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[PMID]:29413004
[Au] Autor:Zobel M; Klotz K; Göen T
[Ad] Endereço:Institute and Outpatient Clinic of Occupational, Social and Environmental Medicine, Friedrich-Alexander Universität Erlangen-Nürnberg (FAU), Schillerstr. 25/29, D-91054 Erlangen, Germany.
[Ti] Título:LC-MS/MS procedure for the simultaneous determination of N-acetyl-S-(1-naphthyl)cysteine and N-acetyl-S-(2-napthyl)cysteine in human urine.
[So] Source:J Chromatogr B Analyt Technol Biomed Life Sci;1074-1075:139-145, 2018 Feb 01.
[Is] ISSN:1873-376X
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:A two-dimensional liquid chromatographic electrospray-ionization tandem mass spectrometric (LC/LC-ESI-MS/MS) procedure for the simultaneous determination of the expected mercapturic acids of naphthalene (1- and 2-naphthylmercapturic acids; 1- and 2-NpMA) and of the well-established parameter for benzene biomonitoring (S-phenylmercapturic acid; PhMA) in human urine was developed, validated and applied to human urine samples. Apart from sample acidification, the enrichment of analytes and sample clean-up as well as the separation of all analytes were completely automated using both a restricted access material column (RAM C18) and a core-shell biphenyl material. Sensitive, specific and reliable detection of all target substances, with limits of detection ranging from 0.03 to 0.04 µg/L, was achieved using structurally well matching isotope-labelled internal standard substances for each analyte. Intraday and interday precision were determined, ranging from 2.2 to 4.3%, and mean accuracy from 98.4 to 100.8%. Due to the low limits of detection, the good precision and accuracy of the developed procedure, it is well suited for application in biomonitoring studies to evaluate the validity of mercapturic acids as biomarkers after naphthalene exposure.
[Mh] Termos MeSH primário: Acetilcisteína/análogos & derivados
Acetilcisteína/urina
Cromatografia Líquida/métodos
Espectrometria de Massas em Tandem/métodos
[Mh] Termos MeSH secundário: Acetilcisteína/química
Seres Humanos
Limite de Detecção
Modelos Lineares
Masculino
Exposição Ocupacional/análise
Hidrocarbonetos Aromáticos Policíclicos/toxicidade
Reprodutibilidade dos Testes
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Polycyclic Aromatic Hydrocarbons); WYQ7N0BPYC (Acetylcysteine)
[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:180208
[St] Status:MEDLINE


  2 / 11748 MEDLINE  
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[PMID]:29331654
[Au] Autor:Xu Y; Mao X; Qin B; Peng Y; Zheng J
[Ad] Endereço:Wuya College of Innovation, Shenyang Pharmaceutical University, Shenyang, Liaoning 110016, PR China.
[Ti] Título:In vitro and in vivo metabolic activation of rhein and characterization of glutathione conjugates derived from rhein.
[So] Source:Chem Biol Interact;283:1-9, 2018 Mar 01.
[Is] ISSN:1872-7786
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Rhein (RH), 4,5-dihydroxyanthrauinone-2-carboxylic acid, is found in rhubarb (Dahuang), a traditional herbal medicine. RH has reportedly demonstrated multiple pharmacologic properties. Previous studies have also shown that RH induced hepatotoxicity, but the mechanisms of the adverse effect remain unknown. The major objective of the present study was to study the metabolic pathways of RH in order to identify potential reactive metabolites. One mono-hydroxylation metabolite (M1) was detected in urine and bile of rats given RH. M1 was also observed in rat and human liver microsomal incubations after exposure to RH. A total of three (GSH) conjugates (M2, M3 and M5) were detected in bile of rats treated with RH. We concluded that M2-M3 were directly derived from parent compound RH through spontaneous reaction with GSH. M5 was derived from M1 by reaction with GSH, which required cytoslic GSTs. M5 was further metabolized to the corresponding NAC conjugate (mercapturic acid) and was excreted in urine. P450 2C9 was mainly involved in the oxidation of RH.
[Mh] Termos MeSH primário: Antraquinonas/metabolismo
Glutationa/química
[Mh] Termos MeSH secundário: Acetilcisteína/química
Animais
Antraquinonas/química
Antraquinonas/farmacologia
Antraquinonas/urina
Bile/química
Bile/efeitos dos fármacos
Bile/metabolismo
Cromatografia Líquida de Alta Pressão
Sistema Enzimático do Citocromo P-450/genética
Sistema Enzimático do Citocromo P-450/metabolismo
Seres Humanos
Masculino
Microssomos Hepáticos/efeitos dos fármacos
Microssomos Hepáticos/metabolismo
Ratos
Ratos Sprague-Dawley
Proteínas Recombinantes/biossíntese
Proteínas Recombinantes/genética
Espectrometria de Massas em Tandem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anthraquinones); 0 (Recombinant Proteins); 9035-51-2 (Cytochrome P-450 Enzyme System); GAN16C9B8O (Glutathione); WYQ7N0BPYC (Acetylcysteine); YM64C2P6UX (rhein)
[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:180115
[St] Status:MEDLINE


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[PMID]:29373603
[Au] Autor:Guo MY; Wang H; Chen YH; Xia MZ; Zhang C; Xu DX
[Ad] Endereço:Department of Toxicology, School of Public Health, Anhui Medical University, Hefei, China.
[Ti] Título:N-acetylcysteine alleviates cadmium-induced placental endoplasmic reticulum stress and fetal growth restriction in mice.
[So] Source:PLoS One;13(1):e0191667, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cadmium (Cd) is a developmental toxicant that induces fetal growth restriction (FGR). Placental endoplasmic reticulum (ER) stress is associated with FGR. This study investigated the effects of N-acetylcysteine (NAC) on Cd-induced placental ER stress and FGR. Pregnant mice were intraperitoneally injected with CdCl2 daily from gestational day (GD)13 to GD17. As expected, Cd reduced fetal weight and crown-rump length. Cd decreased the internal space of blood vessels in the placental labyrinth layer and inhibited placental cell proliferation. Several genes of growth factors, such as Vegf-a, placental growth factor, Igf1 and Igf1r, and several genes of nutrient transport pumps, such as Glut1, Fatp1 and Snat2, were down-regulated in placenta of Cd-treated mice. Moreover, Cd evoked placental ER stress. Of interest, NAC alleviated Cd-induced FGR. Additional experiment showed that NAC inhibited Cd-induced impairment of placental development and placental ER stress. Therefore, NAC may be exploited for prevention of Cd-induced placental insufficiency and FGR.
[Mh] Termos MeSH primário: Acetilcisteína/farmacologia
Cádmio/toxicidade
Estresse do Retículo Endoplasmático/efeitos dos fármacos
Retardo do Crescimento Fetal/prevenção & controle
Placenta/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Regulação para Baixo/efeitos dos fármacos
Feminino
Camundongos
Gravidez
Reação em Cadeia da Polimerase em Tempo Real
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
00BH33GNGH (Cadmium); WYQ7N0BPYC (Acetylcysteine)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180127
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191667


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[PMID]:29248572
[Au] Autor:Xiao C; He P; Han J; Tang M; Wang Z; Mi Y; Liu X
[Ad] Endereço:Laboratory of Functional Chemistry and Nutrition of Food, College of Food Science and Engineering, Northwest A&F University, Yangling, China.
[Ti] Título:1,3-Dichloro-2-propanol evokes inflammation and apoptosis in BV-2 microglia via MAPKs and NF-κB signaling pathways mediated by reactive oxygen species.
[So] Source:Toxicol Lett;284:103-112, 2018 Mar 01.
[Is] ISSN:1879-3169
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:1,3-dichloro-2-propanol (1,3-DCP) is a widely concerned food processing contaminant which has been investigated for decades. While the neurotoxicity of 1,3-DCP and related mechanisms are still elusive. Herein, the effect of 1,3-DCP on neurotoxicity was investigated using BV-2 microglia cells. 1,3-DCP significantly decreased cell viability from 78.6% to 59.2% at doses between 2 and 20 mM. AO/EB and JC-1 staining indicated that 1,3-DCP induced apoptosis by means of the decrease of mitochondrial membrane potential. Meanwhile, western blot showed that 1,3-DCP stimulated inflammation of BV-2 cells through phosphorylation of MAPKs and activation of NF-κB pathways mediated by reactive oxygen species (ROS). Furthermore, the degree of inflammation and apoptosis has eased through MAPKs and NF-κB pathways with cells pretreated by N-acetylcysteine (NAC). Overall, these results presented here suggested that 1,3-DCP has neurotoxic effect on BV-2 microglia mainly via MAPKs and NF-κB pathways mediated by ROS.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Microglia/efeitos dos fármacos
Proteínas Quinases Ativadas por Mitógeno/metabolismo
NF-kappa B/metabolismo
Espécies Reativas de Oxigênio/metabolismo
alfa-Cloridrina/análogos & derivados
[Mh] Termos MeSH secundário: Acetilcisteína/farmacologia
Animais
Linhagem Celular
Sobrevivência Celular/efeitos dos fármacos
Relação Dose-Resposta a Droga
Contaminação de Alimentos
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Camundongos
Microglia/imunologia
Microglia/patologia
Fosforilação
Transdução de Sinais
alfa-Cloridrina/toxicidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (NF-kappa B); 0 (Reactive Oxygen Species); 0F4P2VQC07 (1,3-dichloro-2-propanol); 96-24-2 (alpha-Chlorohydrin); EC 2.7.11.24 (Mitogen-Activated Protein Kinases); WYQ7N0BPYC (Acetylcysteine)
[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:171218
[St] Status:MEDLINE


  5 / 11748 MEDLINE  
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[PMID]:29248134
[Au] Autor:Monti D; Sotgia F; Whitaker-Menezes D; Tuluc M; Birbe R; Berger A; Lazar M; Cotzia P; Draganova-Tacheva R; Lin Z; Domingo-Vidal M; Newberg A; Lisanti MP; Martinez-Outschoorn U
[Ad] Endereço:Marcus Institute of Integrative Health at Thomas Jefferson University, Philadelphia, PA.
[Ti] Título:Pilot study demonstrating metabolic and anti-proliferative effects of in vivo anti-oxidant supplementation with N-Acetylcysteine in Breast Cancer.
[So] Source:Semin Oncol;44(3):226-232, 2017 06.
[Is] ISSN:1532-8708
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: High oxidative stress as defined by hydroxyl and peroxyl activity is often found in the stroma of human breast cancers. Oxidative stress induces stromal catabolism, which promotes cancer aggressiveness. Stromal cells exposed to oxidative stress release catabolites such as lactate, which are up-taken by cancer cells to support mitochondrial oxidative phosphorylation. The transfer of catabolites between stromal and cancer cells leads to metabolic heterogeneity between these cells and increased cancer cell proliferation and reduced apoptosis in preclinical models. N-Acetylcysteine (NAC) is an antioxidant that reduces oxidative stress and reverses stromal catabolism and stromal-carcinoma cell metabolic heterogeneity, resulting in reduced proliferation and increased apoptosis of cancer cells in experimental models of breast cancer. The purpose of this clinical trial was to determine if NAC could reduce markers of stromal-cancer metabolic heterogeneity and markers of cancer cell aggressiveness in human breast cancer. METHODS: Subjects with newly diagnosed stage 0 and I breast cancer who were not going to receive neoadjuvant therapy prior to surgical resection were treated with NAC before definitive surgery to assess intra-tumoral metabolic markers. NAC was administered once a week intravenously at a dose of 150 mg/kg and 600 mg twice daily orally on the days not receiving intravenous NAC. Histochemistry for the stromal metabolic markers monocarboxylate transporter 4 (MCT4) and caveolin-1 (CAV1) and the Ki67 proliferation assay and TUNEL apoptosis assay in carcinoma cells were performed in pre- and post-NAC specimens. RESULTS: The range of days on NAC was 14-27 and the mean was 19 days. Post-treatment biopsies showed significant decrease in stromal MCT4 and reduced Ki67 in carcinoma cells. NAC did not significantly change stromal CAV1 and carcinoma TUNEL staining. NAC was well tolerated. CONCLUSIONS: NAC as a single agent reduces MCT4 stromal expression, which is a marker of glycolysis in breast cancer with reduced carcinoma cell proliferation. This study suggests that modulating metabolism in the tumor microenvironment has the potential to impact breast cancer proliferation.
[Mh] Termos MeSH primário: Acetilcisteína/uso terapêutico
Neoplasias da Mama/tratamento farmacológico
Carcinoma Ductal de Mama/tratamento farmacológico
Carcinoma Intraductal não Infiltrante/tratamento farmacológico
Depuradores de Radicais Livres/uso terapêutico
Mastectomia
[Mh] Termos MeSH secundário: Adulto
Apoptose
Neoplasias da Mama/metabolismo
Neoplasias da Mama/patologia
Carcinoma Ductal de Mama/metabolismo
Carcinoma Ductal de Mama/patologia
Carcinoma Intraductal não Infiltrante/metabolismo
Carcinoma Intraductal não Infiltrante/patologia
Carcinoma Papilar/tratamento farmacológico
Carcinoma Papilar/metabolismo
Carcinoma Papilar/patologia
Caveolina 1/metabolismo
Proliferação Celular
Feminino
Seres Humanos
Imuno-Histoquímica
Marcação In Situ das Extremidades Cortadas
Antígeno Ki-67/metabolismo
Meia-Idade
Transportadores de Ácidos Monocarboxílicos/metabolismo
Proteínas Musculares/metabolismo
Terapia Neoadjuvante
Estadiamento de Neoplasias
Projetos Piloto
Células Estromais/metabolismo
Resultado do Tratamento
Microambiente Tumoral
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (CAV1 protein, human); 0 (Caveolin 1); 0 (Free Radical Scavengers); 0 (Ki-67 Antigen); 0 (Monocarboxylic Acid Transporters); 0 (Muscle Proteins); 0 (SLC16A4 protein, human); WYQ7N0BPYC (Acetylcysteine)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171218
[St] Status:MEDLINE


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[PMID]:29223047
[Au] Autor:Upadhyaya P; Zarth AT; Fujioka N; Fritz VA; Hecht SS
[Ad] Endereço:Masonic Cancer Center, University of Minnesota, 2231 6th Street SE, Minneapolis, MN 55455, USA.
[Ti] Título:Identification and analysis of a mercapturic acid conjugate of indole-3-methyl isothiocyanate in the urine of humans who consumed cruciferous vegetables.
[So] Source:J Chromatogr B Analyt Technol Biomed Life Sci;1072:341-346, 2018 Jan 01.
[Is] ISSN:1873-376X
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Glucobrassicin, a quantitatively significant constituent of Brassica vegetables, gives rise to indole-3-carbinol (I3C) and its dimer di-indolylmethane (DIM) when the vegetables are chewed. I3C and DIM have been extensively studied with respect to their anti-carcinogenic properties. However, the presumed intermediate isothiocyanate in their formation, indole-3-methyl isothiocyanate (IMITC), has to our knowledge never been observed, despite the fact that isothiocyanates derived from cruciferous vegetables are known to have anti-carcinogenic properties. Therefore, we investigated the formation and presence in human urine of IMITC by analyzing for its N-acetylcysteine conjugate, IMITC-NAC, in order to gain a more complete understanding of the biochemical pathways leading to formation of I3C and DIM upon consumption of vegetables rich in glucobrassicin. Standard IMITC-NAC was synthesized and its structure confirmed by NMR and MS. IMITC-NAC was identified in extracts of Brussels sprouts chopped in the presence of N-acetylcysteine. An LC-ESI-MS/MS-SRM method for analysis of IMITC-NAC, with [ C, N]IMITC-NAC as internal standard, was developed and validated. Then, ten subjects (7 females) consumed a salad of Brussels sprouts and cabbage (containing 100-500µmol glucobrassicin) once daily for 3days. Urine was collected at intervals up to 24h after vegetable consumption. Levels of IMITC-NAC in the urine of these 10 subjects ranged from 0.2 to 30.2pmol/mL urine. These results provide the first evidence for the presumed intermediacy of IMITC in the formation of I3C and DIM in humans who consumed Brussels sprouts and cabbage as a source of glucobrassicin.
[Mh] Termos MeSH primário: Acetilcisteína/urina
Brassica
Indóis/urina
Isocianatos/urina
Verduras
[Mh] Termos MeSH secundário: Acetilcisteína/química
Adolescente
Adulto
Feminino
Glucosinolatos
Seres Humanos
Indóis/química
Isocianatos/química
Masculino
Meia-Idade
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glucosinolates); 0 (Indoles); 0 (Isocyanates); EA6EH0IU89 (glucobrassicin); WYQ7N0BPYC (Acetylcysteine)
[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:171210
[St] Status:MEDLINE


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[PMID]:28467574
[Au] Autor:Atayoglu K; Gürleyik G; Demirel G; Özkara S
[Ti] Título:Effect of N-acetylcysteine on neutrophil functions during experimental acute pancreatitis.
[So] Source:Ulus Travma Acil Cerrahi Derg;23(2):100-106, 2017 Mar.
[Is] ISSN:1306-696X
[Cp] País de publicação:Turkey
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Systemic inflammatory responses and extrapancreatic vital organ impairment are mediated by activated neutrophil functions and products, such as oxygen-derived free radicals, in patients with acute pancreatitis (AP). The present study is an examination of effects of an antioxidant, N-acetylcysteine (NAC), on local and systemic histopathological changes and neutrophil functions during AP. METHODS: This experimental study was performed on 24 Wistar albino rats equally divided into 3 groups: Group 1 comprised sham laparotomy, Group 2 had AP induced with taurocholate infusion, and Group 3 consisted of AP with NAC treatment. Histopathological features in pancreas, kidney, and lung tissues were examined for local and systemic changes during AP. Neutrophil functions were evaluated using flow cytometry. RESULTS: Serum levels of pancreatic enzymes were elevated, and histopathological parameters showed acinar cell damage and pancreatic tissue necrosis in the 2 groups with AP. Severe histopathological changes were found in pulmonary and renal tissues, and flow cytometry results indicated defective neutrophil functions in the group with AP alone. NAC treatment significantly ameliorated phagocytosis, chemotaxis, and opsonization of neutrophils (p<0.05). NAC treatment also ameliorated systemic changes in pulmonary and renal tissue damage in all microscopic parameters (p<0.05). CONCLUSION: Uncontrolled and defective neutrophil functions could provoke severe systemic inflammatory responses. In addition to local inflammation and necrosis, severe systemic responses and histopathological changes in extrapancreatic vital organs occur during AP. Treatment with antioxidant NAC significantly reverses detrimental systemic responses in extrapancreatic vital organs by significantly ameliorating neutrophil functions despite ongoing AP.
[Mh] Termos MeSH primário: Acetilcisteína/farmacologia
Neutrófilos
Pancreatite/metabolismo
[Mh] Termos MeSH secundário: Doença Aguda
Animais
Neutrófilos/efeitos dos fármacos
Neutrófilos/metabolismo
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
WYQ7N0BPYC (Acetylcysteine)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180209
[Lr] Data última revisão:
180209
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.5505/tjtes.2016.59844


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[PMID]:29324774
[Au] Autor:Shi T; Yang X; Zhou H; Xi J; Sun J; Ke Y; Zhang J; Shao Y; Jiang X; Pan X; Liu S; Zhuang R
[Ad] Endereço:Department of Pharmaceutical Preparation, The Hangzhou Xixi Hospital Affiliated to Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China.
[Ti] Título:Activated carbon N-acetylcysteine microcapsule protects against nonalcoholic fatty liver disease in young rats via activating telomerase and inhibiting apoptosis.
[So] Source:PLoS One;13(1):e0189856, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Non-alcoholic fatty liver disease (NAFLD) is becoming one of the world's most common chronic liver diseases in childhood, yet no therapy is available that has been approved by the food and drug administration (FDA). Previous studies have reported that telomere and telomerase are involved the development and progression of NAFLD. This study was designed to investigate the potential beneficial effects of activated carbon N-acetylcysteine (ACNAC) microcapsules on the development of NAFLD in young rats as well as the underlying mechanism(s) involved. Three-week old male Sprague Dawley rats were given high-fat diet (HFD) with/without ACNAC treatment for 7 consecutive weeks. Liver pathologies were determined by hematoxylin and eosin (H&E) and Oil Red O staining, as well as by changes in biochemical parameters of plasma alanine transaminase (ALT) and aspartate transaminase (AST) levels, respectively. Glucose homeostasis was evaluated by the glucose tolerance test and the liver telomere length and activity were measured by real time PCR and telomeric repeat amplification protocol (TRAP). Western blot analysis was performed to determine the expression level of Bcl-2, Bax and Caspase-3. Our results demonstrated that ACNAC supplementation improved liver pathologies of rats that received long-term HFD feeding. ACNAC supplementation prevented HFD-induced telomere shortening and improved telomerase activity. Moreover, in comparison to HFD-fed rats, ACNAC supplementation markedly increased the expression of Bcl-2, but significantly decreased the expression of Bax and Caspase-3 in juvenile rats. Together, these results indicate that ACNAC may be a promising choice for preventing and treating NAFLD among children.
[Mh] Termos MeSH primário: Acetilcisteína/farmacologia
Apoptose/efeitos dos fármacos
Hepatopatia Gordurosa não Alcoólica/prevenção & controle
Telomerase/metabolismo
[Mh] Termos MeSH secundário: Alanina Transaminase/sangue
Animais
Aspartato Aminotransferases/sangue
Ativação Enzimática
Glucose/metabolismo
Teste de Tolerância a Glucose
Homeostase
Masculino
Hepatopatia Gordurosa não Alcoólica/enzimologia
Ratos
Ratos Sprague-Dawley
Reação em Cadeia da Polimerase em Tempo Real
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
EC 2.6.1.1 (Aspartate Aminotransferases); EC 2.6.1.2 (Alanine Transaminase); EC 2.7.7.49 (Telomerase); IY9XDZ35W2 (Glucose); WYQ7N0BPYC (Acetylcysteine)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180129
[Lr] Data última revisão:
180129
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180112
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189856


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[PMID]:29273567
[Au] Autor:Huang AM; Lin KW; Lin WH; Wu LH; Chang HC; Ni C; Wang DL; Hsu HY; Su CL; Shih C
[Ad] Endereço:Graduate Institute of Clinical Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, 80708, Taiwan.
[Ti] Título:1-Hydroxy-3-[(E)-4-(piperazine-diium)but-2-enyloxy]-9,10-anthraquinone ditrifluoroactate induced autophagic cell death in human PC3 cells.
[So] Source:Chem Biol Interact;281:60-68, 2018 Feb 01.
[Is] ISSN:1872-7786
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:The autophagy of human prostate cancer cells (PC3 cells) induced by a new anthraquinone derivative, 1-Hydroxy-3-[(E)-4-(piperazine-diium)but-2-enyloxy]-9,10-anthraquinone ditrifluoroactate (PA) was investigated, and the relationship between autophagy and reactive oxygen species (ROS) generation was studied. The results indicated that PA induced PC3 cell death in a time- and dose-dependent manner, could inhibit PC3 cell growth by G1 phase cell cycle arrest and corresponding decrease in the G2/M cell population and induced S-phase arrest accompanied by a significant decrease G2/M and G1 phase numbers after PC3 cells treated with PA for 48 h, and increased the accumulation of autophagolysosomes and microtubule-associated protein LC3-ll, a marker of autophagy. However, these phenomenon were not observed in the group pretreated with the autophagy inhibitor 3-MA or Bafilomycin A1 (BAF), suggesting that PA induced PC3 cell autophagy. In addition, we found that PA triggered ROS generation in cells, while the levels of ROS decreased in the N-acetylcysteine (NAC) co-treatment, indicating that PA-mediated autophagy was partly blocked by NAC. In summary, the autophagic cell death of human PC3 cells mediated by PA-triggered ROS generation.
[Mh] Termos MeSH primário: Antraquinonas/toxicidade
Apoptose/efeitos dos fármacos
Autofagia/efeitos dos fármacos
[Mh] Termos MeSH secundário: Acetilcisteína/farmacologia
Adenina/análogos & derivados
Adenina/farmacologia
Antraquinonas/síntese química
Antraquinonas/química
Caspase 3/metabolismo
Linhagem Celular Tumoral
Pontos de Checagem da Fase G1 do Ciclo Celular/efeitos dos fármacos
Seres Humanos
Macrolídeos/farmacologia
Microscopia Eletrônica de Transmissão
Proteínas Associadas aos Microtúbulos/metabolismo
Espécies Reativas de Oxigênio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anthraquinones); 0 (MAP1LC3A protein, human); 0 (Macrolides); 0 (Microtubule-Associated Proteins); 0 (Reactive Oxygen Species); 5142-23-4 (3-methyladenine); 88899-55-2 (bafilomycin A1); EC 3.4.22.- (Caspase 3); JAC85A2161 (Adenine); WYQ7N0BPYC (Acetylcysteine)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180129
[Lr] Data última revisão:
180129
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171224
[St] Status:MEDLINE


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[PMID]:29225138
[Au] Autor:Jeong M; Kim HM; Ahn JH; Lee KT; Jang DS; Choi JH
[Ad] Endereço:Department of Life and Nanopharmaceutical Sciences, Kyung Hee University, Seoul, South Korea.
[Ti] Título:9-Hydroxycanthin-6-one isolated from stem bark of Ailanthus altissima induces ovarian cancer cell apoptosis and inhibits the activation of tumor-associated macrophages.
[So] Source:Chem Biol Interact;280:99-108, 2018 Jan 25.
[Is] ISSN:1872-7786
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:The stem bark of Ailanthus altissima is used in traditional medicine in Asia to treat a variety of diseases, including cancer. The aim of this study was to identify compounds with tumoricidal activity from A. altissima stem bark and to investigate their mechanisms of action. Among the 13 compounds isolated from the ethyl acetate fraction of A. altissima stem bark, the ß-carboline alkaloid 9-hydroxycanthin-6-one had potent cytotoxicity in all three ovarian cancer cell types examined. 9-Hydroxycanthin-6-one induced apoptosis through the activation of caspases-3, -8, and -9. 9-Hydroxycanthin-6-one increased the intracellular levels of reactive oxygen species (ROS), and pre-treatment with the antioxidant N-acetyl-l-cysteine (NAC) attenuated the pro-apoptotic activity of 9-hydroxycanthin-6-one. Additionally, 9-hydroxycanthin-6-one was found to decrease the expressions of MCP-1 and RANTES, major determinants of macrophage recruitment at tumor sites, in ovarian cancer cells. Treatment with 9-hydroxycanthin-6-one inhibited the levels of M2 phenotype markers and some cancer-promoting factors, such as MMP-2, MMP-9, and VEGF, in macrophages educated in ovarian cancer conditioned medium. Taken together, these data suggest that 9-hydroxycanthin-6-one isolated from A. altissima stem bark induces apoptosis in human ovarian cancer cells through the caspase- and ROS-dependent pathways and inhibits the activation of tumor-associated macrophages.
[Mh] Termos MeSH primário: Ailanthus/química
Antineoplásicos Fitogênicos/farmacologia
Apoptose/efeitos dos fármacos
Alcaloides de Indol/farmacologia
Macrófagos/metabolismo
[Mh] Termos MeSH secundário: Acetilcisteína/farmacologia
Ailanthus/metabolismo
Antineoplásicos Fitogênicos/química
Antineoplásicos Fitogênicos/isolamento & purificação
Antioxidantes/farmacologia
Inibidores de Caspase/farmacologia
Caspases/química
Caspases/metabolismo
Pontos de Checagem do Ciclo Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Quimiocinas/genética
Quimiocinas/metabolismo
Feminino
Seres Humanos
Alcaloides de Indol/química
Alcaloides de Indol/isolamento & purificação
Macrófagos/citologia
Macrófagos/efeitos dos fármacos
Metaloproteinase 2 da Matriz/metabolismo
Metaloproteinase 9 da Matriz/metabolismo
Oligopeptídeos/farmacologia
Neoplasias Ovarianas/metabolismo
Neoplasias Ovarianas/patologia
Casca de Planta/química
Casca de Planta/metabolismo
Espécies Reativas de Oxigênio/metabolismo
Fator A de Crescimento do Endotélio Vascular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (9-hydroxycanthin-6-one); 0 (Antineoplastic Agents, Phytogenic); 0 (Antioxidants); 0 (Caspase Inhibitors); 0 (Chemokines); 0 (Indole Alkaloids); 0 (Oligopeptides); 0 (Reactive Oxygen Species); 0 (Vascular Endothelial Growth Factor A); 0 (benzoylcarbonyl-aspartyl-glutamyl-valyl-aspartyl-fluoromethyl ketone); EC 3.4.22.- (Caspases); EC 3.4.24.24 (Matrix Metalloproteinase 2); EC 3.4.24.35 (Matrix Metalloproteinase 9); WYQ7N0BPYC (Acetylcysteine)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180129
[Lr] Data última revisão:
180129
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171212
[St] Status:MEDLINE



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