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1.
Eur Rev Med Pharmacol Sci ; 22(13): 4341-4349, 2018 07.
Artigo em Inglês | MEDLINE | ID: mdl-30024623

RESUMO

OBJECTIVE: Propofol is one of the most commonly used intravenous anesthetic agents used in cancer resections, but the effect of propofol on non-small cell lung cancer (NSCLC) remains unclear. Previous researches have reported that propofol can inhibit extracellular signal-regulated kinase (ERK) 1/2 phosphorylation or activate p53-upregulated modulator of apoptosis (PUMA) signaling, resulting in apoptosis. In addition, PUMA is negatively regulated by ERK1/2 activation. In the present work, we determined the effect of propofol on NSCLC A549 cells and explored its signaling pathway. MATERIALS AND METHODS: A549 cells were treated with different concentrations of propofol (1-10 µg/mL) for 6 h. After washing, cells were cultured in Dulbecco's Modified Eagle Medium supplemented with 10% fetal bovine serum and antibiotics for another 72 h. Cell survival and apoptosis were determined by MTT, flow cytometry, and TUNEL analyses. To assess whether propofol functions via ERK1/2 and PUMA signaling pathways, A549 cells were transfected with small interfering RNA (siRNA) to target PUMA, or treated with human recombinant ERK1/2 (hrERK1/2) to activate ERK1/2. RESULTS: Propofol treatment inhibited viability and induced apoptosis of A549 cells in a dose-dependent manner in vitro. Propofol inhibited phosphorylation of ERK1/2 (pERK1/2) and increased ERK1/2-dependent PUMA expression. Knockdown of PUMA by siRNA or treatment with hrERK1/2 to activate ERK1/2 blocked propofol-induced apoptosis and cell viability. Upregulation of PUMA expression by propofol requires pERK1/2 inactivation. CONCLUSIONS: Propofol inhibits viability and induces apoptosis of A549 cells via an ERK1/2-dependent PUMA signaling.


Assuntos
Apoptose/efeitos dos fármacos , Propofol/farmacologia , Transdução de Sinais/efeitos dos fármacos , Regulação para Cima/efeitos dos fármacos , Células A549 , Proteínas Reguladoras de Apoptose/metabolismo , Carcinoma Pulmonar de Células não Pequenas/metabolismo , Carcinoma Pulmonar de Células não Pequenas/patologia , Humanos , Neoplasias Pulmonares/metabolismo , Neoplasias Pulmonares/patologia , Proteína Quinase 1 Ativada por Mitógeno/antagonistas & inibidores , Proteína Quinase 1 Ativada por Mitógeno/genética , Proteína Quinase 1 Ativada por Mitógeno/metabolismo , Proteína Quinase 3 Ativada por Mitógeno/antagonistas & inibidores , Proteína Quinase 3 Ativada por Mitógeno/genética , Proteína Quinase 3 Ativada por Mitógeno/metabolismo , Proteínas Proto-Oncogênicas/metabolismo , Interferência de RNA , RNA Interferente Pequeno/metabolismo , Ativação Transcricional , Proteína Supressora de Tumor p53/metabolismo
2.
J Hand Surg Eur Vol ; 40(1): 16-23, 2015 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-25427554

RESUMO

Intra-articular fractures or fracture dislocations of the proximal interphalangeal joint are difficult clinically because the bone and soft tissue structures are small and intricate. Suboptimal treatment of intra-articular fractures typically leads to functional impairment of the hand. This article reviews the current methods of treatment, together with the senior author's experience in treating difficult proximal interphalangeal joint fractures and dislocations. Besides conservative treatments, surgical treatments include open or closed reduction with traditional Osteosynthesis, such as K-wires, screws or plates. Among recent developments are the percutaneous application of thin cannulated compression screws and novel dynamic external fixators. After a preferred minimally invasive treatment with stable reconstruction of the articular surface, sufficient aftercare is necessary to improve surgical outcomes.


Assuntos
Artroplastia , Articulações dos Dedos , Fixação Interna de Fraturas , Fraturas Intra-Articulares/cirurgia , Luxações Articulares/cirurgia , Humanos , Fraturas Intra-Articulares/complicações , Fraturas Intra-Articulares/diagnóstico por imagem , Luxações Articulares/complicações , Luxações Articulares/diagnóstico por imagem , Radiografia
3.
Mutat Res ; 226(2): 99-102, 1989 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-2499785

RESUMO

The enhancing effect of tetrandrine, an antisilicosis, antitumor and antiinflammatory drug, on the genotoxic activity of two known mutagens, mitomycin C (MMC) and cigarette-smoke condensate (CSC), has been studied using cultured Chinese hamster lung (V79) cells. The sister-chromatid exchange (SCE) was used as genetic endpoint to measure genotoxicity. One-day cultured cells were exposed to the test chemicals for 3 h with or without metabolic activation. The results show that the frequencies of SCE induced by MMC or CSC were enhanced by tetrandrine. The percent of enhancement was dependent on the concentration of tetrandrine.


Assuntos
Alcaloides/toxicidade , Benzilisoquinolinas , Mitomicinas/toxicidade , Troca de Cromátide Irmã/efeitos dos fármacos , Fumaça , Animais , Biotransformação , Linhagem Celular , Cricetinae , Sinergismo Farmacológico , Técnicas In Vitro , Mitomicina , Testes de Mutagenicidade , Plantas Tóxicas , Nicotiana
4.
Mutat Res ; 260(3): 233-8, 1991 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-1714540

RESUMO

Diesel-exhaust particles from two sources were dispersed in aqueous mixtures of dipalmitoyl phosphatidyl choline, a major component of pulmonary surfactant, and were tested for genotoxicity. Diesel samples from the same sources were extracted with dichloromethane and transferred into dimethyl sulfoxide and subjected to the same assays. Both types of extractions yielded similar results in both the Salmonella mutagenicity assay and the sister-chromatid exchange assay using V79 cells. After separation of the samples into supernatant and sediment fractions, the activity of both diesel samples was shown to reside exclusively in the supernatant fraction for the solvent-extracted samples, and exclusively in the sedimented fraction for surfactant dispersed samples. These findings indicate that genotoxic activity associated with diesel particles inhaled into the lung may be made bioavailable by virtue of the solubilization/dispersion properties of pulmonary surfactant components.


Assuntos
Poluentes Atmosféricos/toxicidade , Gasolina/toxicidade , Mutagênicos , Surfactantes Pulmonares/química , Emissões de Veículos/toxicidade , Animais , Cricetinae , Cricetulus , Testes de Mutagenicidade , Fosfatidilcolinas/química , Salmonella typhimurium/genética , Troca de Cromátide Irmã
5.
Mutat Res ; 224(1): 5-10, 1989 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-2770774

RESUMO

The genotoxicity of tetrandrine, a drug potentially useful for the treatment of silicosis, was studied using the micronucleus and the sister-chromatid exchange (SCE) assay systems. Cultured Chinese hamster lung (V79) cells were used for the in vitro micronucleus and sister-chromatid exchange studies. Mouse bone marrow was used for the in vivo micronucleus assay and mouse spleen cells for the in vivo/in vitro sister-chromatid exchange analysis. The results show that SCE levels in V79 and in spleen cells were significantly elevated by treatment with tetrandrine at doses above 0.08 mg/ml and 100 mg/kg bw, respectively. Increased tetradrine-induced SCE in vitro was metabolic activation dependent. Tetrandrine failed to induce micronuclei at any of the doses tested. A decrease of replicative index with an increase in the concentration of tetrandrine was found both in vitro and in vivo. These results indicate that tetrandrine is a weak indirect-acting genotoxicant.


Assuntos
Alcaloides/toxicidade , Benzilisoquinolinas , Testes para Micronúcleos , Troca de Cromátide Irmã/efeitos dos fármacos , Alcaloides/farmacocinética , Animais , Biotransformação , Medula Óssea/efeitos dos fármacos , Medula Óssea/ultraestrutura , Divisão Celular/efeitos dos fármacos , Fibroblastos/efeitos dos fármacos , Humanos , Masculino , Camundongos , Pessoa de Meia-Idade , Baço/citologia , Baço/efeitos dos fármacos
7.
Teratog Carcinog Mutagen ; 12(5): 223-30, 1992.
Artigo em Inglês | MEDLINE | ID: mdl-1363495

RESUMO

Transplacental cytogenetic effects of triethylenemelamine (TEM), benzene, and vinblastine on maternal mice and their fetuses have been investigated using micronucleus and sister chromatid exchange (SCE) as genetic endpoints. CD-1 mice were treated on day 14 and 15 of gestation with TEM (0.125, 0.25, and 0.5 mg/kg), benzene (439,878, and 1,318 mg/kg), and vinblastine (0.5, 1, and 2 mg/kg) by intraperitoneal injection at 24 hr intervals, and sacrificed 40 hr after the first injection. Erythrocytic precursor cells in maternal bone marrow and fetal livers (2-4) from each pregnant mouse were used for the micronucleus and/or the SCE analyses. Significant dose-related increases in both micronuclei and SCE were found in maternal bone marrow and fetal liver following TEM treatment. Benzene at the highest dose (1,318 mg/kg) also caused a significant increase in micronuclei and SCE in both maternal bone marrow and fetal liver cells. The embryonic genotoxic effect of TEM was much higher than that of benzene for both genetic endpoints, and the frequency of micronuclei induced by benzene was higher in fetal liver than in maternal bone marrow cells. Vinblastine, a spindle poison, induced micronuclei but not SCE. Micronuclei induction by vinblastine was 7 fold greater in maternal bone marrow than in fetal liver cells. All three chemicals were cytotoxic in maternal bone marrow cells, but not in fetal liver cells except for TEM, which showed a weak cytotoxicity in fetal liver cells in the micronucleus assay. These results indicate that TEM, benzene, and vinblastine are transplacental genotoxicants in mice.


Assuntos
Benzeno/toxicidade , Troca Materno-Fetal , Mutagênicos/administração & dosagem , Trietilenomelamina/toxicidade , Vimblastina/toxicidade , Animais , Benzeno/administração & dosagem , Medula Óssea/efeitos dos fármacos , Células da Medula Óssea , Feminino , Injeções Intraperitoneais , Fígado/citologia , Fígado/efeitos dos fármacos , Camundongos , Camundongos Endogâmicos , Testes para Micronúcleos , Gravidez , Troca de Cromátide Irmã , Trietilenomelamina/administração & dosagem , Vimblastina/administração & dosagem
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