Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 2 de 2
Filtrar
Mais filtros










Base de dados
Intervalo de ano de publicação
1.
Acta Pharmacol Sin ; 35(3): 363-72, 2014 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-24442146

RESUMO

AIM: To investigate the potential interactive effects of a high-fat diet (HFD) and valproic acid (VPA) on hepatic steatosis and hepatotoxicity in rats. METHODS: Male SD rats were orally administered VPA (100 or 500 mg·kg⁻¹·d⁻¹) combined with HFD or a standard diet for 8 weeks. Blood and liver samples were analyzed to determine lipid levels and hepatic function biomarkers using commercial kit assays. Low-molecular-weight compounds in serum, urine and bile samples were analyzed using a metabonomic approach based on GC/TOF-MS. RESULTS: HFD alone induced extensive hepatocyte steatosis and edema in rats, while VPA alone did not cause significant liver lesions. VPA significantly aggravated HFD-induced accumulation of liver lipids, and caused additional spotty or piecemeal necrosis, accompanied by moderate infiltration of inflammatory cells in the liver. Metabonomic analysis of serum, urine and bile samples revealed that HFD significantly increased the levels of amino acids, free fatty acids (FFAs) and 3-hydroxy-butanoic acid, whereas VPA markedly decreased the levels of amino acids, FFAs and the intermediate products of the tricarboxylic acid cycle (TCA) compared with the control group. HFD aggravated VPA-induced inhibition on lipid and amino acid metabolism. CONCLUSION: HFD magnifies VPA-induced impairment of mitochondrial ß-oxidation of FFAs and TCA, thereby increases hepatic steatosis and hepatotoxicity. The results suggest the patients receiving VPA treatment should be advised to avoid eating HFD.


Assuntos
Doença Hepática Induzida por Substâncias e Drogas/etiologia , Dieta Hiperlipídica , Interações Alimento-Droga , Hepatopatia Gordurosa não Alcoólica/etiologia , Ácido Valproico , Animais , Bile/metabolismo , Biomarcadores/sangue , Biomarcadores/urina , Doença Hepática Induzida por Substâncias e Drogas/metabolismo , Doença Hepática Induzida por Substâncias e Drogas/patologia , Ciclo do Ácido Cítrico , Modelos Animais de Doenças , Ácidos Graxos não Esterificados/metabolismo , Cromatografia Gasosa-Espectrometria de Massas , Fígado/metabolismo , Fígado/patologia , Masculino , Metabolômica/métodos , Mitocôndrias Hepáticas/metabolismo , Hepatopatia Gordurosa não Alcoólica/metabolismo , Hepatopatia Gordurosa não Alcoólica/patologia , Ratos Sprague-Dawley , Fatores de Risco , Espectrometria de Massas por Ionização e Dessorção a Laser Assistida por Matriz
2.
Guang Pu Xue Yu Guang Pu Fen Xi ; 31(12): 3315-8, 2011 Dec.
Artigo em Chinês | MEDLINE | ID: mdl-22295785

RESUMO

Ce(1-x)(Fe(0.5)La(0.5))xO(2-delta) solid solutions were obtained via hydrothermal method. The structure of the solid solutions and the cell parameters were characterized by XRD analysis technique, the electron transition properties and doping effectswere measured by UV-Vis diffraction spectrum and Raman spectrum technique. XRD results showed that Ce(1-x)(Fe(0.5)La(0.5))xO(2-delta) id solutions exhibited cubic fluorite structure till the doping content increased to 0.30. Tiny Fe2O3 phase was observed when x = 0.30. The particle size was kept nanoscaled, and location of different kind of doping ions in CeO2 lattice was discussed. By increasing the doping content, the cell parameter was kept increasing gradually till x = 0.18, then it remained almost constant. The UV-Vis diffraction spectrum analysis showed that the absorption threshold edge redshifted, the band gap energy decreased with increasing the doping content. The valence of Fe ions in the lattice of CeO2 was +3. The F2g Raman mode also showed a downshift, and the peak gradually became broader, which further proved the influence of the dopant.

SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA
...