosciences Co. Ltd, A5, 6 Dongsheng West Road, 214437 Jiangyin, Jiangsu, People's Republic of China.
[Ti] Título:Structure of NADP -bound 7ß-hydroxysteroid dehydrogenase reveals two cofactor-binding modes.
[So] Source:Acta Crystallogr F Struct Biol Commun;73(Pt 5):246-252, 2017 May 01.
[Is] ISSN:2053-230X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In mammals, bile acids/salts and their glycine and taurine conjugates are effectively recycled through enterohepatic circulation. 7ß-Hydroxysteroid dehydrogenases (7ß-HSDHs; EC 1.1.1.201), including that from the intestinal microbe Collinsella aerofaciens, catalyse the NADPH-dependent reversible oxidation of secondary bile-acid products to avoid potential toxicity. Here, the first structure of NADP bound to dimeric 7ß-HSDH is presented. In one active site, NADP adopts a conventional binding mode similar to that displayed in related enzyme structures. However, in the other active site a unique binding mode is observed in which the orientation of the nicotinamide is different. Since 7ß-HSDH has become an attractive target owing to the wide and important pharmaceutical use of its product ursodeoxycholic acid, this work provides a more detailed template to support rational protein engineering to improve the enzymatic activities of this useful biocatalyst, further improving the yield of ursodeoxycholic acid and its other applications.
[Mh] Termos MeSH primário: Actinobacteria/química
Proteínas de Bactérias/química
Hidroxiesteroide Desidrogenases/química
NADP/química
Ácido Ursodesoxicólico/química
[Mh] Termos MeSH secundário: Actinobacteria/enzimologia
Sequência de Aminoácidos
Proteínas de Bactérias/genética
Proteínas de Bactérias/metabolismo
Domínio Catalítico
Clonagem Molecular
Cristalografia por Raios X
Escherichia coli/genética
Escherichia coli/metabolismo
Expressão Gênica
Vetores Genéticos/química
Vetores Genéticos/metabolismo
Hidroxiesteroide Desidrogenases/genética
Hidroxiesteroide Desidrogenases/metabolismo
Modelos Moleculares
NADP/metabolismo
Ligação Proteica
Conformação Proteica em alfa-Hélice
Conformação Proteica em Folha beta
Domínios e Motivos de Interação entre Proteínas
Multimerização Proteica
Proteínas Recombinantes/química
Proteínas Recombinantes/genética
Proteínas Recombinantes/metabolismo
Ácido Ursodesoxicólico/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bacterial Proteins); 0 (Recombinant Proteins); 53-59-8 (NADP); 724L30Y2QR (Ursodeoxycholic Acid); EC 1.1.- (Hydroxysteroid Dehydrogenases); EC 1.1.1.- (7 beta-hydroxysteroid dehydrogenase)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171204
[Lr] Data última revisão:
171204
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1107/S2053230X17004460


  4 / 3706 MEDLINE  
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[PMID]:28938442
[Au] Autor:Chan SMH; Lau YS; Miller AA; Ku JM; Potocnik S; Ye JM; Woodman OL; Herbert TP
[Ad] Endereço:School of Health and Biomedical Sciences, Royal Melbourne Institute of Technology University, Bundoora, Victoria 3083, Australia.
[Ti] Título:Angiotensin II Causes ß-Cell Dysfunction Through an ER Stress-Induced Proinflammatory Response.
[So] Source:Endocrinology;158(10):3162-3173, 2017 Oct 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The metabolic syndrome is associated with an increase in the activation of the renin angiotensin system, whose inhibition reduces the incidence of new-onset diabetes. Importantly, angiotensin II (AngII), independently of its vasoconstrictor action, causes ß-cell inflammation and dysfunction, which may be an early step in the development of type 2 diabetes. The aim of this study was to determine how AngII causes ß-cell dysfunction. Islets of Langerhans were isolated from C57BL/6J mice that had been infused with AngII in the presence or absence of taurine-conjugated ursodeoxycholic acid (TUDCA) and effects on endoplasmic reticulum (ER) stress, inflammation, and ß-cell function determined. The mechanism of action of AngII was further investigated using isolated murine islets and clonal ß cells. We show that AngII triggers ER stress, an increase in the messenger RNA expression of proinflammatory cytokines, and promotes ß-cell dysfunction in murine islets of Langerhans both in vivo and ex vivo. These effects were significantly attenuated by TUDCA, an inhibitor of ER stress. We also show that AngII-induced ER stress is required for the increased expression of proinflammatory cytokines and is caused by reactive oxygen species and IP3 receptor activation. These data reveal that the induction of ER stress is critical for AngII-induced ß-cell dysfunction and indicates how therapies that promote ER homeostasis may be beneficial in the prevention of type 2 diabetes.
[Mh] Termos MeSH primário: Angiotensina II/farmacologia
Estresse do Retículo Endoplasmático/fisiologia
Inflamação/fisiopatologia
Células Secretoras de Insulina/efeitos dos fármacos
Células Secretoras de Insulina/fisiologia
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Citocinas/genética
Diabetes Mellitus Tipo 2/etiologia
Diabetes Mellitus Tipo 2/prevenção & controle
Estresse do Retículo Endoplasmático/efeitos dos fármacos
Endorribonucleases/antagonistas & inibidores
Endorribonucleases/genética
Endorribonucleases/fisiologia
Expressão Gênica/efeitos dos fármacos
Técnicas de Silenciamento de Genes
Glucose/farmacologia
Receptores de Inositol 1,4,5-Trifosfato/fisiologia
Insulinoma
Ilhotas Pancreáticas/efeitos dos fármacos
Ilhotas Pancreáticas/fisiopatologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Neoplasias Pancreáticas
Proteínas Serina-Treonina Quinases/antagonistas & inibidores
Proteínas Serina-Treonina Quinases/genética
Proteínas Serina-Treonina Quinases/fisiologia
RNA Interferente Pequeno
Espécies Reativas de Oxigênio/metabolismo
Sistema Renina-Angiotensina/fisiologia
Taurina/farmacologia
Ácido Ursodesoxicólico/farmacologia
eIF-2 Quinase/antagonistas & inibidores
eIF-2 Quinase/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Inositol 1,4,5-Trisphosphate Receptors); 0 (RNA, Small Interfering); 0 (Reactive Oxygen Species); 0 (taurine-ursodeoxycholate conjugate); 11128-99-7 (Angiotensin II); 1EQV5MLY3D (Taurine); 724L30Y2QR (Ursodeoxycholic Acid); EC 2.7.11.1 (Ern1 protein, mouse); EC 2.7.11.1 (PERK kinase); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.1 (eIF-2 Kinase); EC 3.1.- (Endoribonucleases); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170923
[St] Status:MEDLINE
[do] DOI:10.1210/en.2016-1879


  5 / 3706 MEDLINE  
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[PMID]:28934223
[Au] Autor:Adeyemi O; Alvarez-Laviada A; Schultz F; Ibrahim E; Trauner M; Williamson C; Glukhov AV; Gorelik J
[Ad] Endereço:Department of Cardiovascular Sciences, National Heart and Lung Institute, Imperial College London, London, United Kingdom.
[Ti] Título:Ursodeoxycholic acid prevents ventricular conduction slowing and arrhythmia by restoring T-type calcium current in fetuses during cholestasis.
[So] Source:PLoS One;12(9):e0183167, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Increased maternal serum bile acid concentrations in intrahepatic cholestasis of pregnancy (ICP) are associated with fetal cardiac arrhythmias. Ursodeoxycholic acid (UDCA) has been shown to demonstrate anti-arrhythmic properties via preventing ICP-associated cardiac conduction slowing and development of reentrant arrhythmias, although the cellular mechanism is still being elucidated. METHODS: High-resolution fluorescent optical mapping of electrical activity and electrocardiogram measurements were used to characterize effects of UDCA on one-day-old neonatal and adult female Langendorff-perfused rat hearts. ICP was modelled by perfusion of taurocholic acid (TC, 400µM). Whole-cell calcium currents were recorded from neonatal rat and human fetal cardiomyocytes. RESULTS: TC significantly prolonged the PR interval by 11.0±3.5% (P<0.05) and slowed ventricular conduction velocity (CV) by 38.9±5.1% (P<0.05) exclusively in neonatal and not in maternal hearts. A similar CV decline was observed with the selective T-type calcium current (ICa,T) blocker mibefradil 1µM (23.0±6.2%, P<0.05), but not with the L-type calcium current (ICa,L) blocker nifedipine 1µM (6.9±6.6%, NS). The sodium channel blocker lidocaine (30µM) reduced CV by 60.4±4.5% (P<0.05). UDCA co-treatment was protective against CV slowing induced by TC and mibefradil, but not against lidocaine. UDCA prevented the TC-induced reduction in the ICa,T density in both isolated human fetal (-10.2±1.5 versus -5.5±0.9 pA/pF, P<0.05) and neonatal rat ventricular myocytes (-22.3±1.1 versus -9.6±0.8 pA/pF, P<0.0001), whereas UDCA had limited efficacy on the ICa,L. CONCLUSION: Our findings demonstrate that ICa,T plays a significant role in ICP-associated fetal cardiac conduction slowing and arrhythmogenesis, and is an important component of the fetus-specific anti-arrhythmic activity of UDCA.
[Mh] Termos MeSH primário: Canais de Cálcio Tipo T/metabolismo
Colestase/prevenção & controle
Fenômenos Eletrofisiológicos/efeitos dos fármacos
Coração Fetal/efeitos dos fármacos
Ventrículos do Coração/efeitos dos fármacos
Ventrículos do Coração/fisiopatologia
Ácido Ursodesoxicólico/farmacologia
[Mh] Termos MeSH secundário: Animais
Cálcio/farmacologia
Colestase/metabolismo
Colestase/fisiopatologia
Feminino
Coração Fetal/metabolismo
Coração Fetal/fisiopatologia
Seres Humanos
Miócitos Cardíacos/efeitos dos fármacos
Miócitos Cardíacos/metabolismo
Gravidez
Ratos
Ácido Taurocólico/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Calcium Channels, T-Type); 5E090O0G3Z (Taurocholic Acid); 724L30Y2QR (Ursodeoxycholic Acid); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171018
[Lr] Data última revisão:
171018
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170922
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0183167


  6 / 3706 MEDLINE  
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[PMID]:28836457
[Au] Autor:Silveira MG; Lindor KD
[Ad] Endereço:a Section of Digestive Diseases , Yale School of Medicine , New Haven , CT , USA.
[Ti] Título:Investigational drugs in phase II clinical trials for primary biliary cholangitis.
[So] Source:Expert Opin Investig Drugs;26(10):1115-1121, 2017 Oct.
[Is] ISSN:1744-7658
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Primary biliary cholangitis (PBC) is a chronic cholestatic liver disease that may lead to biliary fibrosis, and eventually cirrhosis. The primary treatment for PBC is ursodeoxycholic acid (UDCA), which has favorably altered its natural history. However, up to 40% of patients have an inadequate response to UDCA, and are therefore at high risk of liver-related complications. Obeticholic acid has recently been approved for use in patients with PBC with inadequate response or who are intolerant to UDCA, but improvement in long-term outcomes has not yet been demonstrated. Alternative therapeutic options for PBC are needed. Areas covered: Recent advances in research including epidemiological, genetic and pre-clinical studies in animal models of PBC have yielded numerous agents currently at different stages of development for treatment of patients with PBC; in this review, we cover novel therapies that were recently or are recently being investigated in phase II clinical trials. Expert opinion: Despite the evolving landscape in PBC, the main challenges facing development of novel therapies remain the rarity of the disease and the limitations to design and conduct of controlled clinical trials in PBC, which are needed to determine the long-term effects of novel therapies on the clinical outcomes of PBC.
[Mh] Termos MeSH primário: Colangite/tratamento farmacológico
Desenho de Drogas
Drogas em Investigação/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Ácido Quenodesoxicólico/análogos & derivados
Ácido Quenodesoxicólico/uso terapêutico
Colagogos e Coleréticos/uso terapêutico
Colangite/complicações
Progressão da Doença
Seres Humanos
Cirrose Hepática Biliar/tratamento farmacológico
Ácido Ursodesoxicólico/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Cholagogues and Choleretics); 0 (Drugs, Investigational); 0462Z4S4OZ (obeticholic acid); 0GEI24LG0J (Chenodeoxycholic Acid); 724L30Y2QR (Ursodeoxycholic Acid)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170825
[St] Status:MEDLINE
[do] DOI:10.1080/13543784.2017.1371135


  7 / 3706 MEDLINE  
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[PMID]:28708871
[Au] Autor:Kim EK; Cho JH; Kim E; Kim YJ
[Ad] Endereço:Division of Gastroenterology, Department of Internal medicine, Gachon University Gil Medical Center, Incheon, the Republic of Korea.
[Ti] Título:Ursodeoxycholic acid inhibits the proliferation of colon cancer cells by regulating oxidative stress and cancer stem-like cell growth.
[So] Source:PLoS One;12(7):e0181183, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: The regulation of reactive oxygen species (ROS) exists as a therapeutic target for cancer treatments. Previous studies have shown that ursodeoxycholic acid (UDCA) suppresses the proliferation of colon cancer cells. The aim of this study was to evaluate the effect of UDCA upon the proliferation of colon cancer cells as a direct result of the regulation of ROS. METHOD: Colon cancer cell lines (HT29 and HCT116) were treated with UDCA. The total number of cells and the number of dead cells were determined using cell counters. A fluorescein isothiocyanate-bromodeoxyuridine flow kit was used to analyze cell cycle variations. Upon exposure to UDCA, the protein levels of p27, p21, CDK2, CDK4 and CDK6 were determined using western blotting, and qRT-PCR was used to determine levels of mRNA. We preformed dichlorofluorescindiacetate (DCF-DA) staining to detect alteration of intracellular ROS using fluorescence activated cell sorting (FACS). Colon cancer stem-like cell lines were generated by tumorsphere culture and treated with UDCA for seven days. The total number of tumorspheres was determined using microscopy. RESULTS: We found that UDCA reduced the total number of colon cancer cells, but did not increase the number of dead cells. UDCA inhibited the G1/S and G2/M transition phases in colon cancer cells. UDCA induced expression of cell cycle inhibitors such as p27 and p21. However, it was determined that UDCA suppressed levels of CDK2, CDK4, and CDK6. UDCA regulated intracellular ROS generation in colon cancer cells, and induced activation of Erk1/2. Finally, UDCA inhibited formation of colon cancer stem-like cells. CONCLUSION: Our results indicate that UDCA suppresses proliferation through regulation of oxidative stress in colon cancer cells, as well as colon cancer stem-like cells.
[Mh] Termos MeSH primário: Proliferação Celular/efeitos dos fármacos
Estresse Oxidativo/efeitos dos fármacos
Ácido Ursodesoxicólico/farmacologia
[Mh] Termos MeSH secundário: Pontos de Checagem do Ciclo Celular/efeitos dos fármacos
Neoplasias do Colo/metabolismo
Neoplasias do Colo/patologia
Inibidor de Quinase Dependente de Ciclina p21/genética
Inibidor de Quinase Dependente de Ciclina p21/metabolismo
Inibidor de Quinase Dependente de Ciclina p27/genética
Inibidor de Quinase Dependente de Ciclina p27/metabolismo
Quinases Ciclina-Dependentes/genética
Quinases Ciclina-Dependentes/metabolismo
Células HCT116
Células HT29
Seres Humanos
Proteína Quinase 1 Ativada por Mitógeno/metabolismo
Proteína Quinase 3 Ativada por Mitógeno/metabolismo
Células-Tronco Neoplásicas/citologia
Células-Tronco Neoplásicas/efeitos dos fármacos
Células-Tronco Neoplásicas/metabolismo
RNA Mensageiro/metabolismo
Espécies Reativas de Oxigênio/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cyclin-Dependent Kinase Inhibitor p21); 0 (RNA, Messenger); 0 (Reactive Oxygen Species); 147604-94-2 (Cyclin-Dependent Kinase Inhibitor p27); 724L30Y2QR (Ursodeoxycholic Acid); EC 2.7.11.22 (Cyclin-Dependent Kinases); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170715
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0181183


  8 / 3706 MEDLINE  
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[PMID]:28665991
[Au] Autor:Ko WK; Lee SH; Kim SJ; Jo MJ; Kumar H; Han IB; Sohn S
[Ad] Endereço:Department of Neurosurgery, CHA University, CHA Bundang Medical Center, Seongnam-si, Gyeonggi-do, Republic of Korea.
[Ti] Título:Anti-inflammatory effects of ursodeoxycholic acid by lipopolysaccharide-stimulated inflammatory responses in RAW 264.7 macrophages.
[So] Source:PLoS One;12(6):e0180673, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: The aim of this study was to investigate the anti-inflammatory effects of Ursodeoxycholic acid (UDCA) in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages. METHODS: We induced an inflammatory process in RAW 264.7 macrophages using LPS. The anti-inflammatory effects of UDCA on LPS-stimulated RAW 264.7 macrophages were analyzed using nitric oxide (NO). Pro-inflammatory and anti-inflammatory cytokines were analyzed by quantitative real time polymerase chain reaction (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA). The phosphorylations of extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38 in mitogen-activated protein kinase (MAPK) signaling pathways and nuclear factor kappa-light polypeptide gene enhancer in B-cells inhibitor, alpha (IκBα) signaling pathways were evaluated by western blot assays. RESULTS: UDCA decreased the LPS-stimulated release of the inflammatory mediator NO. UDCA also decreased the pro-inflammatory cytokines tumor necrosis factor-α (TNF-α), interleukin 1-α (IL-1α), interleukin 1-ß (IL-1ß), and interleukin 6 (IL-6) in mRNA and protein levels. In addition, UDCA increased an anti-inflammatory cytokine interleukin 10 (IL-10) in the LPS-stimulated RAW 264.7 macrophages. UDCA inhibited the expression of inflammatory transcription factor nuclear factor kappa B (NF-κB) in LPS-stimulated RAW 264.7 macrophages. Furthermore, UDCA suppressed the phosphorylation of ERK, JNK, and p38 signals related to inflammatory pathways. In addition, the phosphorylation of IκBα, the inhibitor of NF-κB, also inhibited by UDCA. CONCLUSION: UDCA inhibits the pro-inflammatory responses by LPS in RAW 264.7 macrophages. UDCA also suppresses the phosphorylation by LPS on ERK, JNK, and p38 in MAPKs and NF-κB pathway. These results suggest that UDCA can serve as a useful anti-inflammatory drug.
[Mh] Termos MeSH primário: Anti-Inflamatórios/farmacologia
Lipopolissacarídeos/farmacologia
Macrófagos/efeitos dos fármacos
Ácido Ursodesoxicólico/farmacologia
[Mh] Termos MeSH secundário: Animais
Western Blotting
Linhagem Celular
Citocinas/metabolismo
Ensaio de Imunoadsorção Enzimática
Mediadores da Inflamação/metabolismo
Macrófagos/enzimologia
Macrófagos/metabolismo
Camundongos
Óxido Nítrico/metabolismo
Proteínas Quinases/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Cytokines); 0 (Inflammation Mediators); 0 (Lipopolysaccharides); 31C4KY9ESH (Nitric Oxide); 724L30Y2QR (Ursodeoxycholic Acid); EC 2.7.- (Protein Kinases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171006
[Lr] Data última revisão:
171006
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170701
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0180673


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[PMID]:28637315
[Au] Autor:Ma H; Sales VM; Wolf AR; Subramanian S; Matthews TJ; Chen M; Sharma A; Gall W; Kulik W; Cohen DE; Adachi Y; Griffin NW; Gordon JI; Patti ME; Isganaitis E
[Ad] Endereço:Research Division, Joslin Diabetes Center and Harvard Medical School, Boston, Massachusetts 02115.
[Ti] Título:Attenuated Effects of Bile Acids on Glucose Metabolism and Insulin Sensitivity in a Male Mouse Model of Prenatal Undernutrition.
[So] Source:Endocrinology;158(8):2441-2452, 2017 Aug 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Prenatal undernutrition and low birth weight are associated with risk of type 2 diabetes and obesity. Prenatal caloric restriction results in low birth weight, glucose intolerance, obesity, and reduced plasma bile acids (BAs) in offspring mice. Because BAs can regulate systemic metabolism and glucose homeostasis, we hypothesized that BA supplementation could prevent diet-induced obesity and glucose intolerance in this model of developmental programming. Pregnant dams were food restricted by 50% from gestational days 12.5 to 18.5. Offspring of both undernourished (UN) and control (C) dams given unrestricted diets were weaned to high-fat diets with or without supplementation with 0.25% w/w ursodeoxycholic acid (UDCA), yielding four experimental groups: C, UN, C + UDCA, and UN + UDCA. Glucose homeostasis, BA composition, liver and intestinal gene expression, and microbiota composition were analyzed in the four groups. Although UDCA supplementation ameliorated diet-induced obesity in C mice, there was no effect in UN mice. UDCA similarly lowered fasting insulin, and improved glucose tolerance, pyruvate tolerance, and liver steatosis in C, but not UN, animals. BA composition differed significantly, and liver and ileal expression of genes involved in BA metabolism (Cyp7b1, Shp) were differentially induced by UDCA in C vs UN animals. Bacterial taxa in fecal microbiota correlated with treatment groups and metabolic parameters. In conclusion, prenatal undernutrition alters responsiveness to the metabolic benefits of BA supplementation, with resistance to the weight-lowering and insulin-sensitizing effects of UDCA supplementation. Our findings suggest that BA metabolism may be a previously unrecognized contributor to developmentally programmed diabetes risk.
[Mh] Termos MeSH primário: Ácidos e Sais Biliares/farmacologia
Glucose/metabolismo
Resistência à Insulina/fisiologia
Desnutrição
Fenômenos Fisiológicos da Nutrição Pré-Natal
[Mh] Termos MeSH secundário: Animais
Ácidos e Sais Biliares/sangue
Ácidos e Sais Biliares/química
Glicemia
Dieta Hiperlipídica
Feminino
Masculino
Camundongos
Camundongos Endogâmicos ICR
Gravidez
Efeitos Tardios da Exposição Pré-Natal
Ácido Ursodesoxicólico/administração & dosagem
Ácido Ursodesoxicólico/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bile Acids and Salts); 0 (Blood Glucose); 724L30Y2QR (Ursodeoxycholic Acid); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170623
[St] Status:MEDLINE
[do] DOI:10.1210/en.2017-00288


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[PMID]:28602806
[Au] Autor:Stremmel W; Staffer S; Wannhoff A; Pathil A
[Ad] Endereço:Department of Internal Medicine, University Hospital of Heidelberg, INF 410, 69120 Heidelberg, Germany. Electronic address: wolfgang.stremmel@med.uni-heidelberg.de.
[Ti] Título:The overall fatty acid absorption controlled by basolateral chylomicron excretion under regulation of p-JNK1.
[So] Source:Biochim Biophys Acta;1862(9):917-928, 2017 09.
[Is] ISSN:0006-3002
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Suppression of fatty acid absorption is one goal to fight obesity. However, the responsible molecular mechanism is poorly understood. Aim of the present study was the search for the key regulator of the overall fatty acid absorption mechanism and its pharmaceutical modulation. As experimental tool we employed the polarized human intestinal tumor derived cell line CaCo2. Here we showed that influx of fatty acids is mediated by an apical heterotetrameric plasma membrane protein complex of which the calcium-independent membrane phospholipase A (iPLA ß) is one constituent. The newly synthesized bile acid-phospholipid conjugate ursodeoxycholate-lysophosphatidylethanolamide (UDCA-LPE) blocked iPLA ß, which structurally disrupted the fatty acid-uptake complex. Furthermore, the inhibition of iPLA ß lead to reduction of cytosolic lysophosphatidylcholine (LPC) production which suppressed p-JNK1, as a central regulator of metabolism. In a concerted action low p-JNK1 levels prohibited synthesis of the members of the fatty acid uptake complex as well as of apolipoprotein B and the connected members of the basolateral vesicular chylomicron excretion machinery, thereby inhibiting cellular lipid excretion. The basolateral chylomicron release was shown to determine the overall fatty acid-absorption capacity as rate limiting step, whereas apical uptake replenishes the cellular stores, enabling continuous transcellular movement of fatty acids. In conclusion, the UDCA-LPE mediated inhibition of p-JNK1 represents a powerful tool to control intestinal absorption of fatty acids and, thus may be employed as a drug to treat obesity.
[Mh] Termos MeSH primário: Quilomícrons/metabolismo
Ácidos Graxos/metabolismo
Proteína Quinase 8 Ativada por Mitógeno/metabolismo
[Mh] Termos MeSH secundário: Animais
Apolipoproteínas B/metabolismo
Ácidos e Sais Biliares/metabolismo
Células CACO-2
Cálcio/metabolismo
Linhagem Celular Tumoral
Membrana Celular/metabolismo
Feminino
Fosfolipases A2 do Grupo IV/metabolismo
Seres Humanos
Lisofosfatidilcolinas/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Ácido Ursodesoxicólico/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Apolipoproteins B); 0 (Bile Acids and Salts); 0 (Chylomicrons); 0 (Fatty Acids); 0 (Lysophosphatidylcholines); 724L30Y2QR (Ursodeoxycholic Acid); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 8); EC 3.1.1.4 (Group IV Phospholipases A2); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170613
[St] Status:MEDLINE



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