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[PMID]:19883121
[Au] Autor:Mogilenko DA; Dizhe EB; Shavva VS; Lapikov IA; Orlov SV; Perevozchikov AP
[Ad] Endereço:Department of Biochemistry, Institute of Experimental Medicine, Russian Academy of Medical Sciences, 197376 St. Petersburg, Russia. denis@iem.sp.ru
[Ti] Título:Role of the nuclear receptors HNF4 alpha, PPAR alpha, and LXRs in the TNF alpha-mediated inhibition of human apolipoprotein A-I gene expression in HepG2 cells.
[So] Source:Biochemistry;48(50):11950-60, 2009 Dec 22.
[Is] ISSN:1520-4995
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The expression of the apolipoprotein A-I gene (apoA-I) in hepatocytes is repressed by pro-inflammatory cytokines such as IL-1beta and TNFalpha. In this work, we have demonstrated that treatment of HepG2 human hepatoma cells with chemical inhibitors for JNK, p38 protein kinases, and NFkappaB transcription factor abolishes the TNFalpha-mediated inhibition of human apoA-I gene expression in HepG2 cells. In addition, we have shown that TNFalpha decreases also the rate of secretion of apoA-I protein by HepG2 cells, and this effect depends on JNK and p38, but not on NFkappaB and MEK1/2 signaling pathways. The inhibitory effect of TNFalpha has been found to be mediated by the hepatic enhancer of the apoA-I gene. The decrease in the level of human apoA-I gene expression under the impact of TNFalpha appears to be partly mediated by the inhibition of HNF4alpha and PPARalpha gene expression. Treatment of HepG2 cells with PPARalpha antagonist (MK886) or LXR agonist (TO901317) abolishes the TNFalpha-mediated decrease in the level of apoA-I gene expression. PPARalpha agonist (WY-14643) abolishes the negative effect of TNFalpha on apoA-I gene expression in the case of simultaneous inhibition of MEK1/2, although neither inhibition of MEK1/2 nor addition of WY-14643 leads to the blocking of the TNFalpha-mediated decrease in the level of apoA-I gene expression individually. The ligand-dependent regulation of apoA-I gene expression by PPARalpha appears to be affected by the TNFalpha-mediated activation of MEK1/2 kinases, probably through PPARalpha phosphorylation. Treatment of HepG2 cells with PPARalpha and LXR synthetic agonists also blocks the inhibition of apoA-I protein secretion in HepG2 cells under the impact of TNFalpha. A chromatin immunoprecipitation assay demonstrates that TNFalpha leads to a 2-fold decrease in the level of PPARalpha binding with the apoA-I gene hepatic enhancer. At the same time, the level of LXRbeta binding with the apoA-I gene hepatic enhancer is increased 3-fold under the impact of TNFalpha. These results suggest that nuclear receptors HNF4alpha, PPARalpha, and LXRs are involved in the TNFalpha-mediated downregulation of human apoA-I gene expression and apoA-I protein secretion in HepG2 cells.
[Mh] Termos MeSH primário: Apolipoproteína A-I/antagonistas & inibidores
Apolipoproteína A-I/genética
Regulação para Baixo/genética
Fator 4 Nuclear de Hepatócito/fisiologia
Receptores Nucleares Órfãos/fisiologia
PPAR alfa/fisiologia
Fator de Necrose Tumoral alfa/fisiologia
[Mh] Termos MeSH secundário: Apolipoproteína A-I/biossíntese
Linhagem Celular Tumoral
Fator 4 Nuclear de Hepatócito/metabolismo
Seres Humanos
Ligantes
Receptores X do Fígado
MAP Quinase Quinase 1/antagonistas & inibidores
MAP Quinase Quinase 1/fisiologia
MAP Quinase Quinase 2/antagonistas & inibidores
MAP Quinase Quinase 2/fisiologia
NF-kappa B/fisiologia
Nafenopina/metabolismo
Nafenopina/farmacologia
Pirimidinas/metabolismo
Pirimidinas/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Apolipoprotein A-I); 0 (HNF4A protein, human); 0 (Hepatocyte Nuclear Factor 4); 0 (Ligands); 0 (Liver X Receptors); 0 (NF-kappa B); 0 (Orphan Nuclear Receptors); 0 (PPAR alpha); 0 (Pyrimidines); 0 (Tumor Necrosis Factor-alpha); 093W78U96W (Nafenopin); 86C4MRT55A (pirinixic acid); EC 2.7.12.2 (MAP Kinase Kinase 1); EC 2.7.12.2 (MAP Kinase Kinase 2)
[Em] Mês de entrada:1002
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:091104
[St] Status:MEDLINE
[do] DOI:10.1021/bi9015742


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[PMID]:18079279
[Au] Autor:Tamasi V; Miller KK; Ripp SL; Vila E; Geoghagen TE; Prough RA
[Ad] Endereço:Department of Biochemistry and Molecular Biology, U. Louisville School of Medicine, Louisville, KY 40292, USA.
[Ti] Título:Modulation of receptor phosphorylation contributes to activation of peroxisome proliferator activated receptor alpha by dehydroepiandrosterone and other peroxisome proliferators.
[So] Source:Mol Pharmacol;73(3):968-76, 2008 Mar.
[Is] ISSN:1521-0111
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Dehydroepiandrosterone (DHEA), a C19 human adrenal steroid, activates peroxisome proliferator-activated receptor alpha (PPARalpha) in vivo but does not ligand-activate PPARalpha in transient transfection experiments. We demonstrate that DHEA regulates PPARalpha action by altering both the levels and phosphorylation status of the receptor. Human hepatoma cells (HepG2) were transiently transfected with the expression plasmid encoding PPARalpha and a plasmid containing two copies of fatty acyl coenzyme oxidase (FACO) peroxisome-proliferator activated receptor responsive element consensus oligonucleotide in a luciferase reporter gene. Nafenopin treatment increased reporter gene activity in this system, whereas DHEA treatment did not. Okadaic acid significantly decreased nafenopin-induced reporter activity in a concentration-dependent manner. Okadaic acid treatment of primary rat hepatocytes decreased both DHEA- and nafenopin-induced FACO activity in primary rat hepatocytes. DHEA induced both PPARalpha mRNA and protein levels, as well as PP2A message in primary rat hepatocytes. Western blot analysis showed that the serines at positions 12 and 21 were rapidly dephosphorylated upon treatment with DHEA and nafenopin. Results using specific protein phosphatase inhibitors suggested that protein phosphatase 2A (PP2A) is responsible for DHEA action, and protein phosphatase 1 might be involved in nafenopin induction. Mutation of serines at position 6, 12, and 21 to an uncharged alanine residue significantly increased transcriptional activity, whereas mutation to negative charged aspartate residues (mimicking receptor phosphorylation) decreased transcriptional activity. DHEA action involves induction of PPARalpha mRNA and protein levels as well as increased PPARalpha transcriptional activity through decreasing receptor phosphorylation at serines in the AF1 region.
[Mh] Termos MeSH primário: Desidroepiandrosterona/farmacologia
Nafenopina/farmacologia
PPAR alfa/metabolismo
Proliferadores de Peroxissomos/farmacologia
Pirimidinas/farmacologia
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Sobrevivência Celular/efeitos dos fármacos
Células Cultivadas
Interpretação Estatística de Dados
Relação Dose-Resposta a Droga
Genes Reporter
Hepatócitos/efeitos dos fármacos
Hepatócitos/metabolismo
Luciferases/metabolismo
Masculino
Mutação
PPAR alfa/química
PPAR alfa/genética
Fosforilação/efeitos dos fármacos
Plasmídeos
RNA Mensageiro/biossíntese
Ratos
Ratos Sprague-Dawley
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (PPAR alpha); 0 (Peroxisome Proliferators); 0 (Pyrimidines); 0 (RNA, Messenger); 093W78U96W (Nafenopin); 459AG36T1B (Dehydroepiandrosterone); 86C4MRT55A (pirinixic acid); EC 1.13.12.- (Luciferases)
[Em] Mês de entrada:0804
[Cu] Atualização por classe:161122
[Lr] Data última revisão:
161122
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:071215
[St] Status:MEDLINE


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[PMID]:17409492
[Au] Autor:Kawano H; Nagata T; Narahara M; Kanazawa M; Miyake M
[Ad] Endereço:Faculty of Pharmaceutical Sciences, Kobe Gakuin University, Japan. kawano@pharm.kobegakuin.ac.jp
[Ti] Título:Triglyceride accumulation by peroxisome proliferators in rat hepatocytes.
[So] Source:Biol Pharm Bull;30(4):627-32, 2007 Apr.
[Is] ISSN:0918-6158
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Peroxisome proliferators (PxPs) induce peroxisomal beta-oxidation (Px-ox) in the liver of rodents and have a hypolipidemic function. To investigate hypolipidemic effect of PxPs, the relationship between TG fluctuation and Px-ox activity, as an indicator of the function of PxPs, was studied in primary cultured rat hepatocytes. Nafenopin (Nf) treatment of hepatocytes caused an increase in Px-ox activity in association with cellular TG accumulation in a time-dependent manner with a coefficient of r=0.918. This relationship between the activity and cellular TG were obtained using structurally diverse PxPs with a correlation coefficient of r=0.747. Treatment of the hypolipidemic drug, but non-PxP Pravastatin, decreased TG in the medium, but did not have the effects on cellular TG and Px-ox activity. The total amount of TG and diacylglycerol acyltransferase activity, the last enzyme in the TG de novo synthesis pathway, were not affected by Nf treatment. When hepatocytes were cultured with Brefeldin A, cellular TG was accumulated, the same as with Nf, however, Px-ox activity was not enhanced. Nf treatment markedly decreased the level of apolipoprotein B (apo B) in very low density lipoprotein (VLDL) fractions prepared from conditioned media and increased that of cellular apoB by Western blot analysis. Microsomal triglyceride transfer protein activity was not influenced by Nf. Together, with regards to TG lowering effect of PxPs, it is suggested that PxPs cause hepatocellular accumulation of TG without effects on TG biosynthesis and VLDL construction, and they might have inhibitory effect on VLDL secretion process.
[Mh] Termos MeSH primário: Hepatócitos/metabolismo
Hipolipemiantes/farmacologia
Proliferadores de Peroxissomos/farmacologia
Triglicerídeos/biossíntese
[Mh] Termos MeSH secundário: Animais
Apolipoproteínas B/metabolismo
Células Cultivadas
Meios de Cultivo Condicionados/química
Relação Dose-Resposta a Droga
Cinética
Masculino
Nafenopina/farmacologia
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Apolipoproteins B); 0 (Culture Media, Conditioned); 0 (Hypolipidemic Agents); 0 (Peroxisome Proliferators); 0 (Triglycerides); 093W78U96W (Nafenopin)
[Em] Mês de entrada:0705
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:070406
[St] Status:MEDLINE


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[PMID]:16944733
[Au] Autor:Hadzimehmedovic A; Balic A; Balic D
[Ad] Endereço:Ginekolosko-akuserska klinika, Univerzitetski klinicki centar Tuzla. azrahadzi@bih.net.ba
[Ti] Título:[Adolescents and knowledge of sexually transmitted diseases in Tuzla Canton].
[Ti] Título:Adolescenti i poznavanje spolno prenosivih bolesti u Tuzlanskom kantonu..
[So] Source:Med Arh;60(5):304-7, 2006.
[Cp] País de publicação:Bosnia and Herzegovina
[La] Idioma:bos
[Ab] Resumo:INTRODUCTION: Sexually transmitted diseases today are the most spread infectious diseases. Their incidence is constantly increasing. Usually they affect the population age 15 to 19. OBJECTIVE: To examine and determine parameters related to sexual behavior (sexarcha, duration of sexual activity, number of sexual partners), knowledge of adolescents of Tuzla Canton about sexually transmitted diseases and how do they get informed about it. MATERIAL AND METHODS: In period June to September 2003 we conduct a survey with 2995 high school boys and girls age 14 to 19 in Tuzla Canton. The survey contained questions about sexarcha, knowledge on sexually transmitted diseases, usage and knowledge on methods of contraception. RESULTS: Sexually active high school youth was 395 (13,18 %). Of that number 306 (10.22%) were boys and 89 (2.9 %) were girls (p<0.001). Average age of sexarcha for girls was 16.5+0.97 and for boys 15.7+1.2. Earliest average age of sexarcha for girls was in the municipality of Sapna (15.25+0.5) and for the boys in the municipality of Teocak (15 +1.1). In undeveloped municipalities sexual activity of adolescents of both sexes is significantly higher then in developed ones (p<0.5). High school boys and girls of Tuzla Canton showed insufficient knowledge of sexually transmitted diseases. Good knowledge showed only 87 (5 %) of girls and 25 (2 %) of boys. Girls showed statistically significant better knowledge on sexually transmitted diseases than boys p<0.001). Only 208 (19 %) boys and 539 (29 %) girls talks with parents about sexually transmitted diseases and contraception. CONCLUSION: Work on education of youth, especially in undeveloped municipalities in insufficient, as well as knowledge on sexually transmitted diseases and methods of contraception.
[Mh] Termos MeSH primário: Conhecimentos, Atitudes e Prática em Saúde
Doenças Sexualmente Transmissíveis
[Mh] Termos MeSH secundário: Adolescente
Adulto
Bósnia e Herzegóvina
Feminino
Seres Humanos
Masculino
Nafenopina
Comportamento Sexual
[Pt] Tipo de publicação:ENGLISH ABSTRACT; JOURNAL ARTICLE
[Nm] Nome de substância:
093W78U96W (Nafenopin)
[Em] Mês de entrada:0610
[Cu] Atualização por classe:151119
[Lr] Data última revisão:
151119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:060902
[St] Status:MEDLINE


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[PMID]:15728705
[Au] Autor:Bursch W; Wastl U; Hufnagl K; Schulte-Hermann R
[Ad] Endereço:Medizinische Universität Wien, Univ. Klinik für Innere MedizinI, Abtl. Institut für Krebsforschung, Borschkegasse 8a, A-1090 Wien. wilfried.bursch@meduniwien.ac.at
[Ti] Título:No increase of apoptosis in regressing mouse liver after withdrawal of growth stimuli or food restriction.
[So] Source:Toxicol Sci;85(1):507-14, 2005 May.
[Is] ISSN:1096-6080
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In short-term in vivo experiments, liver growth and regression in mice with high (C3H/He), intermediate (B6C3F1) or low (C57BL/6J) susceptibility to hepatocarcinogenesis was compared. Liver growth was induced by dietary administration of phenobarbital (PB; 750 ppm) or nafenopin (NAF; 500 ppm). PB or NAF treatment for 7 days produced moderate increases of liver DNA (15% or 25-28%, respectively) along with pronounced hypertrophy. Liver growth was strongest in C3H/He mice. Cessation of PB or NAF treatment led to a rapid regression of liver hypertrophy. However, the enhanced hepatic DNA content persisted for at least 2 weeks in all mouse strains. Apoptosis was not increased at any time after cessation of treatment in all strains. Food restriction to 60% of the ad libitum intake did not amplify either regression of liver hyperplasia or the occurrence of apoptosis. No strain difference in the occurrence of apoptosis was detected. Mouse hepatocytes in liver regressing after mitogen withdrawal do not enter apoptosis as readily as rat hepatocytes.
[Mh] Termos MeSH primário: Apoptose/fisiologia
Privação de Alimentos/fisiologia
Fígado/patologia
Nafenopina/farmacologia
Fenobarbital/farmacologia
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
DNA/biossíntese
Feminino
Hepatomegalia
Fígado/efeitos dos fármacos
Fígado/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos
Nafenopina/administração & dosagem
Tamanho do Órgão/efeitos dos fármacos
Tamanho do Órgão/fisiologia
Fenobarbital/administração & dosagem
Biossíntese de Proteínas/efeitos dos fármacos
Especificidade da Espécie
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
093W78U96W (Nafenopin); 9007-49-2 (DNA); YQE403BP4D (Phenobarbital)
[Em] Mês de entrada:0508
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:050225
[St] Status:MEDLINE


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[PMID]:12815167
[Au] Autor:Ripp SL; Falkner KC; Pendleton ML; Tamasi V; Prough RA
[Ad] Endereço:Department of Biochemistry and Molecular Biology, University of Louisville School of Medicine, Louisville, KY 40292, USA.
[Ti] Título:Regulation of CYP2C11 by dehydroepiandrosterone and peroxisome proliferators: identification of the negative regulatory region of the gene.
[So] Source:Mol Pharmacol;64(1):113-22, 2003 Jul.
[Is] ISSN:0026-895X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Treatment of rats with peroxisome proliferators is known to affect gene expression, including suppression of CYP2C11. The current study examined the mechanism of negative regulation of CYP2C11, comparing the effects of a classic peroxisome proliferator, nafenopin, with those of the steroid dehydroepiandrosterone (DHEA). In vivo dose-response experiments for DHEA were carried out with rats. Only the highest dose of DHEA in the diet (0.45%), a dose previously shown to produce peroxisome proliferation, caused suppression of CYP2C11 expression. Lower doses of DHEA (0.012 to 0.20% in diet) had little effect on CYP2C11 expression. In HepG2 cells, negative regulation of a CYP2C11 reporter gene by nafenopin required coexpression of PPARalpha, whereas negative regulation by DHEA did not. Deletion analysis revealed that the responsive region for both DHEA and nafenopin was between -108 and -60 relative to the transcription start site. Mutations in several putative transcription factor binding sites in the 5'-flanking region of CYP2C11 were produced. A mutation at -121 bp significantly diminished basal expression of CYP2C11 but did not affect negative regulation by DHEA or nafenopin. A mutation at -75 bp had only a small effect on basal expression but completely abolished negative regulation by DHEA and nafenopin. Gel shift experiments indicated that PPARalpha/RXRalpha heterodimers do not bind DNA in this region. Therefore, the sequence at -75 bp of CYP2C11 is necessary for negative regulation by both DHEA and nafenopin. However, the upstream events leading to suppression at this site must differ for DHEA and nafenopin.
[Mh] Termos MeSH primário: Hidrocarboneto de Aril Hidroxilases/metabolismo
Desidroepiandrosterona/farmacologia
Regulação Enzimológica da Expressão Gênica/efeitos dos fármacos
Proliferadores de Peroxissomos/farmacologia
Sequências Reguladoras de Ácido Nucleico/efeitos dos fármacos
Esteroide 16-alfa-Hidroxilase/metabolismo
[Mh] Termos MeSH secundário: Região 5'-Flanqueadora/efeitos dos fármacos
Região 5'-Flanqueadora/genética
Animais
Hidrocarboneto de Aril Hidroxilases/genética
Sequência de Bases
Família 2 do Citocromo P450
Dimerização
Relação Dose-Resposta a Droga
Regulação para Baixo/efeitos dos fármacos
Deleção de Genes
Seres Humanos
Masculino
Dados de Sequência Molecular
Nafenopina/farmacologia
Ratos
Ratos Sprague-Dawley
Receptores Citoplasmáticos e Nucleares/metabolismo
Receptores do Ácido Retinoico/metabolismo
Receptores X Retinoide
Esteroide 16-alfa-Hidroxilase/genética
Fatores de Transcrição/metabolismo
Transcrição Genética/efeitos dos fármacos
Transfecção
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, U.S. GOV'T, P.H.S.
[Nm] Nome de substância:
0 (Peroxisome Proliferators); 0 (Receptors, Cytoplasmic and Nuclear); 0 (Receptors, Retinoic Acid); 0 (Retinoid X Receptors); 0 (Transcription Factors); 093W78U96W (Nafenopin); 459AG36T1B (Dehydroepiandrosterone); EC 1.14.14.1 (Aryl Hydrocarbon Hydroxylases); EC 1.14.14.1 (CYP2C11 protein, rat); EC 1.14.14.1 (Cytochrome P450 Family 2); EC 1.14.14.1 (Steroid 16-alpha-Hydroxylase)
[Em] Mês de entrada:0307
[Cu] Atualização por classe:161124
[Lr] Data última revisão:
161124
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:030620
[St] Status:MEDLINE


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[PMID]:12606783
[Au] Autor:Gu S; Ripp SL; Prough RA; Geoghegan TE
[Ad] Endereço:Department of Biochemistry and Molecular Biology, the University of Louisville, School of Medicine, Louisville, Kentucky 40292, USA.
[Ti] Título:Dehydroepiandrosterone affects the expression of multiple genes in rat liver including 11 beta-hydroxysteroid dehydrogenase type 1: a cDNA array analysis.
[So] Source:Mol Pharmacol;63(3):722-31, 2003 Mar.
[Is] ISSN:0026-895X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Dehydroepiandrosterone (DHEA) is a C-19 adrenal steroid precursor to the gonadal steroids. In humans, circulating levels of DHEA, as its sulfated conjugate, are high at puberty and throughout early adulthood but decline with age. Dietary supplementation to maintain high levels of DHEA purportedly has beneficial effects on cognitive memory, the immune system, and fat and carbohydrate metabolism. In rodents, DHEA is a peroxisome proliferator that induces genes for the classical peroxisomal and microsomal enzymes associated with this response. These effects are mediated through activation of peroxisome proliferator-activated receptor alpha (PPAR alpha). However, DHEA can affect the expression of genes independently of PPAR alpha, including the gene for the major inducible drug and xenobiotic metabolizing enzyme, cytochrome P450 3A23. To elucidate the biochemistry associated with DHEA treatment, we employed a cDNA gene expression array using liver RNA from rats treated with DHEA or the classic peroxisome proliferator nafenopin. Principal components analysis identified 30 to 35 genes whose expression was affected by DHEA and/or nafenopin. Some were genes previously identified as PPAR-responsive genes. Changes in expression of several affected genes were verified by quantitative reverse transcriptase-polymerase chain reaction. These included aquaporin 3, which was induced by DHEA and to a lesser extent nafenopin, nuclear tyrosine phosphatase, which was induced by both agents, and 11 beta-hydroxysteroid dehydrogenase 1, which was decreased by treatment with DHEA in a dose-dependent fashion. Regulation of 11 beta-hydroxysteroid dehydrogenase 1 expression is important since the enzyme is believed to amplify local glucocorticoid signaling, and its repression may cause some of the metabolic effects associated with DHEA.
[Mh] Termos MeSH primário: Desidroepiandrosterona/farmacologia
Expressão Gênica/efeitos dos fármacos
Hidroxiesteroide Desidrogenases/biossíntese
Fígado/efeitos dos fármacos
[Mh] Termos MeSH secundário: 11-beta-Hidroxiesteroide Desidrogenases
Animais
Aquaporina 3
Aquaporinas/biossíntese
Aquaporinas/genética
Perfilação da Expressão Gênica
Hidroxiesteroide Desidrogenases/genética
Hipolipemiantes/farmacologia
Fígado/enzimologia
Masculino
Nafenopina/farmacologia
Análise de Sequência com Séries de Oligonucleotídeos
Ratos
Ratos Sprague-Dawley
Reação em Cadeia da Polimerase Via Transcriptase Reversa
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, P.H.S.
[Nm] Nome de substância:
0 (Aqp3 protein, rat); 0 (Aquaporins); 0 (Hypolipidemic Agents); 093W78U96W (Nafenopin); 158801-98-0 (Aquaporin 3); 459AG36T1B (Dehydroepiandrosterone); EC 1.1.- (Hydroxysteroid Dehydrogenases); EC 1.1.1.146 (11-beta-Hydroxysteroid Dehydrogenases)
[Em] Mês de entrada:0305
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:030228
[St] Status:MEDLINE


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[PMID]:12586354
[Au] Autor:Coddou C; Loyola G; Boyer JL; Bronfman M; Huidobro-Toro JP
[Ad] Endereço:Centro de Regulación Celular y Patología, Instituto MIFAB, Departamentos de Fisiología y Biologi;a Celular y Molecular, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Casilla 114-D, Santiago, Chile.
[Ti] Título:The hypolipidemic drug metabolites nafenopin-CoA and ciprofibroyl-CoA are competitive P2Y1 receptor antagonists.
[So] Source:FEBS Lett;536(1-3):145-50, 2003 Feb 11.
[Is] ISSN:0014-5793
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Coenzyme A (CoA-SH), endogenous and drug-derived CoA-derivatives were tested as putative antagonists of P2Y receptors expressed in Xenopus laevis oocytes, a method used to determine calcium-activated chloride current, an indicator of the activation of these receptors. CoA-SH antagonized reversibly and in a concentration-dependent manner the ATP-gated currents evoked by the human P2Y(1) but not the P2Y(2) receptor. Palmitoyl-CoA was four-fold more potent than CoA-SH as an antagonist while palmitoyl-carnitine was inactive, highlighting the role of the CoA-SH moiety in the antagonism. The CoA derivatives of nafenopin and ciprofibrate, two clinically relevant hypolipidemic drugs, increased 13 and three-fold the potency of CoA-SH, respectively. The K(B)s of nafenopin-CoA and ciprofibroyl-CoA were 58 and 148 nM, respectively; the slopes of the Schild plots were unitary. Neither 100 microM nafenopin nor ciprofibrate alone altered the P2Y(1) receptor activity. Neither CoA-SH nor ciprofibroyl-CoA antagonized the rat P2X(2) or the P2X(4) nucleotide receptors nor interacted with the 5-HT(2A/C) receptors. The bulky drug CoA-SH derivatives identify a hydrophobic pocket, which may serve as a potential target for novel selective P2Y(1) antagonists.
[Mh] Termos MeSH primário: Acil Coenzima A/farmacologia
Hipolipemiantes/farmacologia
Nafenopina/análogos & derivados
Nafenopina/farmacologia
Antagonistas do Receptor Purinérgico P2
[Mh] Termos MeSH secundário: Acil Coenzima A/química
Trifosfato de Adenosina/antagonistas & inibidores
Animais
Ligação Competitiva
Células Cultivadas
Relação Dose-Resposta a Droga
Condutividade Elétrica
Hipolipemiantes/química
Nafenopina/química
Receptores Purinérgicos P2/classificação
Receptores Purinérgicos P2Y1
Xenopus
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Acyl Coenzyme A); 0 (Hypolipidemic Agents); 0 (P2RY1 protein, human); 0 (P2ry1 protein, rat); 0 (Purinergic P2 Receptor Antagonists); 0 (Receptors, Purinergic P2); 0 (Receptors, Purinergic P2Y1); 0 (ciprofibroyl-coenzyme A); 093W78U96W (Nafenopin); 112195-81-0 (nafenopin-coenzyme A); 8L70Q75FXE (Adenosine Triphosphate)
[Em] Mês de entrada:0303
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:030215
[St] Status:MEDLINE


  9 / 223 MEDLINE  
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Fotocópia
[PMID]:12203361
[Au] Autor:Rossmanith W; Chabicovsky M; Grasl-Kraupp B; Peter B; Schausberger E; Schulte-Hermann R
[Ad] Endereço:Institute for Cancer Research, University of Vienna, Austria.
[Ti] Título:Follistatin overexpression in rodent liver tumors: a possible mechanism to overcome activin growth control.
[So] Source:Mol Carcinog;35(1):1-5, 2002 Sep.
[Is] ISSN:0899-1987
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The activin-follistatin system is a potent growth regulatory system of liver tissue homeostasis. Activin A inhibits hepatocellular DNA synthesis and induces cell death. Follistatin binds activin and sequesters it from the signaling pathway. Consistently, follistatin has been reported to act as an inducer of DNA synthesis in the liver. Using RNase protection analysis, we studied the expression of follistatin in rat and mouse liver tumors as a possible mechanism to overcome activin growth control. Approximately 40% of the tumors (nine of 24 each), most of them hepatocellular carcinomas, displayed increased levels of follistatin mRNA when compared to tumor-surrounding liver tissue. The degree of overexpression was highly variable but independent of the carcinogen treatment that animals had received. It was also independent from the histological stage of malignancy and further found in rat liver adenomas. Follistatin expression was also observed in cell lines derived from human hepatocellular carcinomas. Overexpression of follistatin may represent a unique strategy of hepatic tumors to overcome the inhibitory action of a growth factor, activin, by decreasing its local bioavailability.
[Mh] Termos MeSH primário: Ativinas/genética
Regulação Neoplásica da Expressão Gênica
Neoplasias Hepáticas/genética
[Mh] Termos MeSH secundário: Ativinas/metabolismo
Adenoma/tratamento farmacológico
Adenoma/genética
Adenoma/patologia
Processamento Alternativo
Animais
Western Blotting
Carcinoma Hepatocelular/tratamento farmacológico
Carcinoma Hepatocelular/genética
Carcinoma Hepatocelular/patologia
Divisão Celular/genética
Dietilnitrosamina/farmacologia
Folistatina
Seres Humanos
Neoplasias Hepáticas/tratamento farmacológico
Neoplasias Hepáticas/patologia
Masculino
Camundongos
Camundongos Endogâmicos
Nafenopina/farmacologia
Fenobarbital/farmacologia
RNA Mensageiro/análise
Ratos
Valores de Referência
Fator de Crescimento Transformador alfa/genética
Fator de Crescimento Transformador alfa/metabolismo
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Follistatin); 0 (RNA, Messenger); 0 (Transforming Growth Factor alpha); 093W78U96W (Nafenopin); 104625-48-1 (Activins); 3IQ78TTX1A (Diethylnitrosamine); YQE403BP4D (Phenobarbital)
[Em] Mês de entrada:0210
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:020831
[St] Status:MEDLINE


  10 / 223 MEDLINE  
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[PMID]:12091497
[Au] Autor:Kalderon B; Sheena V; Shachrur S; Hertz R; Bar-Tana J
[Ad] Endereço:Department of Human Nutrition and Metabolism, Hebrew University Medical School, Jerusalem, Israel 91120.
[Ti] Título:Modulation by nutrients and drugs of liver acyl-CoAs analyzed by mass spectrometry.
[So] Source:J Lipid Res;43(7):1125-32, 2002 Jul.
[Is] ISSN:0022-2275
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The profile of liver acyl-CoAs induced by dietary fats of variable compositions or by xenobiotic hypolipidemic amphipathic carboxylates was evaluated in vivo using a novel electrospray ionization tandem mass spectrometry methodology of high resolution, sensitivity, and reliability. The composition of liver fatty acyl-CoAs was found to reflect the composition of dietary fat. Treatment with hypolipidemic carboxylates resulted in liver dominant abundance of their respective acyl-CoAs accompanied by an increase in liver fatty acyl-CoAs. Cellular effects exerted by dietary fatty acids and/or xenobiotic carboxylic drugs may be transduced in vivo by their respective acyl-CoAs.
[Mh] Termos MeSH primário: Acil Coenzima A/análise
Gorduras na Dieta/farmacologia
Fígado/química
Fígado/efeitos dos fármacos
Xenobióticos/farmacologia
[Mh] Termos MeSH secundário: Acil Coenzima A/metabolismo
Animais
Bezafibrato/farmacologia
Dieta
Hipolipemiantes/farmacologia
Masculino
Nafenopina/farmacologia
Ácidos Palmíticos/farmacologia
Ratos
Sensibilidade e Especificidade
Espectrometria de Massas por Ionização por Electrospray/métodos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Acyl Coenzyme A); 0 (Dietary Fats); 0 (Hypolipidemic Agents); 0 (Palmitic Acids); 0 (Xenobiotics); 093W78U96W (Nafenopin); 87272-20-6 (MEDICA 16); Y9449Q51XH (Bezafibrate)
[Em] Mês de entrada:0212
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:020702
[St] Status:MEDLINE



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