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Pesquisa : D02.455.426.559.389.657.393 [Categoria DeCS]
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  1 / 4019 MEDLINE  
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[PMID]:29421518
[Au] Autor:Luo H; Liang H; Chen Y; Chen S; Xu Y; Xu L; Liu J; Zhou K; Peng J; Guo G; Lai B; Song L; Yang H; Liu L; Peng J; Liu Z; Tang L; Chen W; Tang H
[Ad] Endereço:Department of Environmental and Occupational Health, Dongguan Key Laboratory of Environmental Medicine, School of Public Health, Guangdong Medical University, Dongguan, China.
[Ti] Título:miR-7-5p overexpression suppresses cell proliferation and promotes apoptosis through inhibiting the ability of DNA damage repair of PARP-1 and BRCA1 in TK6 cells exposed to hydroquinone.
[So] Source:Chem Biol Interact;283:84-90, 2018 Mar 01.
[Is] ISSN:1872-7786
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Hydroquinone (HQ), one of the major metabolic products of benzene, is a carcinogen, which induces apoptosis and inhibit proliferation in lymphoma cells. microRNA-7-5p (miR-7-5p), a tumor suppressor, participates in various biological processes including cell proliferation and apoptosis regulation by repressing expression of specific oncogenic target genes. To explore whether miR-7-5p is involved in HQ-induced cell proliferation and apoptosis, we assessed the effect of miR-7-5p overexpression on induction of apoptosis analyzed by FACSCalibur flow cytometer in transfection of TK6 cells with miR-7-5p mimic (TK6- miR-7-5p). We observed an increased apoptosis by 25.43% and decreased proliferation by 28.30% in TK6-miR-7-5p cells compared to those negative control cells (TK6-shNC) in response to HQ treatment. Furthermore, HQ might active the apoptotic pathway via partly downregulation the expression of BRCA1 and PARP-1, followed by p53 activation, in TK6-miR-7-5p cells. In contrast, attenuated p53 and BRCA1 expression was observed in shPARP-1 cells than in NC cells after HQ treatment. Therefore, we conclude that HQ may activate apoptotic signals via inhibiting the tumor suppressive effects of miR-7-5p, which may be mediated partly by upregulating the expression of PARP-1 and BRCA1 in control cells. The increase of miR-7-5p expression further intensified downregulation of PARP-1 and BRCA1 in TK6-miR-7-5p cells, resulting in an increase of apoptosis and proliferation inhibited.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Proteína BRCA1/metabolismo
Proliferação Celular/efeitos dos fármacos
Reparo do DNA/efeitos dos fármacos
Hidroquinonas/farmacologia
MicroRNAs/metabolismo
Poli(ADP-Ribose) Polimerase-1/metabolismo
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas
Antagomirs/metabolismo
Proteína BRCA1/genética
Caspase 3/metabolismo
Linhagem Celular Tumoral
Regulação para Baixo/efeitos dos fármacos
Seres Humanos
MicroRNAs/antagonistas & inibidores
MicroRNAs/genética
Poli(ADP-Ribose) Polimerase-1/antagonistas & inibidores
Poli(ADP-Ribose) Polimerase-1/genética
Interferência de RNA
RNA Interferente Pequeno/metabolismo
Proteína Supressora de Tumor p53/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (Antagomirs); 0 (BRCA1 Protein); 0 (BRCA1 protein, human); 0 (Hydroquinones); 0 (MicroRNAs); 0 (RNA, Small Interfering); 0 (Tumor Suppressor Protein p53); EC 2.4.2.30 (PARP1 protein, human); EC 2.4.2.30 (Poly (ADP-Ribose) Polymerase-1); EC 3.4.22.- (Caspase 3); XV74C1N1AE (hydroquinone)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180209
[St] Status:MEDLINE


  2 / 4019 MEDLINE  
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[PMID]:28602139
[Au] Autor:Liu RH; Wang DQ; Zhang PZ; Shao F; Chen LY; Huang HL; Lin S
[Ad] Endereço:a The College of Pharmacy , Jiangxi University of Traditional Chinese Medicine , Nanchang , China.
[Ti] Título:A new diaryl 1, 2-diketone from the heartwood of Dalbergia latifolia.
[So] Source:Nat Prod Res;32(1):91-96, 2018 Jan.
[Is] ISSN:1478-6427
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:A new diaryl 1,2-diketone, named 1-(2,5-dihydroxy-4-methoxyphenyl)-2-phenylethane-1,2-dione (1), along with eight known compounds (2-9), were isolated from the heartwood of Dalbergia latifolia. They were identified on the basis of spectral data. Compounds 1-7 were obtained from the Dalbergia genus for the first time. Compounds 8 and 9 were firstly isolated from the plant. Compound 1 exhibited inactive against Staphylococcus aureus ATCC 6538 and Escherichia coli ATCC 21530 with the minimum inhibitory concentrations of 10.0 and 10.0 mg/mL, respectively.
[Mh] Termos MeSH primário: Antibacterianos/química
Dalbergia/química
Hidroquinonas/química
Cetonas/química
[Mh] Termos MeSH secundário: Antibacterianos/farmacologia
Escherichia coli/efeitos dos fármacos
Hidroquinonas/farmacologia
Cetonas/farmacologia
Espectroscopia de Ressonância Magnética
Testes de Sensibilidade Microbiana
Estrutura Molecular
Staphylococcus aureus/efeitos dos fármacos
Madeira/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (Hydroquinones); 0 (Ketones)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170613
[St] Status:MEDLINE
[do] DOI:10.1080/14786419.2017.1338280


  3 / 4019 MEDLINE  
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[PMID]:28467382
[Au] Autor:Chang NF; Chen YS; Lin YJ; Tai TH; Chen AN; Huang CH; Lin CC
[Ad] Endereço:Department of Cosmetic Science, Providence University, 200, Sec. 7, Taiwan Boulevard, Shalu Dist., Taichung 43301, Taiwan. nfchang@pu.edu.tw.
[Ti] Título:Study of Hydroquinone Mediated Cytotoxicity and Hypopigmentation Effects from UVB-Irradiated Arbutin and DeoxyArbutin.
[So] Source:Int J Mol Sci;18(5), 2017 May 03.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Arbutin (Arb) and deoxyArbutin (dA) are both effective hypopigmentation agents. However, they are glucoside derivatives of hydroquinone (HQ), which may be decayed into HQ under higher energy environments. Therefore, safety and toxicity are very important issues when considering the usage of these compounds. However, no study has verified the properties of Ultra-Violet B (UVB)-irradiated Arb and dA. In this work, we investigated the cytotoxicity and hypopigmentation effects of UVB-irradiated Arb and dA in Detroit 551 human fibroblast cells and B16-F10 mouse melanoma cells. The results showed that UVB-irradiated Arb and dA have strong cytotoxicity for the fibroblast cells, especially for dA, the caspase-3 is also activated by the treatment of UVB-irradiated dA in Detroit 551 cells. The results correlated with the produced HQ. In addition, UVB-irradiated Arb and dA suppressed the production of melanin in melanoma cells; this is due to the release of HQ that compensates for the UVB triggered Arb and dA decomposition.
[Mh] Termos MeSH primário: Arbutina/análogos & derivados
Sobrevivência Celular/efeitos dos fármacos
Hidroquinonas/toxicidade
Hipopigmentação/induzido quimicamente
[Mh] Termos MeSH secundário: Animais
Arbutina/efeitos da radiação
Arbutina/toxicidade
Caspase 3/efeitos dos fármacos
Células Cultivadas
Fibroblastos/efeitos dos fármacos
Glucosídeos
Seres Humanos
Hidroquinonas/efeitos da radiação
Melaninas/antagonistas & inibidores
Melanócitos/efeitos dos fármacos
Melanoma Experimental
Camundongos
Raios Ultravioleta
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glucosides); 0 (Hydroquinones); 0 (Melanins); C5INA23HXF (Arbutin); EC 3.4.22.- (CASP3 protein, human); EC 3.4.22.- (Caspase 3); RG969BY5EN (deoxyarbutin); XV74C1N1AE (hydroquinone)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE


  4 / 4019 MEDLINE  
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[PMID]:28461337
[Au] Autor:Wang Y; Landry AP; Ding H
[Ad] Endereço:From the Department of Biological Sciences, Louisiana State University, Baton Rouge, Louisiana 70803.
[Ti] Título:The mitochondrial outer membrane protein mitoNEET is a redox enzyme catalyzing electron transfer from FMNH to oxygen or ubiquinone.
[So] Source:J Biol Chem;292(24):10061-10067, 2017 06 16.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Increasing evidence suggests that mitoNEET, a target of the type II diabetes drug pioglitazone, is a key regulator of energy metabolism in mitochondria. MitoNEET is anchored to the mitochondrial outer membrane via its N-terminal α helix domain and hosts a redox-active [2Fe-2S] cluster in its C-terminal cytosolic region. The mechanism by which mitoNEET regulates energy metabolism in mitochondria, however, is not fully understood. Previous studies have shown that mitoNEET specifically interacts with the reduced flavin mononucleotide (FMNH ) and that FMNH can quickly reduce the mitoNEET [2Fe-2S] clusters. Here we report that the reduced mitoNEET [2Fe-2S] clusters can be readily oxidized by oxygen. In the presence of FMN, NADH, and flavin reductase, which reduces FMN to FMNH using NADH as the electron donor, mitoNEET mediates oxidation of NADH with a concomitant reduction of oxygen. Ubiquinone-2, an analog of ubiquinone-10, can also oxidize the reduced mitoNEET [2Fe-2S] clusters under anaerobic or aerobic conditions. Compared with oxygen, ubiquinone-2 is more efficient in oxidizing the mitoNEET [2Fe-2S] clusters, suggesting that ubiquinone could be an intrinsic electron acceptor of the reduced mitoNEET [2Fe-2S] clusters in mitochondria. Pioglitazone or its analog NL-1 appears to inhibit the electron transfer activity of mitoNEET by forming a unique complex with mitoNEET and FMNH The results suggest that mitoNEET is a redox enzyme that may promote oxidation of NADH to facilitate enhanced glycolysis in the cytosol and that pioglitazone may regulate energy metabolism in mitochondria by inhibiting the electron transfer activity of mitoNEET.
[Mh] Termos MeSH primário: Mononucleotídeo de Flavina/metabolismo
Hidroquinonas/metabolismo
Membranas Mitocondriais/enzimologia
Proteínas Mitocondriais/metabolismo
Ubiquinona/metabolismo
[Mh] Termos MeSH secundário: Espectroscopia de Ressonância de Spin Eletrônica
Transporte de Elétrons/efeitos dos fármacos
Metabolismo Energético/efeitos dos fármacos
Proteínas de Escherichia coli/genética
Proteínas de Escherichia coli/metabolismo
FMN Redutase/genética
FMN Redutase/metabolismo
Seres Humanos
Hipoglicemiantes/farmacologia
Cinética
Membranas Mitocondriais/efeitos dos fármacos
Membranas Mitocondriais/metabolismo
Proteínas Mitocondriais/química
Proteínas Mitocondriais/genética
Oxirredução
Fragmentos de Peptídeos/química
Fragmentos de Peptídeos/genética
Fragmentos de Peptídeos/metabolismo
Proteínas Recombinantes/química
Proteínas Recombinantes/metabolismo
Tiazóis/farmacologia
Tiazolidinedionas/farmacologia
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (5-(3,5-di-tert-butyl-4-hydroxybenzyl)-4-hydroxythiazol-2(5H)-one); 0 (CISD1 protein, human); 0 (Escherichia coli Proteins); 0 (Hydroquinones); 0 (Hypoglycemic Agents); 0 (Mitochondrial Proteins); 0 (Peptide Fragments); 0 (Recombinant Proteins); 0 (Thiazoles); 0 (Thiazolidinediones); 0 (flavin mononucleotide hydroquinone); 1339-63-5 (Ubiquinone); 7N464URE7E (Flavin Mononucleotide); EC 1.5.1.38 (FMN Reductase); EC 1.5.1.41 (Fre protein, E coli); I7T5V2W47R (Ubiquinone Q2); X4OV71U42S (pioglitazone)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171228
[Lr] Data última revisão:
171228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.789800


  5 / 4019 MEDLINE  
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[PMID]:27774770
[Au] Autor:Chen C; Jiang X; Gu S; Lai Y; Liu Y; Zhang Z
[Ad] Endereço:Department of Occupational and Environmental Health, West China School of Public Health, Sichuan University, Chengdu, Sichuan, People's Republic of China.
[Ti] Título:Protection of Nrf2 against arsenite-induced oxidative damage is regulated by the cyclic guanosine monophosphate-protein kinase G signaling pathway.
[So] Source:Environ Toxicol;32(8):2004-2020, 2017 Aug.
[Is] ISSN:1522-7278
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Arsenite has been shown to induce a variety of oxidative damage in mammalian cells. However, the mechanisms underlying cellular responses to its adverse effects remain unknown. We previously showed that the level of Nrf2, a nuclear transcription factor significantly increased in arsenite-treated human bronchial epithelial (HBE) cells suggesting that Nrf2 is involved in responding to arsenite-induced oxidative damage. To explore how Nrf2 can impact arsenite-induced oxidative damage, in this study, we examined Nrf2 activation and its regulation upon cellular arsenite exposure as well as its effects on arsenite-induced oxidative damage in HBE cells. We found that Nrf2 mRNA and protein levels were significantly increased by arsenite in a dose- and time-dependent manner. Furthermore, we showed that over-expression of Nrf2 significantly reduced the level of arsenite-induced oxidative damage in HBE cells including DNA damage, chromosomal breakage, lipid peroxidation and depletion of antioxidants. This indicates a protective role of Nrf2 against arsenite toxicity. This was further supported by the fact that activation of Nrf2 by its agonists, tertiary butylhydroquinone (t-BHQ) and sulforaphane (SFN) resulted in the same protective effects against arsenite toxicity. Moreover, we demonstrated that arsenite-induced activation of Nrf2 was mediated by the cyclic guanosine monophosphate (cGMP)-protein kinase G (PKG) signaling pathway. This is the first evidence showing that Nrf2 protects against arsenite-induced oxidative damage through the cGMP-PKG pathway. Our study suggests that activation of Nrf2 through the cGMP-PKG signaling pathway in HBE cells may be developed as a new strategy for prevention of arsenite toxicity. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 2004-2020, 2017.
[Mh] Termos MeSH primário: Arsenitos/toxicidade
Proteínas Quinases Dependentes de GMP Cíclico/metabolismo
Fator 2 Relacionado a NF-E2/metabolismo
Estresse Oxidativo/efeitos dos fármacos
[Mh] Termos MeSH secundário: Antioxidantes/metabolismo
Linhagem Celular
Seres Humanos
Hidroquinonas/farmacologia
Isotiocianatos/farmacologia
Fator 2 Relacionado a NF-E2/agonistas
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (Arsenites); 0 (Hydroquinones); 0 (Isothiocyanates); 0 (NF-E2-Related Factor 2); C12674942B (2-tert-butylhydroquinone); EC 2.7.11.12 (Cyclic GMP-Dependent Protein Kinases); GA49J4310U (sulforafan); N5509X556J (arsenite)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171212
[Lr] Data última revisão:
171212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE
[do] DOI:10.1002/tox.22374


  6 / 4019 MEDLINE  
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[PMID]:29061809
[Au] Autor:Maiuthed A; Pinkhien T; Chamni S; Suwanborirux K; Saito N; Petpiroon N; Chanvorachote P
[Ad] Endereço:Department of Pharmacology and Physiology, Faculty of Pharmaceutical Sciences, Chulalongkorn University, Bangkok, Thailand.
[Ti] Título:Apoptosis-inducing Effect of Hydroquinone 5- -Cinnamoyl Ester Analog of Renieramycin M on Non-small Cell Lung Cancer Cells.
[So] Source:Anticancer Res;37(11):6259-6267, 2017 11.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: A newly-synthesized derivative of renieramycin M (RM), an anticancer lead compound isolated from the blue sponge Xestospongia sp., hydroquinone 5-O-cinnamoyl ester (CIN-RM), was investigated here for its activity against non-small cell lung cancer cells. MATERIALS AND METHODS: Cytotoxicity effects of CIN-RM and RM on H292 lung cancer cells were determined by the MTT assay. We also investigated the mechanism of CIN-RM-mediated apoptosis and mechanism of action of this compound by western blotting. RESULTS: CIN-RM showed more potent cytotoxicity than its parental compound (RM) against H292 lung cancer cells. At concentrations of 15-60 µM, CIN-RM significantly induced apoptosis by increasing expression of apoptosis-inducing factor (AIF) and activation of caspase-3 and -9. For up-stream mechanism, CIN-RM mediated apoptosis through a p53-dependent mechanism, that consequently down-regulated anti-apoptotic B-cell lymphoma 2 (BCL2), while increasing the level of pro-apoptotic BCL2-associated X (BAX). In addition, phosphorylation of pro-survival protein AKT was found to be dramatically reduced. CONCLUSION: This study revealed the potential of CIN-RM for apoptosis induction and in the development of a novel anticancer agent.
[Mh] Termos MeSH primário: Carcinoma Pulmonar de Células não Pequenas/metabolismo
Hidroquinonas/farmacologia
Neoplasias Pulmonares/metabolismo
[Mh] Termos MeSH secundário: Apoptose
Fator de Indução de Apoptose/metabolismo
Carcinoma Pulmonar de Células não Pequenas/tratamento farmacológico
Caspase 3/metabolismo
Caspase 9/metabolismo
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Hidroquinonas/síntese química
Hidroquinonas/química
Neoplasias Pulmonares/tratamento farmacológico
Transdução de Sinais/efeitos dos fármacos
Tetra-Hidroisoquinolinas/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (AIFM1 protein, human); 0 (Apoptosis Inducing Factor); 0 (Hydroquinones); 0 (Tetrahydroisoquinolines); 0 (renieramycin M); EC 3.4.22.- (CASP3 protein, human); EC 3.4.22.- (CASP9 protein, human); EC 3.4.22.- (Caspase 3); EC 3.4.22.- (Caspase 9)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171026
[Lr] Data última revisão:
171026
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171025
[St] Status:MEDLINE


  7 / 4019 MEDLINE  
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[PMID]:28917452
[Au] Autor:Chaowattanapanit S; Silpa-Archa N; Kohli I; Lim HW; Hamzavi I
[Ad] Endereço:Department of Dermatology, Henry Ford Hospital, Detroit, Michigan; Department of Medicine, Faculty of Medicine, Srinagarind Hospital, Khon Kaen University, Khon Kaen, Thailand.
[Ti] Título:Postinflammatory hyperpigmentation: A comprehensive overview: Treatment options and prevention.
[So] Source:J Am Acad Dermatol;77(4):607-621, 2017 Oct.
[Is] ISSN:1097-6787
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Postinflammatory hyperpigmentation (PIH) occurs after various dermatoses, exogenous stimuli, and dermatologic procedures. The clinical course of PIH is chronic and unpredictable, although the probability of resolution of epidermal hyperpigmentation is better than those of dermal hyperpigmentation. PIH can be prevented or alleviated. When it does occur, the underlying inflammatory conditions should be sought and treated as the first step to reduce the progression of inflammation and PIH (which is an inflammatory consequence). If the inflammatory conditions subsides or there is no evidence of inflammation at the time of diagnosis, the treatments of PIH should be considered as the next step. Understanding the available treatment options helps the physician choose the appropriate treatment for each patient. Having a reproducible model for PIH is essential for the development of treatment modalities. The second article in this 2-part continuing medical education series on PIH specifically addresses the evidence that supports medical and procedural treatments of PIH and other forms of acquired hyperpigmentation. It also describes a PIH model and provides an algorithm for clinical practice along with discussion about the prevention of PIH.
[Mh] Termos MeSH primário: Dermatite/complicações
Fármacos Dermatológicos/uso terapêutico
Hiperpigmentação/terapia
Preparações Clareadoras de Pele/uso terapêutico
[Mh] Termos MeSH secundário: Antioxidantes/uso terapêutico
Abrasão Química
Combinação de Medicamentos
Seres Humanos
Hidroquinonas/uso terapêutico
Hiperpigmentação/prevenção & controle
Terapia a Laser
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antioxidants); 0 (Dermatologic Agents); 0 (Drug Combinations); 0 (Hydroquinones); 0 (Skin Lightening Preparations); XV74C1N1AE (hydroquinone)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170927
[Lr] Data última revisão:
170927
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170918
[St] Status:MEDLINE


  8 / 4019 MEDLINE  
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[PMID]:28844481
[Au] Autor:Bai J; Yu XJ; Liu KL; Wang FF; Li HB; Shi XL; Zhang Y; Huo CJ; Li X; Gao HL; Qi J; Liu JJ; Zhu GQ; Chen WS; Cui W; Kang YM
[Ad] Endereço:Department of Physiology and Pathophysiology, Xi'an Jiaotong University School of Basic Medical Sciences, Key Laboratory of Environment and Genes Related to Diseases (Xi'an Jiaotong University), Ministry of Education, Xi'an 710061, China.
[Ti] Título:Tert-butylhydroquinone attenuates oxidative stress and inflammation in hypothalamic paraventricular nucleus in high salt-induced hypertension.
[So] Source:Toxicol Lett;281:1-9, 2017 Nov 05.
[Is] ISSN:1879-3169
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Excessive oxidative stress and inflammation in hypothalamic paraventricular nucleus (PVN) are implicated in the pathogenesis of hypertension. It is reported that tert-butylhydroquinone (tBHQ), a nuclear factor erythroid 2-related factor 2(Nrf2)-inducer, has a variety of pharmacological activities such as anti-oxidation and anti-inflammatory effect. The objective of this study was to investigate the effects of tBHQ in high salt induced hypertension and to identify whether the beneficial effects were induced by inhibiting PVN oxidative stress and inflammation. Male Sprague-Dawley rats were fed with high salt diet (HS, 8% NaCl) or normal salt diet (NS, 0.3% NaCl). These rats were administration of tBHQ (150mg/kg/d) by oral gavage for 16 weeks. Our results showed that high salt intake resulted in higher mean arterial pressure, cardiac hypertrophy as well as increased plasma level of norepinephrine and interleukin (IL)-1ß, IL-6 compared with NS rats. It increased PVN level of reactive oxygen species, gp91 , IL-1ß, IL-6, p-IKKß and nuclear factor-kappa B (NF-κB) activity, decreased PVN level of Nrf2 and Cu/Zn-SOD. Chronic administration of tBHQ significantly attenuated these changes in HS rats. These data suggest that the protective effects of tBHQ in salt induced hypertension are partly due to inhibiting oxidative stress and inflammation in PVN.
[Mh] Termos MeSH primário: Hidroquinonas/farmacologia
Hipertensão/tratamento farmacológico
Inflamação/tratamento farmacológico
Estresse Oxidativo/efeitos dos fármacos
Núcleo Hipotalâmico Paraventricular/efeitos dos fármacos
Cloreto de Sódio na Dieta/efeitos adversos
[Mh] Termos MeSH secundário: Animais
Antioxidantes/farmacologia
Pressão Arterial
Modelos Animais de Doenças
Hipertensão/induzido quimicamente
Interleucina-1beta/sangue
Interleucina-6/sangue
Masculino
Glicoproteínas de Membrana/sangue
NADPH Oxidase 2
NADPH Oxidases/sangue
Fator 2 Relacionado a NF-E2/genética
Fator 2 Relacionado a NF-E2/metabolismo
Norepinefrina/sangue
Núcleo Hipotalâmico Paraventricular/metabolismo
Ratos
Ratos Sprague-Dawley
Espécies Reativas de Oxigênio/metabolismo
Cloreto de Sódio na Dieta/administração & dosagem
Superóxido Dismutase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (Hydroquinones); 0 (Interleukin-1beta); 0 (Interleukin-6); 0 (Membrane Glycoproteins); 0 (NF-E2-Related Factor 2); 0 (Nfe2l2 protein, rat); 0 (Reactive Oxygen Species); 0 (Sodium Chloride, Dietary); C12674942B (2-tert-butylhydroquinone); EC 1.15.1.1 (Superoxide Dismutase); EC 1.6.3.- (Cybb protein, rat); EC 1.6.3.- (NADPH Oxidase 2); EC 1.6.3.- (NADPH Oxidases); X4W3ENH1CV (Norepinephrine)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170829
[St] Status:MEDLINE


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[PMID]:28842207
[Au] Autor:Bai J; Yu XJ; Liu KL; Wang FF; Jing GX; Li HB; Zhang Y; Huo CJ; Li X; Gao HL; Qi J; Kang YM
[Ad] Endereço:Department of Physiology and Pathophysiology, Xi'an Jiaotong University School of Basic Medical Sciences, Key Laboratory of Environment and Genes Related to Diseases (Xi'an Jiaotong University), Ministry of Education, Xi'an 710061, China.
[Ti] Título:Central administration of tert-butylhydroquinone attenuates hypertension via regulating Nrf2 signaling in the hypothalamic paraventricular nucleus of hypertensive rats.
[So] Source:Toxicol Appl Pharmacol;333:100-109, 2017 Oct 15.
[Is] ISSN:1096-0333
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Reactive oxygen species (ROS) in the paraventricular nucleus (PVN) play a pivotal role in the pathogenesis of hypertension. Nuclear factor E2-related factor-2 (Nrf2) is an important transcription factor that modulates cell antioxidant defense response against oxidative stress. The present study aimed to explore the efficacy of PVN administration of tert-butylhydroquinone (tBHQ), a selective Nrf2 activator, in hypertensive rats. 16-week-old spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats were used in this study. These rats were chronic bilateral PVN infusion of tBHQ (0.8µg/day), or oxygen free radical scavenger tempol (20µg/h), or vehicle for 2weeks. SHR rats had higher mean arterial pressure (MAP), plasma norepinephrine (NE) levels, and sympathetic nerve activity (RSNA) and lower PVN levels of Nrf2, hemeoxygenase-1 (HO-1), superoxide dismutase-1 (SOD1) and catalase (CAT) as compared with those in the WKY group. Bilateral PVN infusion of tBHQ or tempol significantly reduced MAP, RSNA, plasma NE levels in SHR rats. In addition, tBHQ treatment enhanced the nuclear accumulation of Nrf2 and increased the expression of HO-1, CAT and SOD1 in SHR rats. Furthermore, tBHQ attenuated PVN levels of ROS, the expression of proinflammatory cytokines and restored the imbalance of neurotransmitters in PVN. Knockdown of Nrf2 in the PVN by adeno-associated virus mediated small interfering RNA abrogated the protective effects of tBHQ on hypertension. These findings suggest that PVN administration of tBHQ can attenuate hypertension by activation of the Nrf2-mediated signaling pathway.
[Mh] Termos MeSH primário: Anti-Hipertensivos/farmacologia
Hidroquinonas/farmacologia
Hipertensão/metabolismo
Fator 2 Relacionado a NF-E2/metabolismo
Núcleo Hipotalâmico Paraventricular/efeitos dos fármacos
[Mh] Termos MeSH secundário: Adenoviridae/genética
Animais
Anti-Hipertensivos/uso terapêutico
Pressão Arterial/efeitos dos fármacos
Hidroquinonas/uso terapêutico
Hipertensão/tratamento farmacológico
Hipertensão/fisiopatologia
Interleucina-1beta/genética
Interleucina-1beta/metabolismo
Interleucina-6/genética
Interleucina-6/metabolismo
Masculino
Fator 2 Relacionado a NF-E2/genética
Estresse Oxidativo/efeitos dos fármacos
Núcleo Hipotalâmico Paraventricular/metabolismo
RNA Interferente Pequeno/genética
Ratos Endogâmicos SHR
Ratos Endogâmicos WKY
Transdução de Sinais/efeitos dos fármacos
Sistema Nervoso Simpático/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antihypertensive Agents); 0 (Hydroquinones); 0 (Interleukin-1beta); 0 (Interleukin-6); 0 (NF-E2-Related Factor 2); 0 (RNA, Small Interfering); C12674942B (2-tert-butylhydroquinone)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170920
[Lr] Data última revisão:
170920
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170827
[St] Status:MEDLINE


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[PMID]:28704378
[Au] Autor:Szafran AT; Stossi F; Mancini MG; Walker CL; Mancini MA
[Ad] Endereço:Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas, United States of America.
[Ti] Título:Characterizing properties of non-estrogenic substituted bisphenol analogs using high throughput microscopy and image analysis.
[So] Source:PLoS One;12(7):e0180141, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Animal studies have linked the estrogenic properties of bisphenol A (BPA) to adverse effects on the endocrine system. Because of concerns for similar effects in humans, there is a desire to replace BPA in consumer products, and a search for BPA replacements that lack endocrine-disrupting bioactivity is ongoing. We used multiple cell-based models, including an established multi-parametric, high throughput microscopy-based platform that incorporates engineered HeLa cell lines with visible ERα- or ERß-regulated transcription loci, to discriminate the estrogen-like and androgen-like properties of previously uncharacterized substituted bisphenol derivatives and hydroquinone. As expected, BPA induced 70-80% of the estrogen-like activity via ERα and ERß compared to E2 in the HeLa prolactin array cell line. 2,2' BPA, Bisguaiacol F, CHDM 4-hydroxybuyl acrylate, hydroquinone, and TM modified variants of BPF showed very limited estrogen-like or androgen-like activity (< 10% of that observed with the control compounds). Interestingly, TM-BFP and CHDM 4-hydroxybuyl acrylate, but not their derivatives, demonstrated evidence of anti-estrogenic and anti-androgenic activity. Our findings indicate that Bisguaiacol F, TM-BFP-ER and TM-BPF-DGE demonstrate low potential for affecting estrogenic or androgenic endocrine activity. This suggest that the tested compounds could be suitable commercially viable alternatives to BPA.
[Mh] Termos MeSH primário: Estrogênios não Esteroides/farmacologia
Ensaios de Triagem em Larga Escala/métodos
Transcrição Genética/efeitos dos fármacos
[Mh] Termos MeSH secundário: Compostos Benzidrílicos/farmacologia
Receptor alfa de Estrogênio/metabolismo
Receptor beta de Estrogênio/metabolismo
Estrogênios não Esteroides/química
Células HeLa
Seres Humanos
Hidroquinonas/farmacologia
Células MCF-7
Microscopia
Estrutura Molecular
Fenóis/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benzhydryl Compounds); 0 (ESR2 protein, human); 0 (Estrogen Receptor alpha); 0 (Estrogen Receptor beta); 0 (Estrogens, Non-Steroidal); 0 (Hydroquinones); 0 (Phenols); 0 (estrogen receptor alpha, human); MLT3645I99 (bisphenol A); XV74C1N1AE (hydroquinone)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170921
[Lr] Data última revisão:
170921
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170714
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0180141



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