Base de dados : MEDLINE
Pesquisa : D02.065.064.150 [Categoria DeCS]
Referências encontradas : 2142 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 215 ir para página                         

  1 / 2142 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28192882
[Au] Autor:Kaur P; Kumar M; Singh AP; Kaur S
[Ad] Endereço:Department of Botanical and Environmental Sciences, Guru Nanak Dev University, Amritsar 143005, Punjab, India.
[Ti] Título:Ethyl acetate fraction of Pteris vittata L. alleviates 2-acetylaminofluorene induced hepatic alterations in male Wistar rats.
[So] Source:Biomed Pharmacother;88:1080-1089, 2017 Apr.
[Is] ISSN:1950-6007
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:Pteris vittata L. commonly called 'Brake Fern' possesses some interesting medicinal properties but its chemopreventive potential largely remains unexplored. Therefore, this study was designed to explore the chemopreventive efficacy of P. vittata L. ethyl acetate fraction (PVEA) against 2-acetylaminofluorene (2-AAF) induced liver toxicity in Wistar rats. Antioxidant activity of PVEA was evaluated using various in vitro antioxidant assays. The protective effects of PVEA were evaluated against 2-acetylaminofluorene (2-AAF) induced hepatic damage in Wistar rats. p53 expression in liver tissue was checked using immunohistochemical staining. Phytochemical composition of PVEA was determined using high performance liquid chromatography (HPLC). PVEA showed promising radical scavenging activity with an EC (concentration of a drug that gives half-maximal response) of 41.18µg/ml in DPPH assay, 26.99µg/ml in site specific deoxyribose degradation assay, 13.43µg/ml in non site specific deoxyribose degradation assay and 21.88µg/ml in superoxide anion scavenging assay. Three different doses of PVEA 100, 200 and 400mg/kg body weight (b.w.) followed by administration of 2-AAF (50mg/kg b.w. i.p.) for five consecutive days induced significant changes in activity of liver marker enzymes, thiobarbituric acid reactive substances, lipid hydroperoxides, reduced glutathione content and phase I and II enzymes. Activity of hepatic enzymes and normal hepatic architecture was restored following PVEA treatment. PVEA modulated the expression of p53 in liver tissue as compared to 2-AAF treated group. HPLC analysis of the fraction revealed the abundance of epicatechin (20.809ppm) and umbelliferone (22.308ppm) as major polyphenols. The present study highlights the potentiality of P. vittata in cancer chemoprevention which warrants further investigations.
[Mh] Termos MeSH primário: Acetatos/química
Fígado/patologia
Extratos Vegetais/farmacologia
Pteris/química
[Mh] Termos MeSH secundário: 2-Acetilaminofluoreno
Fosfatase Alcalina/sangue
Animais
Antioxidantes/metabolismo
Compostos de Bifenilo/química
Fracionamento Químico
Cromatografia Líquida de Alta Pressão
Depuradores de Radicais Livres/química
Glutationa/metabolismo
Peroxidação de Lipídeos/efeitos dos fármacos
Fígado/efeitos dos fármacos
Fígado/metabolismo
Masculino
Desentoxicação Metabólica Fase I
Desintoxicação Metabólica Fase II
Estresse Oxidativo/efeitos dos fármacos
Compostos Fitoquímicos/análise
Picratos/química
Substâncias Protetoras/farmacologia
Ratos Wistar
Transaminases/sangue
Proteína Supressora de Tumor p53/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Acetates); 0 (Antioxidants); 0 (Biphenyl Compounds); 0 (Free Radical Scavengers); 0 (Phytochemicals); 0 (Picrates); 0 (Plant Extracts); 0 (Protective Agents); 0 (Tumor Suppressor Protein p53); 76845O8NMZ (ethyl acetate); 9M98QLJ2DL (2-Acetylaminofluorene); DFD3H4VGDH (1,1-diphenyl-2-picrylhydrazyl); EC 2.6.1.- (Transaminases); EC 2.6.1.- (glutamate aminotransferase); EC 3.1.3.1 (Alkaline Phosphatase); GAN16C9B8O (Glutathione)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170314
[Lr] Data última revisão:
170314
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170215
[St] Status:MEDLINE


  2 / 2142 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28127199
[Au] Autor:Gu JJ; Yao M; Yang J; Cai Y; Zheng WJ; Wang L; Yao DB; Yao DF
[Ad] Endereço:Juan-Juan Gu, Wen-Jie Zheng, Deng-Fu Yao, Research Center of Clinical Medicine, Affiliated Hospital of Nantong University, Nantong 226001, Jiangsu Province, China.
[Ti] Título:Mitochondrial carnitine palmitoyl transferase-II inactivity aggravates lipid accumulation in rat hepatocarcinogenesis.
[So] Source:World J Gastroenterol;23(2):256-264, 2017 Jan 14.
[Is] ISSN:2219-2840
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:AIM: To investigate the dynamic alteration of mitochondrial carnitine palmitoyl transferase II (CPT-II) expression during malignant transformation of rat hepatocytes. METHODS: Sprague-Dawley male rats were fed with normal, high fat (HF), and HF containing 2-fluorenylacetamide (2-FAA) diet, respectively. According to the Hematoxylin and Eosin staining of livers, rats were divided into control, fatty liver, degeneration, precancerous, and cancerous groups. Liver lipids were dyed with Oil Red O, CPT-II alterations were analyzed by immunohistochemistry, and compared with CPT-II specific concentration (µg/mg protein). Levels of total cholesterol (Tch), triglyceride (TG), and amino-transferases [alanine aminotransferase (ALT), aspartate aminotransferase (AST)] were determined by the routine methods. RESULTS: After intake of HF and/or HF+2-FAA diets, the rat livers showed mass lipid accumulation. The lipid level in the control group was significantly lower than that in other groups. The changes of serum TG and Tch levels were abnormally increasing, 2-3 times more than those in the controls ( < 0.05). During the rat liver morphological changes from normal to cancer development process with hepatocyte injury, serum AST and ALT levels were significantly higher (4-8 times, < 0.05) than those in the control group. The specific concentration of CPT-II in liver tissues progressively decreased during hepatocyte malignant transformation, with the lowest CPT-II levels in the cancer group than in any of the other groups ( < 0.05). CONCLUSION: Low CPT-II expression might lead to abnormal hepatic lipid accumulation, which should promote the malignant transformation of hepatocytes.
[Mh] Termos MeSH primário: Carcinogênese/metabolismo
Carcinoma Hepatocelular/metabolismo
Carnitina O-Palmitoiltransferase/metabolismo
Hepatócitos/metabolismo
Metabolismo dos Lipídeos
Neoplasias Hepáticas Experimentais/metabolismo
Mitocôndrias/enzimologia
Hepatopatia Gordurosa não Alcoólica/metabolismo
[Mh] Termos MeSH secundário: 2-Acetilaminofluoreno/toxicidade
Alanina Transaminase/sangue
Animais
Aspartato Aminotransferases/sangue
Carcinoma Hepatocelular/sangue
Carcinoma Hepatocelular/induzido quimicamente
Colesterol/sangue
Dieta Hiperlipídica/efeitos adversos
Imuno-Histoquímica
Fígado/citologia
Neoplasias Hepáticas Experimentais/sangue
Neoplasias Hepáticas Experimentais/induzido quimicamente
Masculino
Hepatopatia Gordurosa não Alcoólica/sangue
Hepatopatia Gordurosa não Alcoólica/etiologia
Ratos
Ratos Sprague-Dawley
Triglicerídeos/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Triglycerides); 97C5T2UQ7J (Cholesterol); 9M98QLJ2DL (2-Acetylaminofluorene); EC 2.3.1.21 (Carnitine O-Palmitoyltransferase); EC 2.6.1.1 (Aspartate Aminotransferases); EC 2.6.1.2 (Alanine Transaminase)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170717
[Lr] Data última revisão:
170717
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170128
[St] Status:MEDLINE
[do] DOI:10.3748/wjg.v23.i2.256


  3 / 2142 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28100199
[Au] Autor:Kumar M; Kaur P; Chandel M; Singh AP; Jain A; Kaur S
[Ad] Endereço:Department of Botanical and Environmental Sciences, Guru Nanak Dev University, Amritsar, 143005, Punjab, India.
[Ti] Título:Antioxidant and hepatoprotective potential of Lawsonia inermis L. leaves against 2-acetylaminofluorene induced hepatic damage in male Wistar rats.
[So] Source:BMC Complement Altern Med;17(1):56, 2017 Jan 18.
[Is] ISSN:1472-6882
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Lawsonia inermis (Lythraceae) is an ethnomedicinal plant, traditionally known for curing several ailments such as skin diseases, bacterial infections, jaundice, renal lithiases and inflammation etc. The present work deals with assessment of in vitro antioxidant and in vivo hepatoprotective potential of butanolic fraction (But-LI) of Lawsonia inermis L. leaves. METHODS: Antioxidant activity was evaluated using deoxyribose degradation, lipid peroxidation inhibition and ferric reducing antioxidant power (FRAP) assay. In vivo protective potential of But-LI was assessed at 3 doses [100, 200 & 400 mg/kg body weight (bw)] against 2-acetylaminofluorene (2-AAF) induced hepatic damage in male Wistar rats. RESULTS: But-LI effectively scavenged hydroxyl radicals in deoxyribose degradation assay (IC 149.12 µg/ml). Fraction also inhibited lipid peroxidation and demonstrated appreciable reducing potential in FRAP assay. Treatment of animals with 2-AAF resulted in increased hepatic parameters such as SGOT (2.22 fold), SGPT (1.72 fold), ALP (5.68 fold) and lipid peroxidation (2.94 fold). Different concentration of But-LI demonstrated pronounced protective effects via decreasing levels of SGOT, SGPT, ALP and lipid peroxidation altered by 2-AAF treatment. But-LI administration also restored the normal liver architecture as evident from histopathological studies. CONCLUSIONS: The present experimental findings revealed that phytoconstituents of Lawsonia inermis L. possess potential to effectively protect rats from the 2-AAF induced hepatic damage in vivo possibly by inhibition of reactive oxygen species and lipid peroxidation.
[Mh] Termos MeSH primário: Lawsonia (Planta)/química
Fígado/efeitos dos fármacos
Extratos Vegetais/farmacologia
Substâncias Protetoras/farmacologia
[Mh] Termos MeSH secundário: 2-Acetilaminofluoreno
Animais
Antioxidantes/farmacologia
Doença Hepática Induzida por Substâncias e Drogas/prevenção & controle
Peroxidação de Lipídeos
Fígado/patologia
Masculino
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (Plant Extracts); 0 (Protective Agents); 9M98QLJ2DL (2-Acetylaminofluorene)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170120
[St] Status:MEDLINE
[do] DOI:10.1186/s12906-017-1567-9


  4 / 2142 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27484767
[Au] Autor:Yang CH; Chang HY; Chen YC; Lu CC; Huang SS; Huang GJ; Lai HC
[Ad] Endereço:Graduate Institute of Biomedical Science, Division of Biotechnology, College of Medicine, Chang Gung University, Tao-Yuan, 333, Taiwan, Republic of China.
[Ti] Título:Ethanol extract of Phellinus merrillii protects against diethylnitrosamine- and 2-acetylaminofluorene-induced hepatocarcinogenesis in rats.
[So] Source:Chin J Integr Med;23(2):117-124, 2017 Feb.
[Is] ISSN:1672-0415
[Cp] País de publicação:China
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To study whether the ethanol extract of Phellinus merrillii (EPM) has chemopreventive potential against liver carcinogenesis. METHODS: Thirty male Spraque-Dawley rats were randomly divided into control group, EPM control group, hepatocarcinoma control group, low-dose EPM group and high-dose EPM group, 6 in each group. Using the Solt and Farber protocol in a rat model of hepatocarcinogenesis, the chemopreventive effect of EPM on diethylnitrosamine (DEN)-initiated, 2-acetylaminofluorene (2-AAF) and partial hepatectomy (PH)-promoted liver carcinogenesis in rats was evaluated. Basic pathophysiological and histological examinations, together with the serum levels of glutamic oxaloacetic transaminase (sGOT), glutamic pyruvic transaminase (sGPT) and gamma-glutamyl transpeptidase (γ-GT) were measured. RESULTS: Treatment of EPM at the concentration of 2 g/kg body weight in the diet for 8 weeks clearly prevented the development of carcinogenesis and reduced the levels of sGOT, sGPT, and serum γ-GT of rats as compared with the hepatocarcinoma control group (P<0.05 or P<0.01). These phenotypes were accompanied by a significant increase in natural killer cell activity. CONCLUSION: EPM showed a strong liver preventive effect against DEN+2-AAF+PH-induced hepatocarcinogenesis in a rat model.
[Mh] Termos MeSH primário: 2-Acetilaminofluoreno
Basidiomycota/química
Dietilnitrosamina
Etanol/química
Neoplasias Hepáticas Experimentais/induzido quimicamente
Neoplasias Hepáticas Experimentais/prevenção & controle
Extratos Vegetais/farmacologia
[Mh] Termos MeSH secundário: Animais
Carcinogênese/induzido quimicamente
Citoproteção/efeitos dos fármacos
Masculino
Extratos Vegetais/química
Substâncias Protetoras/farmacologia
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Phellinus linteus extract); 0 (Plant Extracts); 0 (Protective Agents); 3IQ78TTX1A (Diethylnitrosamine); 3K9958V90M (Ethanol); 9M98QLJ2DL (2-Acetylaminofluorene)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:171105
[Lr] Data última revisão:
171105
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160804
[St] Status:MEDLINE
[do] DOI:10.1007/s11655-016-2513-2


  5 / 2142 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27931819
[Au] Autor:Shigano M; Ishii N; Takashima R; Harada H; Takasawa H; Hamada S
[Ad] Endereço:LSI Medience Corporation, 14-1 Sunayama, Kamisu-shi, Ibaraki 314-0255, Japan. Electronic address: shigano.miyuki@ma.medience.co.jp.
[Ti] Título:Results of rat Pig-a/PIGRET assay with a single dose regimen of 1,3-propane sultone and 2-acetyl aminofluorene.
[So] Source:Mutat Res;811:75-79, 2016 Nov 15.
[Is] ISSN:1873-135X
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The Pig-a assay is a useful in vivo mutation detecting test and is easier to perform than the in vivo transgenic mutation assay. This assay is now recognized to be able to detect a number of mutagenic chemicals administered to rats in sub-acute or sub-chronic dose studies. The present investigation was conducted to evaluate the usefulness of peripheral blood Pig-a assays with total red blood cells (RBC Pig-a assay) and with reticulocytes (PIGRET assay) using two genotoxic rodent carcinogens, 1,3-propane sultone (1,3-PS) and 2-acetylaminofluorene (2-AAF). Male rats were orally administered a single dose of each test compound, and both the RBC Pig-a and PIGRET assays were performed using flow cytometry to measure the Pig-a mutant frequency (MF) before and after dosing on Days 8, 15 and 29. In the experiment with 1,3-PS, significant increases in Pig-a MF were observed from Day 15 and Day 8 in the RBC Pig-a and PIGRET assays, respectively. The results of both assays demonstrated that the increases in Pig-a MF were detectable after a single treatment with 1,3-PS. Furthermore, the difference in the kinetics of the increase in Pig-a MF between the RBC Pig-a and PIGRET assays with 1,3-PS suggests that the PIGRET assay has an advantage in detecting the mutant erythrocytes earlier than the RBC Pig-a assay. In contrast, no significant increases were observed in the Pig-a assays using either RBC or reticulocytes with 2-AAF. The negative results in both assays with 2-AAF may indicate the limitation of the single dose method; however, further investigation at higher doses is necessary to determine limitation of the single dose method.
[Mh] Termos MeSH primário: 2-Acetilaminofluoreno/toxicidade
Eritrócitos/efeitos dos fármacos
Proteínas de Membrana/genética
Testes de Mutagenicidade/métodos
Mutagênicos/toxicidade
Reticulócitos/efeitos dos fármacos
Tiofenos/toxicidade
[Mh] Termos MeSH secundário: Animais
Relação Dose-Resposta a Droga
Masculino
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Membrane Proteins); 0 (Mutagens); 0 (Thiophenes); 0 (phosphatidylinositol glycan-class A protein); 9M98QLJ2DL (2-Acetylaminofluorene); L6NTK7VJX9 (1,3-propane sultone)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170531
[Lr] Data última revisão:
170531
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161210
[St] Status:MEDLINE


  6 / 2142 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27444315
[Au] Autor:Pisani GB; Valenti JL; Quintana AB
[Ad] Endereço:Area Morfología, Dto de Ciencias Fisiológicas, Facultad de Ciencias Bioquímicas y Farmacéuticas, Universidad Nacional de Rosario, Argentina.
[Ti] Título:Hepatic preneoplasia induction in male Wistar rats: histological studies up to five months post treatment.
[So] Source:Rev Esp Enferm Dig;108(8):457-63, 2016 Aug.
[Is] ISSN:1130-0108
[Cp] País de publicação:Spain
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Liver preneoplasia development in rats can be mimicked by an initiation-promotion model that induces the appearance of altered hepatocyte foc (FAH). AIMS: We compare two initiation-promotion models to evaluate the presence of FAH or additional hepatic pathologies in which other organs were affected up to five month post treatment. MATERIAL AND METHODS: FAH were induced in male adult Wistar rats with two doses of dietylnitrosamine (DEN, 150 mg/kg bw) followed by 4 doses per week (3 weeks) of 2-acetylaminofluorene (2-AAF, 20 mg/kg bw) or with one dose of DEN (200 mg/kg bw) followed by 2 doses per week (3 weeks) of 2-AAF. DEN 150, DEN 200 and control mice (received the vehicle of the drugs) groups were compared. Rats were euthanized immediately after the last dose of 2-AAF, at 3, 4 and 5 months (n = 3 euthanasia times per group). Samples of livers, lungs, kidneys, pancreatic tissue and small bowel were processed for histological and immunohistochemical analysis. RESULTS: FAH persisted for 5 months in all livers of the DEN groups. Three months after withdrawal of 2-AAF, one rat from the DEN 150 group developed fibrosis and 5 months after 2-AAF removal another rat from the same group presented a microscopic hyperplastic nodule. Only the lungs had damage compatible with lesions induced by gavage-related reflux in DEN groups. CONCLUSION: We concluded that up to five month post treatments, FAH persisted in all the livers from the DEN groups; livers from the DEN 200 group showed no other hepatic lesions besides FAH, and only the lungs suffered pathological alterations in both treated groups.
[Mh] Termos MeSH primário: Neoplasias Hepáticas Experimentais/patologia
Neoplasias Hepáticas Experimentais/terapia
Lesões Pré-Cancerosas/patologia
Lesões Pré-Cancerosas/terapia
[Mh] Termos MeSH secundário: 2-Acetilaminofluoreno
Animais
Carcinógenos
Dietilnitrosamina
Hepatócitos/patologia
Fígado/patologia
Neoplasias Hepáticas Experimentais/induzido quimicamente
Pulmão/patologia
Masculino
Lesões Pré-Cancerosas/induzido quimicamente
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Carcinogens); 3IQ78TTX1A (Diethylnitrosamine); 9M98QLJ2DL (2-Acetylaminofluorene)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171101
[Lr] Data última revisão:
171101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160723
[St] Status:MEDLINE
[do] DOI:10.17235/reed.2016.4183/2015


  7 / 2142 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:26945106
[Au] Autor:Gjymishka A; Pi L; Oh SH; Jorgensen M; Liu C; Protopapadakis Y; Patel A; Petersen BE
[Ad] Endereço:Department of Pediatrics, University of Florida, Gainesville, Florida.
[Ti] Título:miR-133b Regulation of Connective Tissue Growth Factor: A Novel Mechanism in Liver Pathology.
[So] Source:Am J Pathol;186(5):1092-102, 2016 May.
[Is] ISSN:1525-2191
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:miRNAs are involved in liver regeneration, and their expression is dysregulated in hepatocellular carcinoma (HCC). Connective tissue growth factor (CTGF), a direct target of miR-133b, is crucial in the ductular reaction (DR)/oval cell (OC) response for generating new hepatocyte lineages during liver injury in the context of hepatotoxin-inhibited hepatocyte proliferation. Herein, we investigate whether miR-133b regulation of CTGF influences HCC cell proliferation and migration, and DR/OC response. We analyzed miR-133b expression and found it to be down-regulated in HCC patient samples and induced in the rat DR/OC activation model of 2-acetylaminofluorene with partial hepatectomy. Furthermore, overexpression of miR-133b via adenoviral system in vitro led to decreased CTGF expression and reduced proliferation and Transwell migration of both HepG2 HCC cells and WBF-344 rat OCs. In vivo, overexpression of miR-133b in DR/OC activation models of 2-acetylaminofluorene with partial hepatectomy in rats, and 3,5-diethoxycarbonyl-1,4-dihydrocollidine in mice, led to down-regulation of CTGF expression and OC proliferation. Collectively, these results show that miR-133b regulation of CTGF is a novel mechanism critical for the proliferation and migration of HCC cells and OC response.
[Mh] Termos MeSH primário: Fator de Crescimento do Tecido Conjuntivo/metabolismo
MicroRNAs/fisiologia
[Mh] Termos MeSH secundário: 2-Acetilaminofluoreno/farmacologia
Adenoviridae/genética
Idoso
Animais
Carcinógenos/farmacologia
Carcinoma Hepatocelular/fisiopatologia
Movimento Celular/fisiologia
Proliferação Celular/fisiologia
Modelos Animais de Doenças
Regulação para Baixo/fisiologia
Feminino
Vetores Genéticos
Células HEK293
Células Hep G2
Seres Humanos
Neoplasias Hepáticas/fisiopatologia
Masculino
Camundongos
MicroRNAs/metabolismo
Meia-Idade
Ratos
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Carcinogens); 0 (MIRN133 microRNA, human); 0 (MicroRNAs); 139568-91-5 (Connective Tissue Growth Factor); 9M98QLJ2DL (2-Acetylaminofluorene)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170522
[Lr] Data última revisão:
170522
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:160306
[St] Status:MEDLINE


  8 / 2142 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:26919160
[Au] Autor:Seydi E; Rasekh HR; Salimi A; Mohsenifar Z; Pourahmad J
[Ad] Endereço:Department of Pharmacology and Toxicology, Faculty of Pharmacy, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
[Ti] Título:Myricetin Selectively Induces Apoptosis on Cancerous Hepatocytes by Directly Targeting Their Mitochondria.
[So] Source:Basic Clin Pharmacol Toxicol;119(3):249-58, 2016 Sep.
[Is] ISSN:1742-7843
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Hepatocellular carcinoma (HCC) is the third most common cause of cancer-related death. In patients for whom HCC could not be detected early, current treatments show poor tolerance and low efficacy. So, alternative therapies with good efficacy are urgently needed. The aim of this research was to evaluate the selective apoptotic effects of myricetin (MYR), a flavonoid compound, on hepatocytes and mitochondria obtained from the liver of HCC rats. In this study, HCC induced by diethylnitrosamine (DEN), as an initiator, and 2-acetylaminofluorene (2-AAF), as a promoter. To confirm the HCC induction, serum levels of alpha-fetoprotein (AFP), AST, AST and ALP and histopathological changes in the liver tissue were evaluated. Rat liver hepatocytes and mitochondria for evaluation of the selective cytotoxic effects of MYR were isolated, and mitochondrial and cellular parameters related to apoptosis signalling were then determined. Our results showed that MYR was able to induce cytotoxicity only in hepatocytes from the HCC but not from the untreated control group. Besides, MYR (12.5, 25 and 50 µM) induced a considerable increase in reactive oxygen species (ROS) level, mitochondrial swelling, mitochondrial membrane permeabilization (MMP) and cytochrome c release only in cancerous but not in untreated normal hepatocyte mitochondria. MYR selectively increased caspase-3 activation and apoptotic phenotypes in HCC, but not untreated normal hepatocytes. Finally, our finding underlines MYR as a promising therapeutic candidate against HCC and recommends the compound for further studies.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Flavonoides/farmacologia
Hepatócitos/efeitos dos fármacos
Mitocôndrias/efeitos dos fármacos
[Mh] Termos MeSH secundário: 2-Acetilaminofluoreno/toxicidade
Alanina Transaminase/sangue
Fosfatase Alcalina/sangue
Animais
Aspartato Aminotransferases/sangue
Carcinoma Hepatocelular/induzido quimicamente
Carcinoma Hepatocelular/tratamento farmacológico
Caspase 3/metabolismo
Citocromos c/metabolismo
Dietilnitrosamina/toxicidade
Modelos Animais de Doenças
Fígado/citologia
Fígado/efeitos dos fármacos
Neoplasias Hepáticas/induzido quimicamente
Neoplasias Hepáticas/tratamento farmacológico
Masculino
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Dilatação Mitocondrial/efeitos dos fármacos
Tamanho do Órgão/efeitos dos fármacos
Ratos
Ratos Sprague-Dawley
Espécies Reativas de Oxigênio/metabolismo
alfa-Fetoproteínas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Flavonoids); 0 (Reactive Oxygen Species); 0 (alpha-Fetoproteins); 3IQ78TTX1A (Diethylnitrosamine); 76XC01FTOJ (myricetin); 9007-43-6 (Cytochromes c); 9M98QLJ2DL (2-Acetylaminofluorene); EC 2.6.1.1 (Aspartate Aminotransferases); EC 2.6.1.2 (Alanine Transaminase); EC 3.1.3.1 (Alkaline Phosphatase); EC 3.4.22.- (Casp3 protein, rat); EC 3.4.22.- (Caspase 3)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170309
[Lr] Data última revisão:
170309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160227
[St] Status:MEDLINE
[do] DOI:10.1111/bcpt.12572


  9 / 2142 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:26733364
[Au] Autor:Xu L; Cho BP
[Ad] Endereço:Department of Biomedical and Pharmaceutical Sciences, College of Pharmacy, University of Rhode Island , Kingston, Rhode Island 02881, United States.
[Ti] Título:Conformational Insights into the Mechanism of Acetylaminofluorene-dG-Induced Frameshift Mutations in the NarI Mutational Hotspot.
[So] Source:Chem Res Toxicol;29(2):213-26, 2016 Feb 15.
[Is] ISSN:1520-5010
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Frameshift mutagenesis encompasses the gain or loss of DNA base pairs, resulting in altered genetic outcomes. The NarI restriction site sequence 5'-G1G2CG3CX-3' in Escherichia coli is a well-known mutational hotspot, in which lesioning of acetylaminofluorene (AAF) at G3* induces a greater -2 deletion frequency than that at other guanine sites. Its mutational efficiency is modulated by the nature of the nucleotide in the X position (C ∼ A > G ≫ T). Here, we conducted a series of polymerase-free solution experiments that examine the conformational and thermodynamic basis underlying the propensity of adducted G3 to form a slipped mutagenic intermediate (SMI) and its sequence dependence during translesion synthesis (TLS). Instability of the AAF-dG3:dC pair at the replication fork promoted slippage to form a G*C bulge-out SMI structure, consisting of S- ("lesion stacked") and B-SMI ("lesion exposed") conformations, with conformational rigidity increasing as a function of primer elongation. We found greater stability of the S- compared to the B-SMI conformer throughout TLS. The dependence of their population ratios was determined by the 3'-next flanking base X at fully elongated bulge structures, with 59% B/41% S and 86% B/14% S for the dC and dT series, respectively. These results indicate the importance of direct interactions of the hydrophobic AAF lesion with the 3'-next flanking base pair and its stacking fit within the -2 bulge structure. A detailed conformational understanding of the SMI structures and their sequence dependence may provide a useful model for DNA polymerase complexes.
[Mh] Termos MeSH primário: 2-Acetilaminofluoreno/química
Adutos de DNA/química
Desoxirribonucleases de Sítio Específico do Tipo II/metabolismo
Guanina/química
[Mh] Termos MeSH secundário: Varredura Diferencial de Calorimetria
Cromatografia Líquida de Alta Pressão
Dicroísmo Circular
DNA/química
DNA/metabolismo
Adutos de DNA/análise
Adutos de DNA/metabolismo
Reparo do DNA
Escherichia coli/genética
Escherichia coli/metabolismo
Mutação da Fase de Leitura
Conformação de Ácido Nucleico
Espectrometria de Massas por Ionização e Dessorção a Laser Assistida por Matriz
Termodinâmica
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (DNA Adducts); 5Z93L87A1R (Guanine); 9007-49-2 (DNA); 9M98QLJ2DL (2-Acetylaminofluorene); EC 3.1.21.4 (Deoxyribonucleases, Type II Site-Specific)
[Em] Mês de entrada:1610
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160107
[St] Status:MEDLINE
[do] DOI:10.1021/acs.chemrestox.5b00484


  10 / 2142 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:26657500
[Au] Autor:Kindrat I; Tryndyak V; de Conti A; Shpyleva S; Mudalige TK; Kobets T; Erstenyuk AM; Beland FA; Pogribny IP
[Ad] Endereço:Division of Biochemical Toxicology, National Center for Toxicological Research, U.S. Food and Drug Administration, Jefferson, AR, USA.
[Ti] Título:MicroRNA-152-mediated dysregulation of hepatic transferrin receptor 1 in liver carcinogenesis.
[So] Source:Oncotarget;7(2):1276-87, 2016 Jan 12.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Over-expression of transferrin receptor 1 (TFRC) is observed in hepatocellular carcinoma (HCC); however, there is a lack of conclusive information regarding the mechanisms of this dysregulation. In the present study, we demonstrated a significant increase in the levels of TFRC mRNA and protein in preneoplastic livers from relevant experimental models of human hepatocarcinogenesis and in human HCC cells. Additionally, using the TCGA database, we demonstrated an over-expression of TFRC in human HCC tissue samples and a markedly decreased level of microRNA-152 (miR-152) when compared to non-tumor liver tissue. The results indicated that the increase in levels of TFRC in human HCC cells and human HCC tissue samples may be attributed, in part, to a post-transcriptional mechanism mediated by a down-regulation of miR-152. This was evidenced by a strong inverse correlation between the level of TFRC and the expression of miR-152 in human HCC cells (r = -0.99, p = 4. 7 × 10-9), and was confirmed by in vitro experiments showing that transfection of human HCC cell lines with miR-152 effectively suppressed TFRC expression. This suggests that miR-152-specific targeting of TFRC may provide a selective anticancer therapeutic approach for the treatment of HCC.
[Mh] Termos MeSH primário: Antígenos CD/genética
Carcinoma Hepatocelular/genética
Regulação Neoplásica da Expressão Gênica
Neoplasias Hepáticas/genética
MicroRNAs/genética
Receptores da Transferrina/genética
[Mh] Termos MeSH secundário: 2-Acetilaminofluoreno/toxicidade
Animais
Antígenos CD/metabolismo
Western Blotting
Carcinogênese/efeitos dos fármacos
Carcinogênese/genética
Carcinógenos/toxicidade
Carcinoma Hepatocelular/metabolismo
Carcinoma Hepatocelular/patologia
Linhagem Celular Tumoral
Células Hep G2
Seres Humanos
Neoplasias Hepáticas/metabolismo
Neoplasias Hepáticas/patologia
Neoplasias Hepáticas Experimentais/induzido quimicamente
Neoplasias Hepáticas Experimentais/genética
Neoplasias Hepáticas Experimentais/metabolismo
Masculino
Ratos Sprague-Dawley
Receptores da Transferrina/metabolismo
Reação em Cadeia da Polimerase Via Transcriptase Reversa
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.; RESEARCH SUPPORT, U.S. GOV'T, P.H.S.
[Nm] Nome de substância:
0 (Antigens, CD); 0 (CD71 antigen); 0 (Carcinogens); 0 (MIRN152 microRNA, human); 0 (MicroRNAs); 0 (Receptors, Transferrin); 0 (Tfr1 protein, rat); 9M98QLJ2DL (2-Acetylaminofluorene)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151215
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.6004



página 1 de 215 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

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