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[PMID]:27776340
[Au] Autor:Liang L; Yang X; Yu Y; Li X; Wu Y; Shi R; Jiang J; Gao L; Ye F; Zhao Q; Li R; Wei L; Han Z
[Ad] Endereço:Tumor Immunology and Gene Therapy Center, Eastern Hepatobiliary Surgery Hospital, the Second Military Medical University, Shanghai, China.
[Ti] Título:Babao Dan attenuates hepatic fibrosis by inhibiting hepatic stellate cells activation and proliferation via TLR4 signaling pathway.
[So] Source:Oncotarget;7(50):82554-82566, 2016 Dec 13.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Babao Dan (BBD), a traditional Chinese medicine, has been widely used as a complementary and alternative medicine to treat chronic liver diseases. In this study, we aimed to observe the protective effect of BBD on rat hepatic fibrosis induced by diethylnitrosamine (DEN) and explore it possible mechanism. BBD was administrated while DEN was given. After eight weeks, values of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) indicated that BBD significantly protected liver from damaging by DEN and had no obvious side effect on normal rat livers. Meanwhile, BBD attenuated hepatic inflammation and fibrosis in DEN-induced rat livers through histopathological examination and hepatic hydroxyproline content. Furthermore, we found that BBD inhibited hepatic stellate cells activation and proliferation without altering the concentration of lipopolysaccharide (LPS) in portal vein. In vitro study, serum from BBD treated rats (BBD-serum) could also significantly suppress LPS-induced HSCs activation through TLR4/NF-κB pathway. In addition, BBD-serum also inhibited the proliferation of HSCs by regulating TLR4/ERK pathway. Our study demonstrated that BBD may provide a new therapy strategy of hepatic injury and hepatic fibrosis.
[Mh] Termos MeSH primário: Proliferação Celular/efeitos dos fármacos
Doença Hepática Induzida por Substâncias e Drogas/prevenção & controle
Medicamentos de Ervas Chinesas/farmacologia
Células Estreladas do Fígado/efeitos dos fármacos
Cirrose Hepática Experimental/prevenção & controle
Fígado/efeitos dos fármacos
Substâncias Protetoras/farmacologia
Transdução de Sinais/efeitos dos fármacos
Receptor 4 Toll-Like/metabolismo
[Mh] Termos MeSH secundário: Animais
Doença Hepática Induzida por Substâncias e Drogas/metabolismo
Doença Hepática Induzida por Substâncias e Drogas/patologia
Ciclina D1/metabolismo
Citocinas/metabolismo
Citoproteção
Dietilnitrosamina
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Células Estreladas do Fígado/metabolismo
Células Estreladas do Fígado/patologia
Lipopolissacarídeos/farmacologia
Fígado/metabolismo
Fígado/patologia
Cirrose Hepática Experimental/induzido quimicamente
Cirrose Hepática Experimental/metabolismo
Cirrose Hepática Experimental/patologia
Masculino
NF-kappa B/metabolismo
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ccnd1 protein, rat); 0 (Cytokines); 0 (Drugs, Chinese Herbal); 0 (Lipopolysaccharides); 0 (NF-kappa B); 0 (Protective Agents); 0 (Tlr4 protein, rat); 0 (Toll-Like Receptor 4); 136601-57-5 (Cyclin D1); 3IQ78TTX1A (Diethylnitrosamine); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.12783


  2 / 3182 MEDLINE  
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[PMID]:29072132
[Au] Autor:He Q; Wang F; Honda T; Lindquist DM; Dillman JR; Timchenko NA; Redington AN
[Ad] Endereço:1 Heart Institute, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
[Ti] Título:Intravenous miR-144 inhibits tumor growth in diethylnitrosamine-induced hepatocellular carcinoma in mice.
[So] Source:Tumour Biol;39(10):1010428317737729, 2017 Oct.
[Is] ISSN:1423-0380
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Previous in vitro studies have demonstrated that miR-144 inhibits hepatocellular carcinoma cell proliferation, invasion, and migration. We have shown that miR-144, injected intravenously, is taken up by the liver and induces endogenous hepatic synthesis of miR-144. We hypothesized that administered miR-144 has tumor-suppressive effects on liver tumor development in vivo. The effects of miR-144 on tumorigenesis and tumor growth were tested in a diethylnitrosamine-induced hepatocellular carcinoma mouse model. MiR-144 injection had no effect on body weight but significantly reduced diethylnitrosamine-induced liver enlargement compared with scrambled microRNA. MiR-144 had no effect on diethylnitrosamine-induced liver tumor number but reduced the tumor size above 50%, as evaluated by magnetic resonance imaging (scrambled microRNA 23.07 ± 5.67 vs miR-144 10.38 ± 2.62, p < 0.05) and histological analysis (scrambled microRNA 30.75 ± 5.41 vs miR-144 15.20 ± 3.41, p < 0.05). The levels of miR-144 was suppressed in tumor tissue compared with non-tumor tissue in all treatment groups (diethylnitrosamine-phosphate-buffered saline non-tumor 1.05 ± 0.09 vs tumor 0.54 ± 0.08, p < 0.01; diethylnitrosamine-scrambled microRNA non-tumor 1.23 ± 0.33 vs tumor 0.44 ± 0.10, p < 0.05; diethylnitrosamine-miR-144 non-tumor 54.72 ± 11.80 vs tumor 11.66 ± 2.75, p < 0.01), but injection of miR-144 greatly increased miR-144 levels both in tumor and non-tumor tissues. Mechanistic studies showed that miR-144 targets epidermal growth factor receptor and inhibits the downstream Src/AKT signaling pathway which has previously been implicated in hepatocellular carcinoma tumorigenesis. Exogenously delivered miR-144 may be a therapeutic strategy to suppress tumor growth in hepatocellular carcinoma.
[Mh] Termos MeSH primário: Carcinogênese/genética
Carcinoma Hepatocelular/terapia
Neoplasias Hepáticas/terapia
MicroRNAs/administração & dosagem
[Mh] Termos MeSH secundário: Administração Intravenosa
Animais
Apoptose/genética
Carcinoma Hepatocelular/induzido quimicamente
Carcinoma Hepatocelular/genética
Carcinoma Hepatocelular/patologia
Proliferação Celular/genética
Dietilnitrosamina/toxicidade
Modelos Animais de Doenças
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Fígado/metabolismo
Fígado/patologia
Neoplasias Hepáticas/induzido quimicamente
Neoplasias Hepáticas/genética
Neoplasias Hepáticas/patologia
Camundongos
MicroRNAs/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MIRN144 microRNA, mouse); 0 (MicroRNAs); 3IQ78TTX1A (Diethylnitrosamine)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171102
[Lr] Data última revisão:
171102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171027
[St] Status:MEDLINE
[do] DOI:10.1177/1010428317737729


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[PMID]:28943392
[Au] Autor:Romualdo GR; Grassi TF; Goto RL; Tablas MB; Bidinotto LT; Fernandes AAH; Cogliati B; Barbisan LF
[Ad] Endereço:Department of Pathology, Botucatu Medical School, São Paulo State University (UNESP), Botucatu - SP, Brazil.
[Ti] Título:An integrative analysis of chemically-induced cirrhosis-associated hepatocarcinogenesis: Histological, biochemical and molecular features.
[So] Source:Toxicol Lett;281:84-94, 2017 Nov 05.
[Is] ISSN:1879-3169
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:This study aimed the integrative characterization of morphological, biochemical and molecular features of chemically-induced cirrhosis-associated hepatocarcinogenesis. Thus, male Wistar rats were submitted to a diethylnitrosamine (DEN)/thioacetamide (TAA)-induced model. Liver tissue was processed for global gene expression, histopathological and collagen evaluations; as well as immunohistochemical and oxidative stress analysis. Gene Ontology and functional analysis showed the upregulation of extracellular matrix deposition genes, such as collagen type I alpha 1 and 2 (Col1α1 and Col1α2) and tissue inhibitor of metalloproteinase 1 and 2 genes (Timp1 and Timp2). In agreement these findings, animals presented extensive liver cirrhosis with increased collagen deposition (Sirius red). Besides, the animals developed many glutathione S-transferase pi (GST-P)-positive preneoplastic lesions showing high cell proliferation (Ki-67), in keeping with the Gstp1 and Gstp2 increased gene expression. DEN/TAA-treated rats also showed the upregulation of tumorigenesis-related annexin A2 gene (Anxa2) and few neoplastic lesions (hepatocellular adenomas, carcinomas, and cholangiocarcinoma). In contrast, gene expression and activity of antioxidant enzymes were decreased (glutathione peroxidase, total glutathione-S-transferase, and catalase). The model featured remarkable similarities to human hepatocarcinogenesis. Our findings could bring up new molecular insights into cirrhosis-associated hepatocarcinogenesis, and provide a suitable animal model for the establishment of further diagnostic, preventive and therapeutic approaches.
[Mh] Termos MeSH primário: Carcinogênese/genética
Regulação Neoplásica da Expressão Gênica
Cirrose Hepática/genética
Neoplasias Hepáticas Experimentais/genética
[Mh] Termos MeSH secundário: Alanina Transaminase/metabolismo
Animais
Anexina A2/genética
Anexina A2/metabolismo
Aspartato Aminotransferases/metabolismo
Carcinogênese/induzido quimicamente
Colágeno/genética
Colágeno/metabolismo
Dietilnitrosamina/toxicidade
Glutationa Peroxidase/genética
Glutationa Peroxidase/metabolismo
Glutationa Transferase/genética
Glutationa Transferase/metabolismo
Cirrose Hepática/induzido quimicamente
Neoplasias Hepáticas Experimentais/induzido quimicamente
Masculino
Metaloproteinases da Matriz/genética
Metaloproteinases da Matriz/metabolismo
Estresse Oxidativo/efeitos dos fármacos
Ratos
Ratos Wistar
Tioacetamida/toxicidade
Inibidores Teciduais de Metaloproteinases/genética
Inibidores Teciduais de Metaloproteinases/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Annexin A2); 0 (Tissue Inhibitor of Metalloproteinases); 075T165X8M (Thioacetamide); 3IQ78TTX1A (Diethylnitrosamine); 9007-34-5 (Collagen); EC 1.11.1.9 (Glutathione Peroxidase); EC 2.5.1.18 (Glutathione Transferase); EC 2.6.1.1 (Aspartate Aminotransferases); EC 2.6.1.2 (Alanine Transaminase); EC 3.4.24.- (Matrix Metalloproteinases)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171106
[Lr] Data última revisão:
171106
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170926
[St] Status:MEDLINE


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[PMID]:28935427
[Au] Autor:Mahmoud AM; Mohammed HM; Khadrawy SM; Galaly SR
[Ad] Endereço:Physiology Division, Department of Zoology, Faculty of Science, Beni-Suef University, Egypt. Electronic address: ayman.mahmoud@science.bsu.edu.eg.
[Ti] Título:Hesperidin protects against chemically induced hepatocarcinogenesis via modulation of Nrf2/ARE/HO-1, PPARγ and TGF-ß1/Smad3 signaling, and amelioration of oxidative stress and inflammation.
[So] Source:Chem Biol Interact;277:146-158, 2017 Nov 01.
[Is] ISSN:1872-7786
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Hesperidin is a plant-derived bioflavonoid with promising antitumor efficacy, though the underlying mechanisms of action remain poorly elucidated. Thus, we evaluated the in vivo chemopreventive effect of hesperidin against diethylnitrosamine (DEN)-induced hepatocarcinogenesis. We demonstrated the modulatory effect of hesperidin on Nrf2/ARE/HO-1, PPARγ and TGF-ß1/Smad3 signaling. Hepatocarcinogenesis was initiated with DEN and promoted with carbon tetrachloride (CCl ). DEN/CCl -induced rats were treated with 50 and 100 mg/kg hesperidin throughout the experiment. The results revealed that hesperidin significantly reduced circulating liver function marker enzymes, bilirubin, tumor markers and tumor necrosis factor alpha. Hesperidin prevented liver morphological damage, proliferating cell nuclear antigen (PCNA) expression and oxidative stress as evidenced by the reduced lipid peroxidation and enhanced antioxidant defenses. Liver NF-κB and TGF-ß1 expression, and Smad3 phosphorylation were significantly up-regulated in DEN/CCl -induced rats. Hesperidin dramatically abolished NF-κB and TGF-ß1/Smad3 signaling as well as collagen deposition in the liver of DEN/CCl -induced rats. In addition, hesperidin markedly up-regulated the expression of Nrf2, HO-1 and PPARγ in the liver of DEN/CCl -induced rats. In conclusion, hesperidin can inhibit hepatocarcinogenesis by suppressing oxidative stress, inflammation, cell proliferation, TGF-ß1/Smad3 signaling and collagen deposition. These effects are suggested to be mediated by activating Nrf2/ARE/HO-1 and PPARγ pathways.
[Mh] Termos MeSH primário: Anticarcinógenos/uso terapêutico
Carcinogênese/efeitos dos fármacos
Hesperidina/uso terapêutico
Inflamação/prevenção & controle
Neoplasias Hepáticas/prevenção & controle
Fígado/efeitos dos fármacos
Estresse Oxidativo/efeitos dos fármacos
Transdução de Sinais/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Tetracloreto de Carbono
Carcinogênese/induzido quimicamente
Carcinogênese/metabolismo
Proliferação Celular/efeitos dos fármacos
Dietilnitrosamina
Heme Oxigenase-1/metabolismo
Inflamação/metabolismo
Fígado/metabolismo
Neoplasias Hepáticas/induzido quimicamente
Neoplasias Hepáticas/metabolismo
Masculino
Fator 2 Relacionado a NF-E2/metabolismo
NF-kappa B/metabolismo
PPAR gama/metabolismo
Ratos
Ratos Wistar
Fator de Crescimento Transformador beta1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anticarcinogenic Agents); 0 (NF-E2-Related Factor 2); 0 (NF-kappa B); 0 (PPAR gamma); 0 (Transforming Growth Factor beta1); 3IQ78TTX1A (Diethylnitrosamine); CL2T97X0V0 (Carbon Tetrachloride); E750O06Y6O (Hesperidin); EC 1.14.14.18 (Heme Oxygenase-1)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171108
[Lr] Data última revisão:
171108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170923
[St] Status:MEDLINE


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[PMID]:28830415
[Au] Autor:Khan F; Khan TJ; Kalamegam G; Pushparaj PN; Chaudhary A; Abuzenadah A; Kumosani T; Barbour E; Al-Qahtani M
[Ad] Endereço:Biochemistry Department, Faculty of Science, King Abdulaziz University, Jeddah, Saudi Arabia.
[Ti] Título:Anti-cancer effects of Ajwa dates (Phoenix dactylifera L.) in diethylnitrosamine induced hepatocellular carcinoma in Wistar rats.
[So] Source:BMC Complement Altern Med;17(1):418, 2017 Aug 22.
[Is] ISSN:1472-6882
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Hepatocellular carcinoma (HCC) accounts for major cancer-related deaths despite current advanced therapies. Treatment and prognosis of HCC is better in patients with preserved liver function. Many natural products including ajwa dates (Phoenix dactylifera L.), are claimed to have hepatoprotective and HCC inhibitory effects, but most lack scientific validation. To prove our hypothesis, we attempted to evaluate the HCC inhibitory effects, and other beneficial properties of the aqueous extract of ajwa dates (ADE) in a rat model of diethylnitrosamine (DEN) induced liver cancer. METHODS: Thirty-two male rats were divided into four groups of eight each as follows, Group A: untreated control; Group B: DEN control (180 mg/kg bw), Group C: DEN + ADE 0.5 g/kg bw; and Group D: DEN +1.0 g/kg bw. Rats from all groups were assessed for liver cancer progression or inhibition by evaluating histological, biochemical, antioxidant enzyme status, cytokines and gene expression profiles. RESULTS: DEN treatment Groups (B, C, D) showed histological features of HCC and in rats treated with ADE (Groups C, D) partial to complete reversal of normal liver architecture was observed. Antioxidant enzymes such as superoxide dismutase (SOD), glutathione reductase (GR), glutatione peroxidase (GPx) and catalase (CAT) were increased, while the liver enzymes alanine aminotransferase (ALT), aspartate aminotransferase (AST) and alkaline phosphatase (ALP) levels and lipid peroxidation were significantly decreased in Group C and Group D compared to Group B. Pro-inflammatory cytokines such as interleukin (IL)-1α, IL-1ß,, GM-CSF) were increased in the serum of rats in Group B while the anti-tumor cytokines (IL-2, IL-12) were increased in ADE treated Groups (C, D). In addition, Alpha-Feto Protein (AFP) and IL-6 gene expression levels were upregulated in Group B, while they were significantly downregulated in ADE treated Groups (C, D). CONCLUSIONS: ADE helped in the reversal of DEN damaged liver towards normal. Restoration of anti-oxidant enzymes, liver enzymes, cytokines balance and gene expression to normal levels following ADE treatment indicates that ADE improves liver function and inhibits HCC. ADE can, therefore, be used together with conventional therapeutics for HCC.
[Mh] Termos MeSH primário: Antineoplásicos
Carcinoma Hepatocelular/tratamento farmacológico
Neoplasias Hepáticas/tratamento farmacológico
Phoeniceae/química
Extratos Vegetais
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/química
Antineoplásicos/farmacologia
Antineoplásicos/uso terapêutico
Antioxidantes/análise
Carcinoma Hepatocelular/induzido quimicamente
Carcinoma Hepatocelular/metabolismo
Carcinoma Hepatocelular/patologia
Citocinas/sangue
Dietilnitrosamina/toxicidade
Frutas/química
Fígado/efeitos dos fármacos
Fígado/patologia
Neoplasias Hepáticas/induzido quimicamente
Neoplasias Hepáticas/metabolismo
Neoplasias Hepáticas/patologia
Masculino
Extratos Vegetais/química
Extratos Vegetais/farmacologia
Extratos Vegetais/uso terapêutico
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Antioxidants); 0 (Cytokines); 0 (Plant Extracts); 3IQ78TTX1A (Diethylnitrosamine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170911
[Lr] Data última revisão:
170911
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170824
[St] Status:MEDLINE
[do] DOI:10.1186/s12906-017-1926-6


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[PMID]:28810822
[Au] Autor:Elsonbaty SM; Zahran WE; Moawed FS
[Ad] Endereço:1 National Center for Radiation Research and Technology, Atomic Energy Authority, Cairo, Egypt.
[Ti] Título:Gamma-irradiated ß-glucan modulates signaling molecular targets of hepatocellular carcinoma in rats.
[So] Source:Tumour Biol;39(8):1010428317708703, 2017 Aug.
[Is] ISSN:1423-0380
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:ß-glucans are one of the most abundant forms of polysaccharides known as biological response modifiers which influence host's biological response and stimulate immune system. Accordingly, this study was initiated to evaluate irradiated ß-glucan as a modulator for cellular signaling growth factors involved in the pathogenesis of hepatocellular carcinoma in rats. Hepatocellular carcinoma was induced with 20 mg diethylnitrosamine/kg BW. Rats received daily by gastric gavage 65 mg irradiated ß-glucan/kg BW. It was found that treatment of rats with diethylnitrosamine induced hepatic injury and caused significant increase in liver injury markers with a concomitant significant increase in both hepatic oxidative and inflammatory indices: alpha-fetoprotein, interferon gamma, and interleukin 6 in comparison with normal and irradiated ß-glucan-treated groups. Western immunoblotting showed a significant increase in the signaling growth factors: extracellular signal-regulated kinase 1 and phosphoinositide 3-kinase proteins in a diethylnitrosamine-treated group while both preventive and therapeutic irradiated ß-glucan treatments recorded significant improvement versus diethylnitrosamine group via the modulation of growth factors that encounters hepatic toxicity. The transcript levels of vascular endothelial growth factor A and inducible nitric oxide synthase genes were significantly higher in the diethylnitrosamine-treated group in comparison with controls. Preventive and therapeutic treatments with irradiated ß-glucan demonstrated that the transcript level of these genes was significantly decreased which demonstrates the protective effect of ß-glucan. Histological investigations revealed that diethylnitrosamine treatment affects the hepatic architecture throughout the significant severe appearance of inflammatory cell infiltration in the portal area and congestion in the portal vein in association with severe degeneration and dysplasia in hepatocytes all over hepatic parenchyma. The severity of hepatic architecture changes was significantly decreased with both ß-glucan therapeutic and preventive treatments. In conclusion, irradiated ß-glucan modulated signal growth factors, vascular endothelial growth factor A, extracellular signal-regulated kinase 1, and phosphatidylinositol-3-kinase, which contributed to experimental hepatocarcinogenesis.
[Mh] Termos MeSH primário: Carcinoma Hepatocelular/tratamento farmacológico
Neoplasias Hepáticas/tratamento farmacológico
Fígado/efeitos dos fármacos
beta-Glucanas/administração & dosagem
[Mh] Termos MeSH secundário: Animais
Carcinoma Hepatocelular/induzido quimicamente
Carcinoma Hepatocelular/genética
Carcinoma Hepatocelular/patologia
Dietilnitrosamina/toxicidade
Modelos Animais de Doenças
Raios gama
Seres Humanos
Fígado/lesões
Fígado/patologia
Neoplasias Hepáticas/induzido quimicamente
Neoplasias Hepáticas/genética
Neoplasias Hepáticas/patologia
Proteína Quinase 3 Ativada por Mitógeno/genética
Fosfatidilinositol 3-Quinases/genética
Ratos
Transdução de Sinais/efeitos dos fármacos
Fator A de Crescimento do Endotélio Vascular/genética
beta-Glucanas/química
beta-Glucanas/efeitos da radiação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Vascular Endothelial Growth Factor A); 0 (beta-Glucans); 3IQ78TTX1A (Diethylnitrosamine); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170828
[Lr] Data última revisão:
170828
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170817
[St] Status:MEDLINE
[do] DOI:10.1177/1010428317708703


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[PMID]:28720064
[Au] Autor:Medhat A; Mansour S; El-Sonbaty S; Kandil E; Mahmoud M
[Ad] Endereço:1 Department of Biochemistry, Faculty of Science, Ain Shams University, Cairo, Egypt.
[Ti] Título:Evaluation of the antitumor activity of platinum nanoparticles in the treatment of hepatocellular carcinoma induced in rats.
[So] Source:Tumour Biol;39(7):1010428317717259, 2017 Jul.
[Is] ISSN:1423-0380
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:This study aimed to evaluate the antitumor activity of platinum nanoparticles compared with cis-platin both in vitro and in vivo in the treatment of hepatocellular carcinoma induced in rats. The treatment efficacy of platinum nanoparticles was evaluated by measuring antioxidant activities against oxidative stress caused by diethylnitrosamine in liver tissue. The measurements included reduced glutathione content and superoxide dismutase activity, as well as malondialdehyde level. Liver function tests were also determined, in addition to the evaluation of serum alpha-fetoprotein, caspase-3, and cytochrome c in liver tissue. Total RNA extraction from liver tissue samples was also done for the relative quantification of B-cell lymphoma 2, matrix metallopeptidase 9, and tumor protein p53 genes. Histopathological examination was also performed for liver tissue. Results showed that platinum nanoparticles are more potent than cis-platin in treatment of hepatocellular carcinoma induced by diethylnitrosamine in rats as it ameliorated the investigated parameters toward normal control animals. These findings were well appreciated with histopathological studies of diethylnitrosamine group treated with platinum nanoparticles, suggesting that platinum nanoparticles can serve as a good therapeutic agent for the treatment of hepatocellular carcinoma which should attract further studies.
[Mh] Termos MeSH primário: Carcinoma Hepatocelular/tratamento farmacológico
Neoplasias Hepáticas Experimentais/tratamento farmacológico
Neoplasias Hepáticas/tratamento farmacológico
Nanopartículas Metálicas/administração & dosagem
Platina/administração & dosagem
[Mh] Termos MeSH secundário: Animais
Antioxidantes/metabolismo
Carcinoma Hepatocelular/induzido quimicamente
Carcinoma Hepatocelular/genética
Carcinoma Hepatocelular/patologia
Dietilnitrosamina/toxicidade
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Neoplasias Hepáticas/induzido quimicamente
Neoplasias Hepáticas/genética
Neoplasias Hepáticas/patologia
Neoplasias Hepáticas Experimentais/induzido quimicamente
Neoplasias Hepáticas Experimentais/genética
Neoplasias Hepáticas Experimentais/patologia
Masculino
Metaloproteinase 9 da Matriz/biossíntese
Estresse Oxidativo/efeitos dos fármacos
Proteínas Proto-Oncogênicas c-bcl-2/biossíntese
Ratos
Proteína Supressora de Tumor p53/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (Proto-Oncogene Proteins c-bcl-2); 0 (Tumor Suppressor Protein p53); 3IQ78TTX1A (Diethylnitrosamine); 49DFR088MY (Platinum); EC 3.4.24.35 (Matrix Metalloproteinase 9)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170726
[Lr] Data última revisão:
170726
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170720
[St] Status:MEDLINE
[do] DOI:10.1177/1010428317717259


  8 / 3182 MEDLINE  
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[PMID]:28693887
[Au] Autor:Radwan RR; Zaher NH; El-Gazzar MG
[Ad] Endereço:Drug Radiation Research Department, National Center for Radiation Research and Technology (NCRRT), Egyptian Atomic Energy Authority (EAEA), P.O. Box 29, Nasr City, Cairo, Egypt. Electronic address: rasha_radwan33@yahoo.com.
[Ti] Título:Novel 1,2,4-triazole derivatives as antitumor agents against hepatocellular carcinoma.
[So] Source:Chem Biol Interact;274:68-79, 2017 Aug 25.
[Is] ISSN:1872-7786
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Fifteen novel 1,2,3-triazole derivatives were prepared in series of synthetic steps starting from 4-amino-5-hydrazino-4H-1,2,4-triazole-3-thiol 1. The structures of the obtained compounds were verified through micoanalytical and spectral data. All the compounds were screened for their anticancer activity against liver human cancer cell lines (HEPG2) using Doxorubicin as standard. The most promising triazolothiadiazine derivative 12 was further tested for its degree of toxicity by estimating the median lethal dose (LD 50) and its antitumor activity through inhibiting the angiogenesis and progression of tumor against diethylnitrosamine (DENA)/CCl induced hepatocellular carcinoma (HCC) in rats. To elucidate its mechanism of action, the following parameters were determined including: vascular endothelial growth factor (VEGF) as a marker of angiogenesis; hepatic tyrosine kinase (HTK) as a marker for tumor growth; serum alpha fetoprotein (AFP) as a marker for hepatocarcinoma; aspartate and alanine aminotransferases (AST & ALT) as liver function test; malondialdehyde (MDA) and glutathione (GSH) as markers of antioxidant activity. Liver histopathological analysis was also evaluated. Carcinogenic rats showed drastic elevation in all investigated parameters accompanied by reduction in hepatic glutathione. Administration of compound 12 into rats after induction of experimental HCC, improved the biochemical changes induced by DENA/CCl . These observations were supported by histopathological study of liver sections. It was concluded that triazolothiadiazine compound 12 could be promising anti HCC agent after more investigations on higher animals.
[Mh] Termos MeSH primário: Antineoplásicos/toxicidade
Fígado/efeitos dos fármacos
Tiadiazóis/toxicidade
Triazóis/toxicidade
[Mh] Termos MeSH secundário: Alanina Transaminase/sangue
Animais
Antineoplásicos/química
Antineoplásicos/uso terapêutico
Aspartato Aminotransferases/sangue
Carcinoma Hepatocelular/metabolismo
Carcinoma Hepatocelular/patologia
Linhagem Celular Tumoral
Sobrevivência Celular/efeitos dos fármacos
Dietilnitrosamina/toxicidade
Glutationa/metabolismo
Seres Humanos
Fígado/metabolismo
Fígado/patologia
Testes de Função Hepática
Neoplasias Hepáticas/metabolismo
Neoplasias Hepáticas/patologia
Neoplasias Hepáticas Experimentais/induzido quimicamente
Neoplasias Hepáticas Experimentais/tratamento farmacológico
Neoplasias Hepáticas Experimentais/patologia
Masculino
Malondialdeído
Ratos
Ratos Wistar
Relação Estrutura-Atividade
Tiadiazóis/síntese química
Tiadiazóis/uso terapêutico
Triazóis/síntese química
Triazóis/química
Triazóis/uso terapêutico
Fator A de Crescimento do Endotélio Vascular/metabolismo
alfa-Fetoproteínas/análise
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (1-phenyl-2-(2-(7-phenyl-5H-(1,2,4)triazolo(3,4-b)(1,3,4)thiadiazin-3-yl)hydrazinyl)ethanone); 0 (Antineoplastic Agents); 0 (Thiadiazoles); 0 (Triazoles); 0 (Vascular Endothelial Growth Factor A); 0 (alpha-Fetoproteins); 288-88-0 (1,2,4-triazole); 3IQ78TTX1A (Diethylnitrosamine); 4Y8F71G49Q (Malondialdehyde); EC 2.6.1.1 (Aspartate Aminotransferases); EC 2.6.1.2 (Alanine Transaminase); GAN16C9B8O (Glutathione)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170712
[St] Status:MEDLINE


  9 / 3182 MEDLINE  
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[PMID]:28655791
[Au] Autor:Ngo HKC; Kim DH; Cha YN; Na HK; Surh YJ
[Ad] Endereço:Tumor Microenvironment Global Core Research Center, College of Pharmacy, Seoul National University, Seoul, South Korea.
[Ti] Título:Nrf2 Mutagenic Activation Drives Hepatocarcinogenesis.
[So] Source:Cancer Res;77(18):4797-4808, 2017 Sep 15.
[Is] ISSN:1538-7445
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Nrf2, a master regulator of oxidative stress, is considered a prominent target for prevention of hepatocellular carcinoma (HCC), one of the leading causes of cancer-related deaths worldwide. Here we report that -deficient mice resisted diethylnitrosamine (DEN)-induced hepatocarcinogenesis without affecting P450-mediated metabolic activation of DEN. Nrf2 expression, nuclear translocation, and transcriptional activity were enhanced in liver tumors. Overactivated Nrf2 was required for hepatoma growth in DEN-induced HCC. Following DEN treatment, genetic disruption reduced expression of pentose phosphate pathway-related enzymes, the depletion of which has been associated with an amelioration of HCC incidence. Conversely, enhanced Nrf2 activity was attributable to alterations in the ability to bind its endogenous inhibitor Keap1. Our findings provide a mechanistic rationale for Nrf2 blockade to prevent and possibly treat liver cancer. .
[Mh] Termos MeSH primário: Dietilnitrosamina/toxicidade
Neoplasias Hepáticas Experimentais/patologia
Subunidade p45 do Fator de Transcrição NF-E2/fisiologia
[Mh] Termos MeSH secundário: Alquilantes/toxicidade
Animais
Apoptose
Proliferação Celular
Feminino
Seres Humanos
Neoplasias Hepáticas Experimentais/induzido quimicamente
Neoplasias Hepáticas Experimentais/genética
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Mutagênicos/toxicidade
Transdução de Sinais
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Alkylating Agents); 0 (Mutagens); 0 (NF-E2 Transcription Factor, p45 Subunit); 0 (Nfe2 protein, mouse); 3IQ78TTX1A (Diethylnitrosamine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170629
[St] Status:MEDLINE
[do] DOI:10.1158/0008-5472.CAN-16-3538


  10 / 3182 MEDLINE  
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[PMID]:28628031
[Au] Autor:Van TM; Polykratis A; Straub BK; Kondylis V; Papadopoulou N; Pasparakis M
[Ad] Endereço:Institute for Genetics.
[Ti] Título:Kinase-independent functions of RIPK1 regulate hepatocyte survival and liver carcinogenesis.
[So] Source:J Clin Invest;127(7):2662-2677, 2017 Jun 30.
[Is] ISSN:1558-8238
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The mechanisms that regulate cell death and inflammation play an important role in liver disease and cancer. Receptor-interacting protein kinase 1 (RIPK1) induces apoptosis and necroptosis via kinase-dependent mechanisms and exhibits kinase-independent prosurvival and proinflammatory functions. Here, we have used genetic mouse models to study the role of RIPK1 in liver homeostasis, injury, and cancer. While ablating either RIPK1 or RelA in liver parenchymal cells (LPCs) did not cause spontaneous liver pathology, mice with combined deficiency of RIPK1 and RelA in LPCs showed increased hepatocyte apoptosis and developed spontaneous chronic liver disease and cancer that were independent of TNF receptor 1 (TNFR1) signaling. In contrast, mice with LPC-specific knockout of Ripk1 showed reduced diethylnitrosamine-induced (DEN-induced) liver tumorigenesis that correlated with increased DEN-induced hepatocyte apoptosis. Lack of RIPK1 kinase activity did not inhibit DEN-induced liver tumor formation, showing that kinase-independent functions of RIPK1 promote DEN-induced hepatocarcinogenesis. Moreover, mice lacking both RIPK1 and TNFR1 in LPCs displayed normal tumor formation in response to DEN, demonstrating that RIPK1 deficiency decreases DEN-induced liver tumor formation in a TNFR1-dependent manner. Therefore, these findings indicate that RIPK1 cooperates with NF-κB signaling to prevent TNFR1-independent hepatocyte apoptosis and the development of chronic liver disease and cancer, but acts downstream of TNFR1 signaling to promote DEN-induced liver tumorigenesis.
[Mh] Termos MeSH primário: Transformação Celular Neoplásica/metabolismo
Hepatócitos/enzimologia
Neoplasias Hepáticas Experimentais/enzimologia
Proteínas de Neoplasias/metabolismo
Proteína Serina-Treonina Quinases de Interação com Receptores/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Animais
Sobrevivência Celular/efeitos dos fármacos
Sobrevivência Celular/genética
Transformação Celular Neoplásica/induzido quimicamente
Transformação Celular Neoplásica/patologia
Dietilnitrosamina/toxicidade
Hepatócitos/patologia
Neoplasias Hepáticas Experimentais/induzido quimicamente
Neoplasias Hepáticas Experimentais/genética
Neoplasias Hepáticas Experimentais/patologia
Camundongos
Camundongos Transgênicos
Proteínas de Neoplasias/genética
Proteína Serina-Treonina Quinases de Interação com Receptores/genética
Receptores Tipo I de Fatores de Necrose Tumoral/genética
Receptores Tipo I de Fatores de Necrose Tumoral/metabolismo
Fator de Transcrição RelA/genética
Fator de Transcrição RelA/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Neoplasm Proteins); 0 (Receptors, Tumor Necrosis Factor, Type I); 0 (Rela protein, mouse); 0 (Tnfrsf1a protein, mouse); 0 (Transcription Factor RelA); 3IQ78TTX1A (Diethylnitrosamine); EC 2.7.11.1 (Receptor-Interacting Protein Serine-Threonine Kinases); EC 2.7.11.1 (Ripk1 protein, mouse)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171005
[Lr] Data última revisão:
171005
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170620
[St] Status:MEDLINE



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