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[PMID]:27980003
[Au] Autor:Das RK; Banerjee S; Shapiro BH
[Ti] Título:Growth hormone: a newly identified developmental organizer.
[So] Source:J Endocrinol;232(3):377-389, 2017 Mar.
[Is] ISSN:1479-6805
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The sexually dimorphic expression of cytochromes P450 (CYP) drug-metabolizing enzymes has been reported in all species examined. These sex differences are only expressed during adulthood and are solely regulated by sex differences in circulating growth hormone (GH) profiles. Once established, however, the different male- and female-dependent CYP isoform profiles are permanent and immutable, suggesting that adult CYP expression requires imprinting. As the hormone that regulates an adult function is likely the same hormone that imprints the function, we selectively blocked GH secretion in some newborn male rats, whereas others received concurrent physiologic replacement of rat GH. The results demonstrate that adult male GH activation of the signal transduction pathway regulating expression of the principal CYP2C11 isoform is obligatorily dependent on perinatal GH imprinting, without which CYP2C11 and drug metabolism would be permanently and profoundly suppressed. As there are other adult metabolic functions also regulated by GH, pediatric drug therapy known to disrupt GH secretion could unintentionally impair adult health.
[Mh] Termos MeSH primário: Regulação Enzimológica da Expressão Gênica/efeitos dos fármacos
Hormônio do Crescimento/farmacologia
Hepatócitos/efeitos dos fármacos
Transdução de Sinais/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Hidrocarboneto de Aril Hidroxilases/genética
Hidrocarboneto de Aril Hidroxilases/metabolismo
Família 2 do Citocromo P450/genética
Família 2 do Citocromo P450/metabolismo
Feminino
Hormônio do Crescimento/sangue
Hepatócitos/metabolismo
Masculino
Ratos
Esteroide 16-alfa-Hidroxilase/genética
Esteroide 16-alfa-Hidroxilase/metabolismo
Proteínas Supressoras da Sinalização de Citocinas/genética
Proteínas Supressoras da Sinalização de Citocinas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Suppressor of Cytokine Signaling Proteins); 0 (cytokine inducible SH2-containing protein); 9002-72-6 (Growth Hormone); 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:1706
[Cu] Atualização por classe:170620
[Lr] Data última revisão:
170620
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161217
[St] Status:MEDLINE
[do] DOI:10.1530/JOE-16-0471


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[PMID]:26354504
[Au] Autor:Lu J; Ding T; Qin X; Liu M; Wang X
[Ad] Endereço:Shanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai, 200241, China.
[Ti] Título:In vitro and in vivo evaluation of cucurbitacin E on rat hepatic CYP2C11 expression and activity using LC-MS/MS.
[So] Source:Sci China Life Sci;60(2):215-224, 2017 Feb.
[Is] ISSN:1869-1889
[Cp] País de publicação:China
[La] Idioma:eng
[Ab] Resumo:This study explored the effects of cucurbitacin E (CuE), a bioactive compound from Cucurbitaceae, on the metabolism/pharmacokinetic of tolbutamide, a model CYP2C9/11 probe substrate, and hepatic CYP2C11 expression in rats. Liquid chromatography-(tandem) mass spectrometry (LC-MS/MS) assay was used to detect tolbutamide as well as 4-hydroxytolbutamide, and then successfully applied to the pharmacokinetic study of tolbutamide in rats. The effect of CuE on CYP2C11 expression was determined by western blot. CuE (1.25-100 µmol L ) competitively inhibited tolbutamide 4-hydroxylation (CYP2C11) activity only in concentration-dependent manner with a K value of 55.5 µmol L in vitro. In whole animal studies, no significant difference in metabolism/pharmacokinetic of tolbutamide was found for the single pretreatment groups. In contrast, multiple pretreatments of CuE (200 µg kg d , 3 d, i.p.) significantly decreased tolbutamide clearance (CL) by 25% and prolonged plasma half-time (T ) by 37%. Moreover, CuE treatment (50-200 µg kg d , i.p.) for 3 d did not affect CYP2C11 expression. These findings demonstrated that CuE competitively inhibited the metabolism of CYP2C11 substrates but had no effect on rat CYP2C11 expression. This study may provide a useful reference for the reasonable and safe use of herbal or natural products containing CuE to avoid unnecessary drug-drug interactions.
[Mh] Termos MeSH primário: Hidrocarboneto de Aril Hidroxilases/metabolismo
Família 2 do Citocromo P450/metabolismo
Fígado/efeitos dos fármacos
Esteroide 16-alfa-Hidroxilase/metabolismo
Triterpenos/farmacologia
[Mh] Termos MeSH secundário: Animais
Cromatografia Líquida de Alta Pressão
Hidroxilação
Masculino
Microssomos Hepáticos/efeitos dos fármacos
Ratos
Ratos Sprague-Dawley
Espectrometria de Massas em Tandem
Tolbutamida/análogos & derivados
Tolbutamida/farmacocinética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (4'-hydroxytolbutamide); 0 (Triterpenes); 982XCM1FOI (Tolbutamide); 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); V8A45XYI21 (cucurbitacin E)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150911
[St] Status:MEDLINE
[do] DOI:10.1007/s11427-015-4911-7


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[PMID]:27224941
[Au] Autor:Ramakrishna R; Bhateria M; Singh R; Bhatta RS
[Ad] Endereço:Pharmacokinetics and Metabolism Division, CSIR-Central Drug Research Institute, Lucknow, 226031, Uttar Pradesh, India; Academy of Scientific and Innovative Research, New Delhi, 110001, India.
[Ti] Título:Evaluation of the impact of 16-dehydropregnenolone on the activity and expression of rat hepatic cytochrome P450 enzymes.
[So] Source:J Steroid Biochem Mol Biol;163:183-92, 2016 10.
[Is] ISSN:1879-1220
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:16-dehydropregnenolone (DHP) is a promising novel antihyperlipidemic agent developed and patented by Central Drug Research Institute (CDRI), India. The purpose of the present study was to investigate whether DHP influences the activities and mRNA expression of hepatic drug-metabolizing cytochrome P450 (CYP) enzymes (CYP1A2, CYP2C11, CYP2D2, CYP2E1 and CYP3A1) in Sprague-Dawley (SD) rats. A cocktail suspension of CYP probe substrates which contained caffeine (CYP1A2), tolbutamide (CYP2C11), dextromethorphan (CYP2D2), chlorzoxazone (CYP2E1) and dapsone (CYP3A1) was administered orally on eighth- or fifteenth-day to rats pre-treated with DHP intragastrically at a dose of 36 and 72mg/kg for one week and two weeks. The concentrations of probe drugs in plasma were estimated by liquid chromatography-tandem mass spectrometry (LC-MS/MS). Alongside, the effect of DHP on CYPs activity and mRNA expression levels were assayed in isolated rat liver microsomes and by real-time reverse transcription-polymerase chain reaction (RT-PCR), respectively. DHP had significant inducing effects on CYP1A2, 2C11, 2D2 and 2E1 with no effect on CYP3A1 in dose- and time-dependent manner, as revealed from the pharmacokinetic profiles of the probe drugs in rats. In-vitro microsomal activities and mRNA expression results were in good agreement with the in-vivo pharmacokinetic results. Collectively, the results unveiled that DHP is an inducer of rat hepatic CYP enzymes. Hence, intense attention should be paid when DHP is co-administered with drugs metabolized by CYP1A2, 2C11, 2D2 and 2E1, which might result in drug-drug interactions and therapeutic failure.
[Mh] Termos MeSH primário: Hidrocarboneto de Aril Hidroxilases/genética
Citocromo P-450 CYP1A2/genética
Citocromo P-450 CYP2E1/genética
Citocromo P-450 CYP3A/genética
Família 2 do Citocromo P450/genética
Hipolipemiantes/farmacocinética
Pregnenolona/análogos & derivados
Esteroide 16-alfa-Hidroxilase/genética
[Mh] Termos MeSH secundário: Administração Oral
Animais
Hidrocarboneto de Aril Hidroxilases/metabolismo
Cafeína/metabolismo
Cafeína/farmacologia
Clorzoxazona/metabolismo
Clorzoxazona/farmacologia
Citocromo P-450 CYP1A2/metabolismo
Citocromo P-450 CYP2E1/metabolismo
Citocromo P-450 CYP3A/metabolismo
Família 2 do Citocromo P450/metabolismo
Dapsona/metabolismo
Dapsona/farmacologia
Dextrometorfano/metabolismo
Dextrometorfano/farmacologia
Regulação da Expressão Gênica
Hipolipemiantes/administração & dosagem
Fígado/efeitos dos fármacos
Fígado/enzimologia
Masculino
Microssomos Hepáticos/efeitos dos fármacos
Microssomos Hepáticos/enzimologia
Pregnenolona/administração & dosagem
Pregnenolona/farmacocinética
Ratos
Ratos Sprague-Dawley
Esteroide 16-alfa-Hidroxilase/metabolismo
Tolbutamida/metabolismo
Tolbutamida/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hypolipidemic Agents); 3G6A5W338E (Caffeine); 7349506P5S (16-dehydropregnenolone); 7355X3ROTS (Dextromethorphan); 73R90F7MQ8 (Pregnenolone); 8W5C518302 (Dapsone); 982XCM1FOI (Tolbutamide); EC 1.14.13.- (Cytochrome P-450 CYP2E1); EC 1.14.14.1 (Aryl Hydrocarbon Hydroxylases); EC 1.14.14.1 (CYP2C11 protein, rat); EC 1.14.14.1 (Cyp1a2 protein, rat); EC 1.14.14.1 (Cyp2d2 protein, rat); EC 1.14.14.1 (Cyp3a1 protein, rat); EC 1.14.14.1 (Cytochrome P-450 CYP1A2); EC 1.14.14.1 (Cytochrome P-450 CYP3A); EC 1.14.14.1 (Cytochrome P450 Family 2); EC 1.14.14.1 (Steroid 16-alpha-Hydroxylase); H0DE420U8G (Chlorzoxazone)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171113
[Lr] Data última revisão:
171113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160526
[St] Status:MEDLINE


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[PMID]:27137992
[Au] Autor:Rysz M; Bromek E; Haduch A; Liskova B; Wójcikowski J; Daniel WA
[Ad] Endereço:Institute of Pharmacology, Polish Academy of Sciences, Smetna 12, 31-343 Kraków, Poland.
[Ti] Título:The reverse role of the hypothalamic paraventricular (PVN) and arcuate (ARC) nuclei in the central serotonergic regulation of the liver cytochrome P450 isoform CYP2C11.
[So] Source:Biochem Pharmacol;112:82-9, 2016 Jul 15.
[Is] ISSN:1873-2968
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Our recent work showed that the brain serotonergic system negatively regulated liver cytochrome P450. The aim of our present research was to study the effect of damage to the serotonergic innervation of the paraventricular (PVN) or arcuate nuclei (ARC) of the hypothalamus on the neuroendocrine regulation of cytochrome P450 (CYP). Male rats received bilateral injections of the serotonergic neurotoxin 5,7-dihydroxytryptamine (5,7-DHT) into the PVN or ARC. One week after the injection brain neurotransmitters, serum hormones (growth hormone, testosterone, corticosterone, thyroid hormones), pituitary somatostatin and liver cytochrome P450 expression and activity were measured. Lesion of the serotonergic innervation of the PVN decreased serotonin level in the hypothalamic area containing the PVN, causing an increase in growth hormone and testosterone concentrations in the blood and, subsequently, an increase in the expression (mRNA and protein level) and activity of isoform CYP2C11 in the liver. In contrast, damage to the serotonergic innervation of the ARC, which caused a decrease in serotonin level in the hypothalamic area containing the ARC, reduced the concentration of growth hormone and the expression and activity of CYP2C11. In conclusion, the obtained results show a reverse effect of the serotonergic innervation of the hypothalamic paraventricular (a negative effect) and arcuate nuclei (a positive effect) on growth hormone secretion and growth hormone-dependent CYP2C11 expression. They also suggest that CYP2C11 expression may be changed by drugs acting via the serotonergic system, their effect depending on their mechanism of action, route of administration (intracerebral, peripheral) and distribution pattern within the hypothalamus.
[Mh] Termos MeSH primário: 5,7-Di-Hidroxitriptamina/farmacologia
Núcleo Arqueado do Hipotálamo/efeitos dos fármacos
Hidrocarboneto de Aril Hidroxilases/genética
Família 2 do Citocromo P450/genética
Fígado/efeitos dos fármacos
Núcleo Hipotalâmico Paraventricular/efeitos dos fármacos
Serotonina/metabolismo
Esteroide 16-alfa-Hidroxilase/genética
[Mh] Termos MeSH secundário: Animais
Núcleo Arqueado do Hipotálamo/metabolismo
Masculino
Núcleo Hipotalâmico Paraventricular/metabolismo
Hormônios Hipofisários/sangue
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Pituitary Hormones); 31363-74-3 (5,7-Dihydroxytryptamine); 333DO1RDJY (Serotonin); 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:1705
[Cu] Atualização por classe:170523
[Lr] Data última revisão:
170523
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160504
[St] Status:MEDLINE


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[PMID]:26887802
[Au] Autor:Liu Y; Pu QH; Wu MJ; Yu C
[Ad] Endereço:a Institute of Life Science, Chongqing Medical University , Chongqing , P.R. China.
[Ti] Título:Proteomic analysis for the impact of hypercholesterolemia on expressions of hepatic drug transporters and metabolizing enzymes.
[So] Source:Xenobiotica;46(10):940-7, 2016 Oct.
[Is] ISSN:1366-5928
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:1. Our objective is to investigate the alterations of hepatic drug transporters and metabolizing enzymes in hypercholesterolemia. Male Sprague-Dawley rats were fed high-cholesterol chows for 8 weeks to induce hypercholesterolemia. Protein levels of hepatic drug transporters and metabolizing enzymes were analyzed by iTRAQ labeling coupled with LC TRIPLE-TOF. 2. Total 239 differentially expressed proteins were identified using proteomic analysis. Among those, protein levels of hepatic drug transporters (MRP2, ABCD3, OAT2, SLC25A12, SCL38A3, SLC2A2 and SLC25A5) and metabolizing enzymes (CYP2B3, CYP2C7, CYP2C11, CYP2C13, CYP4A2 and UGT2B) were markedly reduced, but the levels of CYP2C6 and CYP2E1 were increased in hypercholesterolemia group compared to control. Decreased expressions of drug transporters MRP2 and OAT2 were further confirmed by real time quantitative PCR (RT-qPCR) and western blot. 3. Ingenuity pathway analysis revealed that these differentially expressed proteins were regulated by various signaling pathways including nuclear receptors and inflammatory cytokines. One of the nuclear receptor candidates, liver X receptor alpha (LXRα), was further validated by RT-qPCR and western blot. Additionally, LXRα agonist T0901317 rescued the reduced expressions of MRP2 and OAT2 in HepG2 cells in hypercholesterolemic serum treatment. 4. Our present results indicated that hypercholesterolemia affected the expressions of various drug transporters and metabolizing enzymes in liver via nuclear receptors pathway. Especially, decreased function of LXRα contributes to the reduced expressions of MRP2 and OAT2.
[Mh] Termos MeSH primário: Hipercolesterolemia/metabolismo
Fígado/metabolismo
Proteoma/metabolismo
[Mh] Termos MeSH secundário: Transportadores de Cassetes de Ligação de ATP/metabolismo
Translocador 2 do Nucleotídeo Adenina/metabolismo
Animais
Hidrocarboneto de Aril Hidroxilases/metabolismo
Transporte Biológico
Sistema Enzimático do Citocromo P-450/metabolismo
Família 2 do Citocromo P450/metabolismo
Transportador de Glucose Tipo 2/metabolismo
Glucuronosiltransferase/metabolismo
Masculino
Proteínas dos Microfilamentos/metabolismo
Antígenos de Histocompatibilidade Menor/metabolismo
Proteínas de Transporte da Membrana Mitocondrial/metabolismo
Transportadores de Ânions Orgânicos Sódio-Independentes/metabolismo
Ratos
Ratos Sprague-Dawley
Esteroide 16-alfa-Hidroxilase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Abcd3 protein, rat); 0 (Adenine Nucleotide Translocator 2); 0 (Glucose Transporter Type 2); 0 (Microfilament Proteins); 0 (Minor Histocompatibility Antigens); 0 (Mitochondrial Membrane Transport Proteins); 0 (Organic Anion Transporters, Sodium-Independent); 0 (Proteome); 0 (Slc22a7 protein, rat); 0 (Slc25a12 protein, rat); 9035-51-2 (Cytochrome P-450 Enzyme System); EC 1.14.14.1 (Aryl Hydrocarbon Hydroxylases); EC 1.14.14.1 (CYP2C11 protein, rat); EC 1.14.14.1 (Cyp2b3 protein, rat); EC 1.14.14.1 (Cyp2c13 protein, rat); EC 1.14.14.1 (Cyp2c7 protein, rat); EC 1.14.14.1 (Cytochrome P450 Family 2); EC 1.14.14.1 (Steroid 16-alpha-Hydroxylase); EC 1.14.15.3 (cytochrome P-450 CYP4A2 (rat)); EC 2.4.1.17 (Glucuronosyltransferase); EC 2.4.1.17 (glucuronosyltransferase 2B, rat)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170201
[Lr] Data última revisão:
170201
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160219
[St] Status:MEDLINE
[do] DOI:10.3109/00498254.2016.1144228


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[PMID]:26797788
[Au] Autor:Korashy HM; Ansari MA; Maayah ZH; Imam F; Raish M; Attafi IM; Alharbi NO; Moraished BA
[Ad] Endereço:Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh, Saudi Arabia.
[Ti] Título:Differential Effects of Sunitinib on the Expression Profiles of Xenobiotic-Metabolizing Enzymes and Transporters in Rat Liver and Kidneys.
[So] Source:Basic Clin Pharmacol Toxicol;119(2):173-83, 2016 Aug.
[Is] ISSN:1742-7843
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Sunitinib (SUN) is a multi-targeted tyrosine kinase inhibitor that was recently approved for the treatment of gastrointestinal tract and renal cancers. To date, very little is known about the effects of SUN on the expression of hepatic and renal xenobiotic-metabolizing enzymes (XMEs) and transporters. The present study was designed to investigate the capacity of chronic SUN treatment to modulate the mRNA and protein expression levels of phase I cytochrome P450 (CYP), phase II conjugating enzymes, and phase III transporters in rat liver and kidneys. For this purpose, SUN (25, 50 and 100 mg/kg) was injected IP into Wistar albino rats for 4 weeks; thereafter, the mRNA and protein expression levels of several XMEs and transporters were determined by RT-PCR and Western blot analysis, respectively. Real-time PCR analysis showed that SUN significantly induced the hepatic and renal CYP1A1, 1A2, 1B1, 2E1 and 4F4, whereas it inhibited CYP2C11 and 4A2. Furthermore, SUN specifically induced renal, but not hepatic, CYP2J3 and 3A2, while it induced only hepatic CYP4A1. With regard to phase II, SUN induced hepatic GSTA1 and UGT1A and renal NQO1 and UGT1A mRNA levels, whereas it inhibited renal GST1A expression. On the other hand, both renal and hepatic P-gp, MRP2 and BCRP transporters were significantly induced by SUN at the mRNA and protein expression levels. Importantly, these differential effects were associated with changes in oxidative stress genes and lipid peroxidation levels. In conclusion, SUN can serve as XME and transporters modulator, which potentially may counteract the efficacy of the treatment, adverse reactions and drug interactions in SUN treatment.
[Mh] Termos MeSH primário: Indóis/farmacologia
Rim/efeitos dos fármacos
Fígado/efeitos dos fármacos
Pirróis/farmacologia
[Mh] Termos MeSH secundário: Membro 2 da Subfamília G de Transportadores de Cassetes de Ligação de ATP/genética
Membro 2 da Subfamília G de Transportadores de Cassetes de Ligação de ATP/metabolismo
Transportadores de Cassetes de Ligação de ATP/genética
Transportadores de Cassetes de Ligação de ATP/metabolismo
Animais
Hidrocarboneto de Aril Hidroxilases/antagonistas & inibidores
Hidrocarboneto de Aril Hidroxilases/genética
Hidrocarboneto de Aril Hidroxilases/metabolismo
Citocromo P-450 CYP1A1/genética
Citocromo P-450 CYP1A1/metabolismo
Citocromo P-450 CYP1A2/genética
Citocromo P-450 CYP1A2/metabolismo
Citocromo P-450 CYP1B1/genética
Citocromo P-450 CYP1B1/metabolismo
Citocromo P-450 CYP2E1/genética
Citocromo P-450 CYP2E1/metabolismo
Sistema Enzimático do Citocromo P-450/genética
Sistema Enzimático do Citocromo P-450/metabolismo
Família 2 do Citocromo P450/antagonistas & inibidores
Família 2 do Citocromo P450/genética
Família 2 do Citocromo P450/metabolismo
Família 4 do Citocromo P450/genética
Família 4 do Citocromo P450/metabolismo
Glucuronosiltransferase/genética
Glucuronosiltransferase/metabolismo
Glutationa Transferase/genética
Glutationa Transferase/metabolismo
Isoenzimas/genética
Isoenzimas/metabolismo
Rim/enzimologia
Peroxidação de Lipídeos/efeitos dos fármacos
Fígado/enzimologia
Masculino
NAD(P)H Desidrogenase (Quinona)/genética
NAD(P)H Desidrogenase (Quinona)/metabolismo
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Ratos
Ratos Wistar
Esteroide 16-alfa-Hidroxilase/antagonistas & inibidores
Esteroide 16-alfa-Hidroxilase/genética
Esteroide 16-alfa-Hidroxilase/metabolismo
Transcriptoma
Xenobióticos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ATP Binding Cassette Transporter, Sub-Family G, Member 2); 0 (Abcc2 protein, rat); 0 (Abcg2 protein, rat); 0 (Indoles); 0 (Isoenzymes); 0 (Pyrroles); 0 (RNA, Messenger); 0 (Ugt1a1 protein, rat); 0 (Xenobiotics); 9035-51-2 (Cytochrome P-450 Enzyme System); EC 1.14.13.- (Cytochrome P-450 CYP2E1); EC 1.14.14.1 (Aryl Hydrocarbon Hydroxylases); EC 1.14.14.1 (CYP2C11 protein, rat); EC 1.14.14.1 (Cyp1a2 protein, rat); EC 1.14.14.1 (Cyp1b1 protein, rat); EC 1.14.14.1 (Cyp4f4 protein, rat); EC 1.14.14.1 (Cytochrome P-450 CYP1A1); EC 1.14.14.1 (Cytochrome P-450 CYP1A2); EC 1.14.14.1 (Cytochrome P-450 CYP1B1); EC 1.14.14.1 (Cytochrome P450 Family 2); EC 1.14.14.1 (Cytochrome P450 Family 4); EC 1.14.14.1 (Steroid 16-alpha-Hydroxylase); EC 1.14.15.3 (cytochrome P-450 CYP4A2 (rat)); EC 1.6.5.2 (NAD(P)H Dehydrogenase (Quinone)); EC 1.6.5.2 (NQO1 protein, rat); EC 2.4.1.17 (Glucuronosyltransferase); EC 2.5.1.18 (Glutathione Transferase); EC 2.5.1.18 (glutathione S-transferase alpha); V99T50803M (sunitinib)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170308
[Lr] Data última revisão:
170308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160123
[St] Status:MEDLINE
[do] DOI:10.1111/bcpt.12555


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[PMID]:26772189
[Au] Autor:Hye Khan MA; Fish B; Wahl G; Sharma A; Falck JR; Paudyal MP; Moulder JE; Imig JD; Cohen EP
[Ad] Endereço:Department of Pharmacology & Toxicology, Medical College of Wisconsin, Milwaukee, WI 53226, U.S.A.
[Ti] Título:Epoxyeicosatrienoic acid analogue mitigates kidney injury in a rat model of radiation nephropathy.
[So] Source:Clin Sci (Lond);130(8):587-99, 2016 Apr.
[Is] ISSN:1470-8736
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Arachidonic acid is metabolized to epoxyeicosatrienoic acids (EETs) by CYP epoxygenases, and EETs are kidney protective in multiple pathologies. We determined the ability of an EET analogue, EET-A, to mitigate experimental radiation nephropathy. The kidney expression of the EET producing enzyme CYP2C11 was lower in rats that received total body irradiation (TBI rat) compared with non-irradiated control. At 12 weeks after TBI, the rats had higher systolic blood pressure and impaired renal afferent arteriolar function compared with control, and EET-A or captopril mitigated these abnormalities. The TBI rats had 3-fold higher blood urea nitrogen (BUN) compared with control, and EET-A or captopril decreased BUN by 40-60%. The urine albumin/creatinine ratio was increased 94-fold in TBI rats, and EET-A or captopril attenuated that increase by 60-90%. In TBI rats, nephrinuria was elevated 30-fold and EET-A or captopril decreased it by 50-90%. Renal interstitial fibrosis, tubular and glomerular injury were present in the TBI rats, and each was decreased by EET-A or captopril. We further demonstrated elevated renal parenchymal apoptosis in TBI rats, which was mitigated by EET-A or captopril. Additional studies revealed that captopril or EET-A mitigated renal apoptosis by acting on the p53/Fas/FasL (Fas ligand) apoptotic pathway. The present study demonstrates a novel EET analogue-based strategy for mitigation of experimental radiation nephropathy by improving renal afferent arteriolar function and by decreasing renal apoptosis.
[Mh] Termos MeSH primário: Lesão Renal Aguda/prevenção & controle
Eicosanoides/farmacologia
Rim/efeitos dos fármacos
Rim/efeitos da radiação
Lesões Experimentais por Radiação/prevenção & controle
Protetores contra Radiação/farmacologia
[Mh] Termos MeSH secundário: Lesão Renal Aguda/metabolismo
Lesão Renal Aguda/patologia
Lesão Renal Aguda/fisiopatologia
Albuminúria/metabolismo
Albuminúria/prevenção & controle
Inibidores da Enzima Conversora de Angiotensina/farmacologia
Animais
Apoptose/efeitos dos fármacos
Hidrocarboneto de Aril Hidroxilases/metabolismo
Pressão Sanguínea/efeitos dos fármacos
Nitrogênio da Ureia Sanguínea
Captopril/farmacologia
Família 2 do Citocromo P450
Citoproteção
Proteína Ligante Fas/metabolismo
Fibrose
Hipertensão/metabolismo
Hipertensão/fisiopatologia
Hipertensão/prevenção & controle
Rim/irrigação sanguínea
Rim/metabolismo
Rim/patologia
Masculino
Lesões Experimentais por Radiação/metabolismo
Lesões Experimentais por Radiação/patologia
Lesões Experimentais por Radiação/fisiopatologia
Ratos
Circulação Renal/efeitos dos fármacos
Transdução de Sinais/efeitos dos fármacos
Esteroide 16-alfa-Hidroxilase/metabolismo
Receptor fas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (Angiotensin-Converting Enzyme Inhibitors); 0 (Eicosanoids); 0 (Fas Ligand Protein); 0 (Radiation-Protective Agents); 0 (Tnfrsf6 protein, rat); 0 (Tnfsf6 protein, rat); 0 (fas Receptor); 9G64RSX1XD (Captopril); 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:1607
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160117
[St] Status:MEDLINE
[do] DOI:10.1042/CS20150778


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[PMID]:25834921
[Au] Autor:Yin S; Cheng Y; Li T; Dong M; Zhao H; Liu G
[Ad] Endereço:a Department of Pharmacy , The Second Affiliated Hospital, Harbin Medical University , Harbin , PR China and.
[Ti] Título:Effects of notoginsenoside R1 on CYP1A2, CYP2C11, CYP2D1, and CYP3A1/2 activities in rats by cocktail probe drugs.
[So] Source:Pharm Biol;54(2):231-6, 2016.
[Is] ISSN:1744-5116
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:CONTEXT: Notoginsenoside R1 (NGR1) is the main component with cardiovascular activity in Panax notoginseng (Burk.) F. H. Chen, an herbal medicine that is widely used to enhance blood circulation and dissipate blood stasis. OBJECTIVE: The objective of this study is to investigate NGR1's effects on CYP1A2, CYP2C11, CYP2D1, and CYP3A1/2 activities in rats in vivo through the use of the Cytochrome P450 (CYP450) probe drugs. MATERIALS AND METHODS: After pretreatment with NGR1 or physiological saline, the rats were administered intraperitoneally with a mixture solution of cocktail probe drugs containing caffeine (10 mg/kg), tolbutamide (15 mg/kg), metoprolol (20 mg/kg), and dapsone (10 mg/kg). The bloods were then collected at a set of time-points for the ultra-performance liquid chromatography/tandem mass spectrometry (UPLC-MS/MS) analysis. RESULTS: NGR1 was shown to exhibit an inhibitory effect on CYP1A2 by increased caffeine Cmax (43.13%, p < 0.01) and AUC0 - ∞ (40.57%, p < 0.01), and decreased CL/F (62.16%, p < 0.01) in the NGR1-treated group compared with those of the control group, but no significant changes in pharmacokinetic parameters of tolbutamide, metoprolol, and dapsone were observed between the two groups, indicating that NGR1 had no effects on rat CYP2C11, CYP2D1, and CYP3A1/2. DISCUSSION AND CONCLUSION: When NGR1 is co-administered with drugs that are metabolized by CYP1A2, the pertinent potential herb-drug interactions should be monitored.
[Mh] Termos MeSH primário: Oxirredutases do Álcool/antagonistas & inibidores
Hidrocarboneto de Aril Hidroxilases/antagonistas & inibidores
Citocromo P-450 CYP3A/metabolismo
Citocromos/antagonistas & inibidores
Ginsenosídeos/farmacologia
Interações Ervas-Drogas
Preparações Farmacêuticas/sangue
Esteroide 16-alfa-Hidroxilase/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Citocromo P-450 CYP1A2
Família 2 do Citocromo P450
Ginsenosídeos/administração & dosagem
Ginsenosídeos/isolamento & purificação
Masculino
Panax notoginseng/química
Preparações Farmacêuticas/administração & dosagem
Ratos Wistar
Especificidade por Substrato
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cytochromes); 0 (Ginsenosides); 0 (Pharmaceutical Preparations); EC 1.1.- (Alcohol Oxidoreductases); EC 1.14.14.1 (Aryl Hydrocarbon Hydroxylases); EC 1.14.14.1 (CYP2C11 protein, rat); EC 1.14.14.1 (Cyp1a2 protein, rat); EC 1.14.14.1 (Cyp2d1 protein, rat); EC 1.14.14.1 (Cyp3a1 protein, rat); EC 1.14.14.1 (Cyp3a2 protein, rat); EC 1.14.14.1 (Cytochrome P-450 CYP1A2); EC 1.14.14.1 (Cytochrome P-450 CYP3A); EC 1.14.14.1 (Cytochrome P450 Family 2); EC 1.14.14.1 (Steroid 16-alpha-Hydroxylase); Z62692362Z (notoginsenoside R1)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150404
[St] Status:MEDLINE
[do] DOI:10.3109/13880209.2015.1029051


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[PMID]:26757108
[Au] Autor:Borek-Dohalska L; Valaskova P; Kubickova B; Sulc M; Kresinova Z; Cajthaml T; Stiborova M
[Ad] Endereço:Department of Biochemistry, Faculty of Science, Charles University, Prague, Czech Republic.
[Ti] Título:A study on 17alpha-ethinylestradiol metabolism in rat and Pleurotus ostreatus.
[So] Source:Neuro Endocrinol Lett;36 Suppl 1:5-12, 2015.
[Is] ISSN:0172-780X
[Cp] País de publicação:Sweden
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: 17α-Ethinylestradiol (EE2) is an endocrine disruptor that is an ingredient of oral contraceptives. Here, EE2 metabolism catalyzed by cytochromes P450 (CYP) was studied. Two model organisms, rat and ligninolytic fungus Pleurotus ostreatus, were used. METHODS: To resolve the role of rat and/or fungal CYPs in EE2 oxidation, microsomes were incubated with EE2 and NADPH or cumene hydroperoxide. Using Supersomes™, we examined which of rat CYPs oxidize EE2. RESULTS: EE2 is effectively degraded by P. ostreatus in vivo. In vitro, EE2 is metabolized by CYPs by the NADPH-dependent and organic hydroperoxide-dependent mechanisms. Rat hepatic microsomes metabolize EE2 in the presence of NADPH to three products; two of them are hydroxylated EE2 derivatives. Using rat Supersomes™ we found that EE2 is hydroxylated by several rat CYPs, among them CYP2C6 and 2C11 are most efficient in 2-hydroxy-EE2 formation, while CYP2A and 3A catalyze EE2 hydroxylation to the second product. On the contrary, the products of the NADPH-dependent hydroxylating reactions were not detected in Pleurotus ostreatus. During the reaction of EE2 in microsomes isolated from rat and P. ostreatus in the presence of the alternate oxidant, cumene hydroperoxide, another metabolite, different from the above mentioned products, is generated. Rat CYP1A1 is the most efficient enzyme catalyzing formation of this EE2 product. CONCLUSION: The results suggest that CYPs play a role in EE2 metabolism in rat and P. ostreatus. To our knowledge this is the first finding describing ligninolythic fungal metabolism of EE2 by CYP in the presence of cumene hydroperoxide.
[Mh] Termos MeSH primário: Sistema Enzimático do Citocromo P-450/metabolismo
Etinilestradiol/metabolismo
Microssomos Hepáticos/metabolismo
[Mh] Termos MeSH secundário: Animais
Hidrocarboneto de Aril Hidroxilases/metabolismo
Cromatografia Líquida de Alta Pressão
Citocromo P-450 CYP1A1/metabolismo
Citocromo P-450 CYP3A/metabolismo
Família 2 do Citocromo P450
Hidroxilação
Masculino
Microssomos Hepáticos/enzimologia
Oxirredução
Pleurotus
Ratos
Ratos Wistar
Esteroide 16-alfa-Hidroxilase/metabolismo
Esteroide 21-Hidroxilase/metabolismo
Esteroide Hidroxilases/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
423D2T571U (Ethinyl Estradiol); 9035-51-2 (Cytochrome P-450 Enzyme System); EC 1.14.- (Steroid Hydroxylases); EC 1.14.14.1 (Aryl Hydrocarbon Hydroxylases); EC 1.14.14.1 (CYP2C11 protein, rat); EC 1.14.14.1 (Cyp2c6v1 protein, rat); EC 1.14.14.1 (Cytochrome P-450 CYP1A1); EC 1.14.14.1 (Cytochrome P-450 CYP3A); EC 1.14.14.1 (Cytochrome P450 Family 2); EC 1.14.14.1 (Steroid 16-alpha-Hydroxylase); EC 1.14.14.1 (steroid hormone 7-alpha-hydroxylase); EC 1.14.14.16 (Steroid 21-Hydroxylase)
[Em] Mês de entrada:1604
[Cu] Atualização por classe:161126
[Lr] Data última revisão:
161126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160113
[St] Status:MEDLINE


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[PMID]:26434126
[Au] Autor:Ahmad A; Khan RM; Alkharfy KM; Raish M; Al-Jenoobi FI; Al-Mohizea AM
[Ti] Título:Effects of Thymoquinone on the Pharmacokinetics and Pharmacodynamics of Glibenclamide in a Rat Model.
[So] Source:Nat Prod Commun;10(8):1395-8, 2015 Aug.
[Is] ISSN:1934-578X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Glibenclamide and thymoquinone plasma concentrations were analysed using a sensitive RP-HPLC method, and non-compartmental model pharmacokinetic parameters were calculated. The maximum reduction in blood glucose level was observed 3 hours following glibenclamide administration, which reached 47.4% of baseline, whereas it was reduced by 53.0% to 56.2% when co-administrated with thymoquinone. Plasma concentration of glibenclamide was increased by 13.4% and 21.8% by the co-administration of thymoquinone as single and multiple doses, respectively (P<0.05). The AUC and TI/2 of glibenclamide were also increased respectively by 32.0% and 17.4% with a thymoquinone single dose, and by 52.5% and 92.8% after chronic treatment. Furthermore, diabetic rats treated with thymoquinone demonstrated a marked decrease in hepatic protein expressions of CYP3A2 and CYP2C 11 enzymes that are responsible for the metabolism of glibenclamide. The current data suggest that thymoquinone exhibits a synergistic effect with glibenclamide on glucose level, which could be explained by reducing CYP450 activity at the protein level.
[Mh] Termos MeSH primário: Benzoquinonas/administração & dosagem
Diabetes Mellitus Experimental/tratamento farmacológico
Glibureto/farmacocinética
Hipoglicemiantes/farmacocinética
Nigella/química
Extratos Vegetais/administração & dosagem
[Mh] Termos MeSH secundário: Animais
Hidrocarboneto de Aril Hidroxilases/genética
Hidrocarboneto de Aril Hidroxilases/metabolismo
Glicemia/metabolismo
Citocromo P-450 CYP3A/genética
Citocromo P-450 CYP3A/metabolismo
Família 2 do Citocromo P450
Diabetes Mellitus Experimental/enzimologia
Diabetes Mellitus Experimental/genética
Diabetes Mellitus Experimental/metabolismo
Modelos Animais de Doenças
Interações Medicamentosas
Seres Humanos
Masculino
Ratos
Ratos Wistar
Esteroide 16-alfa-Hidroxilase/genética
Esteroide 16-alfa-Hidroxilase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benzoquinones); 0 (Blood Glucose); 0 (Hypoglycemic Agents); 0 (Plant Extracts); 490-91-5 (thymoquinone); EC 1.14.14.1 (Aryl Hydrocarbon Hydroxylases); EC 1.14.14.1 (CYP2C11 protein, rat); EC 1.14.14.1 (Cyp3a2 protein, rat); EC 1.14.14.1 (Cytochrome P-450 CYP3A); EC 1.14.14.1 (Cytochrome P450 Family 2); EC 1.14.14.1 (Steroid 16-alpha-Hydroxylase); SX6K58TVWC (Glyburide)
[Em] Mês de entrada:1511
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151006
[St] Status:MEDLINE



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