Base de dados : MEDLINE
Pesquisa : C06.552.645 [Categoria DeCS]
Referências encontradas : 4868 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 487 ir para página                         

  1 / 4868 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29381966
[Au] Autor:Liu MX; Wen XY; Leung YK; Zheng YJ; Jin MS; Jin QL; Niu JQ
[Ad] Endereço:Department of Hepatology, The First Hospital of Jilin University.
[Ti] Título:Hemolytic anemia in alcoholic liver disease: Zieve syndrome: A case report and literature review.
[So] Source:Medicine (Baltimore);96(47):e8742, 2017 Nov.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Zieve syndrome, a rarely reported disease resulting from alcohol abuse, consists of a triad of symptoms: hemolytic anemia, cholestatic jaundice, and transient hyperlipidemia. It is largely under-recognized and under-reported, possibly because of unawareness of the condition by physicians. Here, we report a case of Zieve syndrome managed at the Jilin University First Bethune Hospital. PATIENT CONCERNS: A 30-year-old Chinese woman presented with a 4-month history of fatigue, yellowish discoloration of the eyes, and tea-colored urine. She had been a heavy drinker for 2 years prior to onset of the disease with an average daily alcohol intake of 60 g/d and more than 80 g/d for the previous 6 months. DIAGNOSIS: The diagnosis of Zieve syndrome was confirmed based on hemolysis and cholestatic jaundice secondary to alcoholic liver disease and heavy drinking. Bone marrow biopsy and liver biopsy both supported the diagnosis. INTERVENTIONS: We treated her with abstinence from alcohol and supportive therapy. OUTCOMES: The patient was discharged 14 days after admission with an improvement in symptoms, which continued to subside during the 2-month follow-up period. LESSONS: Doctors confronted with hemolysis in a patient with alcoholic liver disease should be aware of the under-reported Zieve syndrome. Recognition of this syndrome could help doctors avoid unnecessary invasive procedures and emphasize the importance of alcohol abstinence as the mainstay of management. Glucocorticoids may not be useful in treating hemolytic anemia in Zieve syndrome.
[Mh] Termos MeSH primário: Anemia Hemolítica/complicações
Hepatopatias Alcoólicas/complicações
[Mh] Termos MeSH secundário: Adulto
Feminino
Seres Humanos
Hiperlipidemias/etiologia
Icterícia/etiologia
Síndrome
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180201
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000008742


  2 / 4868 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29236785
[Au] Autor:Sandahl TD; Støy SH; Laursen TL; Rødgaard-Hansen S; Møller HJ; Møller S; Vilstrup H; Grønbæk H
[Ad] Endereço:Department of Hepatology & Gastroenterology, Aarhus University Hospital, Aarhus, Denmark.
[Ti] Título:The soluble mannose receptor (sMR) is elevated in alcoholic liver disease and associated with disease severity, portal hypertension, and mortality in cirrhosis patients.
[So] Source:PLoS One;12(12):e0189345, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND AIMS: Hepatic macrophages (Kupffer cells) are involved in the immunopathology of alcoholic liver disease (ALD). The mannose receptor (MR, CD206), expressed primarily by macrophages, mediates endocytosis, antigen presentation and T-cell activation. A soluble form, sMR, has recently been identified in humans. We aimed to study plasma sMR levels and its correlation with disease severity and survival in ALD patients. METHODS: We included 50 patients with alcoholic hepatitis (AH), 68 alcoholic cirrhosis (AC) patients (Child-Pugh A (23), B (24), C (21)), and 21 healthy controls (HC). Liver status was described by the Glasgow Alcoholic Hepatitis Score (GAHS), Child-Pugh (CP) and MELD-scores, and in AC patients the hepatic venous pressure gradient (HVPG) was measured by liver vein catheterisation. We used Kaplan-Meier statistics for short-term survival (84-days) in AH patients and long-term (4 years) in AC patients. We measured plasma sMR by ELISA. RESULTS: Median sMR concentrations were significantly elevated in AH 1.32(IQR:0.69) and AC 0.46(0.5) compared to HC 0.2(0.06) mg/L; p<0.001 and increased in a stepwise manner with the CP-score (p<0.001). In AC sMR predicted portal hypertension (HVPG ≥10 mmHg) with an area under the Receiver Operator Characteristics curve of 0.86 and a high sMR cut-off (>0.43 mg/l) was associated with increased mortality (p = 0.005). CONCLUSION: The soluble mannose receptor is elevated in alcoholic liver disease, especially in patients with AH. Its blood level predicts portal hypertension and long-term mortality in AC patients.
[Mh] Termos MeSH primário: Hipertensão Portal/metabolismo
Lectinas Tipo C/metabolismo
Cirrose Hepática/mortalidade
Hepatopatias Alcoólicas/metabolismo
Lectinas de Ligação a Manose/metabolismo
Receptores de Superfície Celular/metabolismo
[Mh] Termos MeSH secundário: Adulto
Feminino
Seres Humanos
Hipertensão Portal/complicações
Hipertensão Portal/fisiopatologia
Cirrose Hepática/complicações
Cirrose Hepática/metabolismo
Cirrose Hepática/fisiopatologia
Hepatopatias Alcoólicas/patologia
Masculino
Meia-Idade
Índice de Gravidade de Doença
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Lectins, C-Type); 0 (Mannose-Binding Lectins); 0 (Receptors, Cell Surface); 0 (mannose receptor)
[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:171214
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189345


  3 / 4868 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:29188945
[Au] Autor:Jokelainen K
[Ti] Título:Elevated liver enzymes - what next?
[So] Source:Duodecim;132(18):1688-92, 2016.
[Is] ISSN:0012-7183
[Cp] País de publicação:Finland
[La] Idioma:eng
[Ab] Resumo:Owing to laboratory automation, elevated liver enzymes are increasingly found in persons who are either asymptomatic or present with vague symptoms. The majority of slightly elevated liver enzymes detected in Finland result from excessive alcohol use, a drug or non-alcoholic fatty liver disease. On the other hand, disregarding pathological liver enzymes may lead to a delay of the treatment of a liver disease. In addition to careful anamnesis and status, systematic targeting of investigations is often the quickest way to correct diagnosis and assessment of need for treatment.
[Mh] Termos MeSH primário: Hepatopatias/diagnóstico
Hepatopatias/enzimologia
[Mh] Termos MeSH secundário: Fígado Gorduroso/enzimologia
Finlândia
Seres Humanos
Hepatopatias Alcoólicas/enzimologia
Testes de Função Hepática
Fatores de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171201
[St] Status:MEDLINE


  4 / 4868 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29020055
[Au] Autor:Ding L; Wo L; Du Z; Tang L; Song Z; Dou X
[Ad] Endereço:College of Life Science, Zhejiang Chinese Medical University, Hangzhou, Zhejiang, P. R. China.
[Ti] Título:Danshen protects against early-stage alcoholic liver disease in mice via inducing PPARα activation and subsequent 4-HNE degradation.
[So] Source:PLoS One;12(10):e0186357, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Alcoholic liver disease (ALD) is a type of chronic liver disease caused by long-term heavy ethanol consumption. Danshen is one of the most commonly used substances in traditional Chinese medicine and has been widely used for the treatment of various diseases, and most frequently, the ALD. The current study aims to determine the potential beneficial effect of Danshen administration on ALD and to clarify the underlying molecular mechanisms. Danshen administration improved liver pathologies of ALD, attenuated alcohol-induced increment of hepatic 4-Hydroxynonenal (4-HNE) formation, and prevented hepatic Peroxisome proliferators activated receptor alpha (PPARα) suppression in response to chronic alcohol consumption. Cell culture studies revealed that both hepatoprotective effect and increased intracellular 4-HNE clearance instigated by Danshen supplementation are PPARα-dependent. In conclusion, Danshen administration can protect against ALD via inducing PPARα activation and subsequent 4-HNE degradation.
[Mh] Termos MeSH primário: Aldeídos/metabolismo
Medicamentos de Ervas Chinesas/uso terapêutico
Hepatopatias Alcoólicas/tratamento farmacológico
Hepatopatias Alcoólicas/prevenção & controle
PPAR alfa/metabolismo
[Mh] Termos MeSH secundário: Alcoolismo/tratamento farmacológico
Alcoolismo/metabolismo
Alcoolismo/patologia
Animais
Morte Celular/efeitos dos fármacos
Suplementos Nutricionais
Medicamentos de Ervas Chinesas/administração & dosagem
Medicamentos de Ervas Chinesas/farmacologia
Etanol/administração & dosagem
Células Hep G2
Hepatócitos/efeitos dos fármacos
Hepatócitos/metabolismo
Hepatócitos/patologia
Seres Humanos
Fígado/efeitos dos fármacos
Fígado/metabolismo
Fígado/patologia
Hepatopatias Alcoólicas/metabolismo
Masculino
Camundongos Endogâmicos C57BL
Fitoterapia
Substâncias Protetoras/administração & dosagem
Substâncias Protetoras/farmacologia
Substâncias Protetoras/uso terapêutico
Triglicerídeos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aldehydes); 0 (Drugs, Chinese Herbal); 0 (PPAR alpha); 0 (Protective Agents); 0 (Triglycerides); 3K9958V90M (Ethanol); 79483-68-4 (dan-shen root extract); K1CVM13F96 (4-hydroxy-2-nonenal)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171012
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0186357


  5 / 4868 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28890346
[Au] Autor:Li C; Li L; Yang CF; Zhong YJ; Wu D; Shi L; Chen L; Li YW
[Ad] Endereço:College of Pharmacy, Guilin Medical University, Guilin 541004, PR China.
[Ti] Título:Hepatoprotective effects of Methyl ferulic acid on alcohol-induced liver oxidative injury in mice by inhibiting the NOX4/ROS-MAPK pathway.
[So] Source:Biochem Biophys Res Commun;493(1):277-285, 2017 Nov 04.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:AIMS: The present study aimed to investigate the hepatoprotective effects of Methyl ferulic acid (MFA) against oxidative stress and apoptosis as well as inflammation in mice with liver injury induced by alcohol and its underlying mechanisms. METHODS: C57BL/6 mice were divided into a control group,a model group, and Methyl ferulic acid with high dosage (20 mg/kg), moderate dosage (10 mg/kg) and low dosage (5 mg/kg) groups. The general condition and organ index of each group were investigated. Histopathological analysis was performed to determine the degree of hepatic injury. Biochemical analyses of functional liver enzymes, lipid peroxidation enzymes and lipid content in each group. The levels of inflammatory cytokines were measured by enzyme-linked immunosorbent assay (ELISA). The mechanisms were investigated by detecting levels of NADPH Oxidase 4 (NOX4),p22phox, cytochrome P4502E1 (CYP2E1),Bax,B-cell lymphoma 2 (Bcl-2),cleaved-caspase 3 and 9 and phosphorylated extracellular regulated protein kinases(ERK),phosphorylated c-Jun N-terminal kinase (JNK), and phosphorylated p38 mitogen-activated protein kinase (MAPK) using real-time polymerase chain reaction (PCR) and Western blotting. RESULTS: MFA treatment significantly decreased serum enzymatic activities of alanine aminotransferase (ALT) and aspartate aminotransaminase (AST). MFA markedly increased levels of superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), glutathione peroxidase (GSH-Px) and total antioxidative capacity (T-AOC), and reduced the concentration of malondialdehyde (MDA) and reactive oxygen species (ROS). Histopathological examination of livers showed that MFA reduced cytoplasmic vacuolisation necrosis and inflammatory cell infiltration in alcohol-treated mice. MFA treatment remarkably reduced the levels of trigyceride (TG), total cholesterol (TC) and low-density lipoprotein (LDL), decreasing the levels of high-density lipoprotein (HDL), alcohol dehydrogenase(ADL) and aldehyde dehydrogenase (ALDH). MFA treatment remarkably inhibited the expression of inflammatory factors tumour necrosis factor (TNF)-α, monocyte chemoattractant protein 1 (MCP-1), interleukin (IL)-1ß and IL-6. MFA attenuated both mRNA and protein expression of NOX4,p22phox,CYP2E1,Bax/Bcl-2. In addition, MFA inhibited the activation of caspase 3 and 9 and downregulated the levels of p-JNK,p-p38 MAPK and p-ERK in liver. CONCLUSION: MFA has a protective effect on alcohol-induced liver injury, which may be related to its antioxidant,anti-inflammatory,lipid-eliminating properties and its ability to regulate the NOX4/ROS-MAPK signalling pathway.
[Mh] Termos MeSH primário: Ácidos Cafeicos/administração & dosagem
Hepatopatias Alcoólicas/tratamento farmacológico
Hepatopatias Alcoólicas/metabolismo
NADPH Oxidases/metabolismo
Estresse Oxidativo/efeitos dos fármacos
Espécies Reativas de Oxigênio/metabolismo
[Mh] Termos MeSH secundário: Animais
Antioxidantes/administração & dosagem
Doença Hepática Induzida por Substâncias e Drogas
Relação Dose-Resposta a Droga
Etanol
Hepatopatias Alcoólicas/patologia
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
NADPH Oxidase 4
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (Caffeic Acids); 0 (Reactive Oxygen Species); 3K9958V90M (Ethanol); EC 1.6.3.- (NADPH Oxidase 4); EC 1.6.3.- (NADPH Oxidases); EC 1.6.3.- (Nox4 protein, mouse); Y98BUA66RX (methyl ferulate)
[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:170912
[St] Status:MEDLINE


  6 / 4868 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28867186
[Au] Autor:Ikaga R; Li D; Yamazaki T
[Ad] Endereço:Department of Nutritional Science, National Institute of Health and Nutrition, National Institutes of Biomedical Innovation, Health and Nutrition, 1-23-1 Toyama, Shinjuku-ku, Tokyo, 162-8636, Japan.
[Ti] Título:Dietary ß-conglycinin prevents acute ethanol-induced fatty liver in mice.
[So] Source:Biochem Biophys Res Commun;493(1):542-547, 2017 Nov 04.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Alcoholic fatty liver is the earliest stage of alcohol-induced liver disease leading to liver cirrhosis. ß-Conglycinin, one of the soy proteins, is known to prevent non-alcoholic fatty liver, hyperlipidemia and obesity. Therefore, we examined whether ß-conglycinin feeding has an effect on the prevention of acute ethanol-induced fatty liver in mice. Male C57BL/6J mice were fed with 20 energy% ß-conglycinin or casein for 4 weeks prior to ethanol administration and were then given ethanol or glucose, as a control, by gavage. Ethanol significantly increased liver triglyceride (TG) in mice fed casein due to the activation of peroxisome proliferator-activated receptor (PPAR) γ2, a nuclear transcription factor known for regulating lipid metabolism and de novo lipogenesis. The liver TG of ethanol-administered ß-conglycinin-fed mice was significantly lower than that in those fed casein, although ethanol increased the amount of liver TG in mice fed ß-conglycinin. The increased levels of PPARγ2 protein and its target gene CD36 in response to an ethanol were not observed in mice fed ß-conglycinin. Moreover, ß-conglycinin decreased the basal expression of de novo lipogenesis-related genes such as stearoyl-CoA desaturase-1, and therefore, the expressions of these genes were lower in the ethanol-administered ß-conglycinin-fed mice than in the casein-fed mice. In conclusion, ß-conglycinin supplementation appears to prevent the development of fatty liver in mice caused by ethanol consumption via the suppression of alcohol-induced activation of PPARγ2 and the downregulation of the basal expression of de novo lipogenesis.
[Mh] Termos MeSH primário: Antígenos de Plantas/administração & dosagem
Suplementos Nutricionais
Globulinas/administração & dosagem
Lipogênese/efeitos dos fármacos
Hepatopatias Alcoólicas/metabolismo
Hepatopatias Alcoólicas/prevenção & controle
PPAR gama/metabolismo
Proteínas de Armazenamento de Sementes/administração & dosagem
Proteínas de Soja/administração & dosagem
[Mh] Termos MeSH secundário: Animais
Relação Dose-Resposta a Droga
Etanol/envenenamento
Hepatopatias Alcoólicas/etiologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Plant); 0 (Globulins); 0 (PPAR gamma); 0 (Seed Storage Proteins); 0 (Soybean Proteins); 0 (beta-conglycinin protein, Glycine max); 3K9958V90M (Ethanol)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170905
[St] Status:MEDLINE


  7 / 4868 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28849551
[Au] Autor:Shafaghati L; Razaghi-Moghadam Z; Mohammadnejad J
[Ad] Endereço:Faculty of New Sciences and Technologies, University of Tehran, Tehran, Iran.
[Ti] Título:A Systems Biology Approach to Understanding Alcoholic Liver Disease Molecular Mechanism: The Development of Static and Dynamic Models.
[So] Source:Bull Math Biol;79(11):2450-2473, 2017 Nov.
[Is] ISSN:1522-9602
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Alcoholic liver disease (ALD) is a complex disease characterized by damages to the liver and is the consequence of excessive alcohol consumption over years. Since this disease is associated with several pathway failures, pathway reconstruction and network analysis are likely to explicit the molecular basis of the disease. To this aim, in this paper, a network medicine approach was employed to integrate interactome (protein-protein interaction and signaling pathways) and transcriptome data to reconstruct both a static network of ALD and a dynamic model for it. Several data sources were exploited to assemble a set of ALD-associated genes which further was used for network reconstruction. Moreover, a comprehensive literature mining reveals that there are four signaling pathways with crosstalk (TLR4, NF- [Formula: see text]B, MAPK and Apoptosis) which play a major role in ALD. These four pathways were exploited to reconstruct a dynamic model of ALD. The results assure that these two models are consistent with a number of experimental observations. The static network of ALD and its dynamic model are the first models provided for ALD which offer potentially valuable information for researchers in this field.
[Mh] Termos MeSH primário: Hepatopatias Alcoólicas/etiologia
Modelos Biológicos
[Mh] Termos MeSH secundário: Simulação por Computador
Seres Humanos
Hepatopatias Alcoólicas/genética
Hepatopatias Alcoólicas/metabolismo
Conceitos Matemáticos
Mapas de Interação de Proteínas
Transdução de Sinais
Biologia de Sistemas
Transcriptoma
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171113
[Lr] Data última revisão:
171113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170830
[St] Status:MEDLINE
[do] DOI:10.1007/s11538-017-0336-8


  8 / 4868 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28822232
[Ti] Título:This Month in AJP.
[So] Source:Am J Pathol;187(10):2129, 2017 Oct.
[Is] ISSN:1525-2191
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The following highlights summarize research articles that are published in the current issue of The American Journal of Pathology.
[Mh] Termos MeSH primário: Publicações Periódicas como Assunto
[Mh] Termos MeSH secundário: Animais
Proliferação Celular
Síndrome de Ehlers-Danlos/patologia
Seres Humanos
Hepatopatias Alcoólicas/patologia
Degeneração Macular/terapia
Neoplasias/patologia
Fibrose Pulmonar/prevenção & controle
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171004
[Lr] Data última revisão:
171004
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170820
[St] Status:MEDLINE


  9 / 4868 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28803762
[Au] Autor:Wang F; Liu JC; Zhou RJ; Zhao X; Liu M; Ye H; Xie ML
[Ad] Endereço:Department of Pharmacology, Jiangsu Key Laboratory of Preventive and Translational Medicine for Geriatric Diseases, College of Pharmaceutical Sciences, Soochow University, Suzhou 215123, Jiangsu Province, China.
[Ti] Título:Apigenin protects against alcohol-induced liver injury in mice by regulating hepatic CYP2E1-mediated oxidative stress and PPARα-mediated lipogenic gene expression.
[So] Source:Chem Biol Interact;275:171-177, 2017 Sep 25.
[Is] ISSN:1872-7786
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Alcohol is a major cause of liver injury, and there are currently no ideal pharmacological reagents that can prevent or reverse this disease. Apigenin is one of the most common flavonoids present in numerous plants and has many beneficial effects. But whether or not apigenin may protect against alcohol-induced liver injury remains unknown. Our aim was to examine the effect and potential mechanisms. The experimental mice were given 56% erguotou wine or simultaneously given apigenin 150-300 mg/kg by gavage for 30 days. The results showed that in the apigenin-treated mice, the expression of hepatic cytochrome P450 2E1 (CYP2E1) and nuclear factor kappa B proteins as well as contents of hepatic malondialdehyde and tumor necrosis factor-alpha were reduced, while the levels of hepatic reduced glutathione, glutathione reductase, glutathione peroxidase, and glutathione S-transferase were increased, especially in the 300 mg/kg group. A significant change in hepatic steatosis was also observed in the apigenin 300 mg/kg group. Apigenin pretreatment could increase the expression of hepatic peroxisome proliferator-activated receptor alpha (PPARα) and carnitine palmitoyltransferase-1 proteins, and decrease the expression of hepatic sterol regulatory element binding protein-1c, fatty acid synthase, and diacylglycerol acyltransferase proteins. These findings demonstrated that apigenin might exert a protective effect on alcohol-induced liver injury, and its mechanisms might be related to the regulations of hepatic CYP2E1-mediated oxidative stress and PPARα-mediated lipogenic gene expression.
[Mh] Termos MeSH primário: Apigenina/farmacologia
Citocromo P-450 CYP2E1/metabolismo
Regulação da Expressão Gênica/efeitos dos fármacos
Hepatopatias Alcoólicas/prevenção & controle
Estresse Oxidativo/efeitos dos fármacos
PPAR alfa/metabolismo
Substâncias Protetoras/farmacologia
[Mh] Termos MeSH secundário: Animais
Apigenina/uso terapêutico
Etanol/toxicidade
Ácido Graxo Sintases/metabolismo
Glutationa/metabolismo
Glutationa Peroxidase/metabolismo
Glutationa Redutase/metabolismo
Glutationa Transferase/metabolismo
Hepatopatias Alcoólicas/etiologia
Hepatopatias Alcoólicas/patologia
Masculino
Malondialdeído/metabolismo
Camundongos
PPAR alfa/genética
Substâncias Protetoras/uso terapêutico
Proteína de Ligação a Elemento Regulador de Esterol 1/metabolismo
Fator de Transcrição RelA/metabolismo
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (PPAR alpha); 0 (Protective Agents); 0 (Sterol Regulatory Element Binding Protein 1); 0 (Transcription Factor RelA); 0 (Tumor Necrosis Factor-alpha); 3K9958V90M (Ethanol); 4Y8F71G49Q (Malondialdehyde); 7V515PI7F6 (Apigenin); EC 1.11.1.9 (Glutathione Peroxidase); EC 1.14.13.- (Cytochrome P-450 CYP2E1); EC 1.8.1.7 (Glutathione Reductase); EC 2.3.1.85 (Fatty Acid Synthases); EC 2.5.1.18 (Glutathione Transferase); GAN16C9B8O (Glutathione)
[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:170815
[St] Status:MEDLINE


  10 / 4868 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28777049
[Au] Autor:Moriggia A; Stickel F
[Ad] Endereço:1 Epatocentro Ticino SA, Lugano.
[Ti] Título:Alkoholische Lebererkrankung ­ Update 2017..
[So] Source:Ther Umsch;74(3):133-144, 2017 Jul.
[Is] ISSN:0040-5930
[Cp] País de publicação:Switzerland
[La] Idioma:ger
[Mh] Termos MeSH primário: Etanol/administração & dosagem
Hepatopatias Alcoólicas/diagnóstico
Hepatopatias Alcoólicas/fisiopatologia
Fígado/efeitos dos fármacos
Fígado/fisiopatologia
Modelos Biológicos
[Mh] Termos MeSH secundário: Seres Humanos
Hepatopatias Alcoólicas/terapia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
3K9958V90M (Ethanol)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171005
[Lr] Data última revisão:
171005
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170805
[St] Status:MEDLINE
[do] DOI:10.1024/0040-5930/a000896



página 1 de 487 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde